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gal3  (R&D Systems)


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    R&D Systems gal3
    Infarct size correlations with peri‐infarct immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 <t>(Gal3),</t> and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 in a standard environment (SE) mouse at peri‐infarct area (at ×20 magnification). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at peri‐infarct area (at ×20 magnification). (C) Quantification of indirect infarct area measurements. (D) Correlation of infarct area with Neuroscore per group. (E) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (H) Correlation of infarct area with Gal3 coverage. (I) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (J) Correlation of infarct area with P2RY12 coverage. Peri‐infarct area is shown as dashed red lines in A and B. In (C, E, G, and I), values are expressed as individual experimental replicates with mean ± SEM. In (D, F, H, and J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C, E, G, and I), unpaired t ‐test was performed. n = 4/6 mice in SE and n = 7 mice in EE (2 mice in SE were not behaviorally characterized). P ‐values and r values are expressed with 3 decimals. P ‐values were not corrected for multiple comparisons.
    Gal3, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/gal3/product/R&D Systems
    Average 94 stars, based on 63 article reviews
    gal3 - by Bioz Stars, 2026-05
    94/100 stars

    Images

    1) Product Images from "Environmental enrichment modulates chronic poststroke inflammation and links white matter TREM2‐positive microglia in recovery in mice"

    Article Title: Environmental enrichment modulates chronic poststroke inflammation and links white matter TREM2‐positive microglia in recovery in mice

    Journal: Neuroprotection

    doi: 10.1002/nep3.70028

    Infarct size correlations with peri‐infarct immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 in a standard environment (SE) mouse at peri‐infarct area (at ×20 magnification). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at peri‐infarct area (at ×20 magnification). (C) Quantification of indirect infarct area measurements. (D) Correlation of infarct area with Neuroscore per group. (E) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (H) Correlation of infarct area with Gal3 coverage. (I) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (J) Correlation of infarct area with P2RY12 coverage. Peri‐infarct area is shown as dashed red lines in A and B. In (C, E, G, and I), values are expressed as individual experimental replicates with mean ± SEM. In (D, F, H, and J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C, E, G, and I), unpaired t ‐test was performed. n = 4/6 mice in SE and n = 7 mice in EE (2 mice in SE were not behaviorally characterized). P ‐values and r values are expressed with 3 decimals. P ‐values were not corrected for multiple comparisons.
    Figure Legend Snippet: Infarct size correlations with peri‐infarct immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 in a standard environment (SE) mouse at peri‐infarct area (at ×20 magnification). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at peri‐infarct area (at ×20 magnification). (C) Quantification of indirect infarct area measurements. (D) Correlation of infarct area with Neuroscore per group. (E) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (H) Correlation of infarct area with Gal3 coverage. (I) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (J) Correlation of infarct area with P2RY12 coverage. Peri‐infarct area is shown as dashed red lines in A and B. In (C, E, G, and I), values are expressed as individual experimental replicates with mean ± SEM. In (D, F, H, and J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C, E, G, and I), unpaired t ‐test was performed. n = 4/6 mice in SE and n = 7 mice in EE (2 mice in SE were not behaviorally characterized). P ‐values and r values are expressed with 3 decimals. P ‐values were not corrected for multiple comparisons.

    Techniques Used: Immunofluorescence, Binding Assay, Immunostaining

    Infarct size correlations with white matter immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 (at ×20 magnification) in a standard environment (SE) mouse at white matter area (corpus callosum + external capsule). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at white matter area (at ×20 magnification). (C) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (D) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (E) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Correlation of infarct area with Gal3 coverage. (H) Correlation of infarct area with P2RY12 coverage. White matter area is shown as dashed red lines in (A, B). In (C–E) values are expressed as individual experimental replicates with mean ± SEM. In (F–H) values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C–E) unpaired t ‐test was performed n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.
    Figure Legend Snippet: Infarct size correlations with white matter immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 (at ×20 magnification) in a standard environment (SE) mouse at white matter area (corpus callosum + external capsule). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at white matter area (at ×20 magnification). (C) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (D) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (E) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Correlation of infarct area with Gal3 coverage. (H) Correlation of infarct area with P2RY12 coverage. White matter area is shown as dashed red lines in (A, B). In (C–E) values are expressed as individual experimental replicates with mean ± SEM. In (F–H) values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C–E) unpaired t ‐test was performed n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.

    Techniques Used: Immunofluorescence, Binding Assay, Immunostaining

    Quantification of peri‐infarct myelin debris, white matter myelin loss, and their correlations with microglial markers. (A) Representative myelin staining in a standard environment mouse (at ×20 magnification). (B) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in a standard environment (SE) mouse. (C) Representative myelin staining in an enriched environment mouse (at ×20 magnification). (D) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in an enriched environment (EE) mouse. (E) Myelin debris coverage quantification measured as the percentage of peri‐infarct image covered by Black Gold Myelin dark debris area (%area). (F) Correlation of infarct area with myelin debris coverage. (G) Myelin loss quantification measured as the percentage of myelin lost at corpus callosum in ipsilateral versus contralateral infarct. (H) Correlation of infarct area with myelin loss. (I) Correlations of myelin debris with ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), purinergic receptor P2Y12 (P2RY12), cluster of differentiation 68 (CD68), and triggering receptor expressed on myeloid cells 2 (TREM2) coverages at peri‐infarct. (J) Correlations of myelin loss with Iba1, Gal3, P2RY12, CD68, and TREM2 coverages at white matter. In (E, G) values are expressed as individual experimental replicates with mean ± SEM. In (F, H, I, J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (E, G) unpaired t‐test was performed. n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.
    Figure Legend Snippet: Quantification of peri‐infarct myelin debris, white matter myelin loss, and their correlations with microglial markers. (A) Representative myelin staining in a standard environment mouse (at ×20 magnification). (B) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in a standard environment (SE) mouse. (C) Representative myelin staining in an enriched environment mouse (at ×20 magnification). (D) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in an enriched environment (EE) mouse. (E) Myelin debris coverage quantification measured as the percentage of peri‐infarct image covered by Black Gold Myelin dark debris area (%area). (F) Correlation of infarct area with myelin debris coverage. (G) Myelin loss quantification measured as the percentage of myelin lost at corpus callosum in ipsilateral versus contralateral infarct. (H) Correlation of infarct area with myelin loss. (I) Correlations of myelin debris with ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), purinergic receptor P2Y12 (P2RY12), cluster of differentiation 68 (CD68), and triggering receptor expressed on myeloid cells 2 (TREM2) coverages at peri‐infarct. (J) Correlations of myelin loss with Iba1, Gal3, P2RY12, CD68, and TREM2 coverages at white matter. In (E, G) values are expressed as individual experimental replicates with mean ± SEM. In (F, H, I, J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (E, G) unpaired t‐test was performed. n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.

    Techniques Used: Staining, Binding Assay



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    Spinal cord injury (SCI) increases galectin-3 (GAL3) expression in spinal neurons. (A) Relative GAL3 mRNA expression in the spinal cord after SCI. One-way ANOVA, n = 3/group. (B) Western blot analysis of GAL3 protein after SCI. (C) Statistical data show relative GAL3 protein expression after SCI. One-way ANOVA, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) detection of GAL3 protein levels in rat serum after SCI. One-way ANOVA, n = 6/group. (E) Immunofluorescence microscopy reveals GAL3 co-localization with NeuN post-SCI. (F) Fluorescence intensity of GAL3 after SCI. One-way ANOVA, n = 3/group. (G,H) Immunofluorescence double staining of GAL3 and GFAP (G) or IBA1 (H) after SCI. (I) Determination of optimal glutamate concentration and duration using CCK8 assay. (J) Relative GAL3 mRNA expression in the glutamate-stimulated spinal cord neurons. Unpaired Student’s t -test, n = 3/group. (K) Western blot analysis of GAL3 protein in neuronal injury model. (L) Relative GAL3 protein expression in neuronal injury model. Unpaired Student’s t -test, n = 3/group. (M) ELISA detection of GAL3 in cell supernatant of neuronal injury model. Unpaired Student’s t -test, n = 3/group. (N) Immunofluorescence microscopy showing GAL3 expression in neuronal injury model. (O) Quantification of GAL3 fluorescence intensity in neuronal injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Spinal cord injury (SCI) increases galectin-3 (GAL3) expression in spinal neurons. (A) Relative GAL3 mRNA expression in the spinal cord after SCI. One-way ANOVA, n = 3/group. (B) Western blot analysis of GAL3 protein after SCI. (C) Statistical data show relative GAL3 protein expression after SCI. One-way ANOVA, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) detection of GAL3 protein levels in rat serum after SCI. One-way ANOVA, n = 6/group. (E) Immunofluorescence microscopy reveals GAL3 co-localization with NeuN post-SCI. (F) Fluorescence intensity of GAL3 after SCI. One-way ANOVA, n = 3/group. (G,H) Immunofluorescence double staining of GAL3 and GFAP (G) or IBA1 (H) after SCI. (I) Determination of optimal glutamate concentration and duration using CCK8 assay. (J) Relative GAL3 mRNA expression in the glutamate-stimulated spinal cord neurons. Unpaired Student’s t -test, n = 3/group. (K) Western blot analysis of GAL3 protein in neuronal injury model. (L) Relative GAL3 protein expression in neuronal injury model. Unpaired Student’s t -test, n = 3/group. (M) ELISA detection of GAL3 in cell supernatant of neuronal injury model. Unpaired Student’s t -test, n = 3/group. (N) Immunofluorescence microscopy showing GAL3 expression in neuronal injury model. (O) Quantification of GAL3 fluorescence intensity in neuronal injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Microscopy, Fluorescence, Double Staining, Concentration Assay, CCK-8 Assay

    Galectin-3 (GAL3) contributes to spinal cord injury (SCI)-induced motor impairment. (A) The mRNA level of GAL3 after siR-GAL3 treatment. Unpaired Student’s t -test, n = 3/group. (B) Western blot shows the protein level of GAL3 after siR-GAL3 treatment. (C) Statistical data show the knockdown of GAL3 by siRNA. Unpaired Student’s t -test, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) shows the secretory GAL3 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (E) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. (F) The inclined plane angles were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-GAL3 group was compared with SCI + Vehicle group, ** P < 0.01, *** P < 0.001; when SCI + TD139 group was compared with SCI + Vehicle group, # P < 0.05, ### P < 0.001; when SCI + GAL3 group was compared with SCI + Vehicle group, + P < 0.05,++ P < 0.01.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) contributes to spinal cord injury (SCI)-induced motor impairment. (A) The mRNA level of GAL3 after siR-GAL3 treatment. Unpaired Student’s t -test, n = 3/group. (B) Western blot shows the protein level of GAL3 after siR-GAL3 treatment. (C) Statistical data show the knockdown of GAL3 by siRNA. Unpaired Student’s t -test, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) shows the secretory GAL3 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (E) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. (F) The inclined plane angles were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-GAL3 group was compared with SCI + Vehicle group, ** P < 0.01, *** P < 0.001; when SCI + TD139 group was compared with SCI + Vehicle group, # P < 0.05, ### P < 0.001; when SCI + GAL3 group was compared with SCI + Vehicle group, + P < 0.05,++ P < 0.01.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Western Blot, Knockdown, Enzyme-linked Immunosorbent Assay

    Galectin-3 (GAL3) is closely related to programmed cell death after spinal cord injury (SCI). (A) The four datasets before the batch effect were removed. (B) The four datasets after the batch effect were removed. (C) Volcano map shows DEGs in the SCI dataset. (D) Biological Process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the SCI dataset. Each column represents the P -value score of the pathway between the Sham group and the SCI group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (E) Protein-Protein Interaction Networks (PPI) analysis of differentially expressed genes (DEGs) in SCI dataset. In the PPI nodes, red signifies an increase in expression level, while blue indicates a decrease. The intensity of the color corresponds to the magnitude of the differential expression, with darker shades representing a higher differential expression multiple.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) is closely related to programmed cell death after spinal cord injury (SCI). (A) The four datasets before the batch effect were removed. (B) The four datasets after the batch effect were removed. (C) Volcano map shows DEGs in the SCI dataset. (D) Biological Process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the SCI dataset. Each column represents the P -value score of the pathway between the Sham group and the SCI group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (E) Protein-Protein Interaction Networks (PPI) analysis of differentially expressed genes (DEGs) in SCI dataset. In the PPI nodes, red signifies an increase in expression level, while blue indicates a decrease. The intensity of the color corresponds to the magnitude of the differential expression, with darker shades representing a higher differential expression multiple.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Expressing, Quantitative Proteomics

    Galectin-3 (GAL3) regulates neuronal autophagy. (A) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in neurons. (B-E) Quantification of western blot detection of GAL3 (B) , ATG7 (C) , P62 (D) , and LC3 II/I (E) in neurons. One-way ANOVA, n = 3/group. (F) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in the spinal cord of rats. (G–I) Quantification of western blot detection of ATG7 (G) , P62 (H) , and LC3 II/I (I) in the spinal cord of rats. One-way ANOVA, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) regulates neuronal autophagy. (A) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in neurons. (B-E) Quantification of western blot detection of GAL3 (B) , ATG7 (C) , P62 (D) , and LC3 II/I (E) in neurons. One-way ANOVA, n = 3/group. (F) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in the spinal cord of rats. (G–I) Quantification of western blot detection of ATG7 (G) , P62 (H) , and LC3 II/I (I) in the spinal cord of rats. One-way ANOVA, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Western Blot

    Sequencing analysis of spinal cord neurons with galectin-3 (GAL3) knocked down. (A) Volcano map shows differential expression genes (DEGs) in the neuron dataset. (B) Biological process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the neuron dataset. Each column represents the P -value score of the pathway between the Sham group and the spinal cord injury (SCI) group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (C) The Protein-Protein Interaction Networks (PPI) analysis of DEGs in the neuron dataset. In the PPI nodes, red indicates that the expression level increases and blue indicates that the expression level decreases. The darker the color, the greater the differential expression multiple.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Sequencing analysis of spinal cord neurons with galectin-3 (GAL3) knocked down. (A) Volcano map shows differential expression genes (DEGs) in the neuron dataset. (B) Biological process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the neuron dataset. Each column represents the P -value score of the pathway between the Sham group and the spinal cord injury (SCI) group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (C) The Protein-Protein Interaction Networks (PPI) analysis of DEGs in the neuron dataset. In the PPI nodes, red indicates that the expression level increases and blue indicates that the expression level decreases. The darker the color, the greater the differential expression multiple.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Sequencing, Quantitative Proteomics, Expressing

    Galectin-3 (GAL3) interacts with Cell-division-cycle-42 (CDC42) to regulate neuronal autophagy. (A) Intersected 29 core nodes from the neuron dataset with 22 core nodes from the spinal cord injury (SCI) dataset by the Venn diagram. (B) Correlation analysis between GAL3 and CDC42 expression level in SCI dataset. (C) Correlation analysis between GAL3 and CDC42 expression level in the neuron dataset. (D) Co-immunoprecipitation (Co-IP) shows a direct interaction between GAL3 and CDC42 in the glutamate-induced neuronal damage model. (E) Western blot shows the expression of CDC42, ATG7, P62, and LC3 II/I. (F–I) Quantification of western blot detection of CDC42 (F) , ATG7 (G) , P62 (H) , and LC3 II/I (I) . One-way ANOVA, n = 3/group. (J) Enzyme-linked immunosorbent assay (ELISA) detection of CDC42 in cell supernatant of GAL3-injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) interacts with Cell-division-cycle-42 (CDC42) to regulate neuronal autophagy. (A) Intersected 29 core nodes from the neuron dataset with 22 core nodes from the spinal cord injury (SCI) dataset by the Venn diagram. (B) Correlation analysis between GAL3 and CDC42 expression level in SCI dataset. (C) Correlation analysis between GAL3 and CDC42 expression level in the neuron dataset. (D) Co-immunoprecipitation (Co-IP) shows a direct interaction between GAL3 and CDC42 in the glutamate-induced neuronal damage model. (E) Western blot shows the expression of CDC42, ATG7, P62, and LC3 II/I. (F–I) Quantification of western blot detection of CDC42 (F) , ATG7 (G) , P62 (H) , and LC3 II/I (I) . One-way ANOVA, n = 3/group. (J) Enzyme-linked immunosorbent assay (ELISA) detection of CDC42 in cell supernatant of GAL3-injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Expressing, Immunoprecipitation, Co-Immunoprecipitation Assay, Western Blot, Enzyme-linked Immunosorbent Assay

    Cell-division-cycle-42 (CDC42) contributes to spinal cord injury (SCI)-induced motor function impairment. (A) The mRNA level after siR-CDC42 treatment. Unpaired Student’s t -test, n = 3/group. (B) Enzyme-linked immunosorbent assay (ELISA) shows the secretory CDC42 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (C) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. (D) The inclined plane angles were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-CDC42 group was compared with SCI + Vehicle group, * P < 0.05, ** P < 0.01, *** P < 0.001; when SCI + ML141 group was compared with SCI + Vehicle group, ## P < 0.01, ### P < 0.001. (E,F) Detection of the protein expression level of galectin-3 (GAL3) (E) and CDC42 (F) in serum of healthy volunteers and SCI patients by ELISA. Unpaired Student’s t -test, n = 8/group. *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Cell-division-cycle-42 (CDC42) contributes to spinal cord injury (SCI)-induced motor function impairment. (A) The mRNA level after siR-CDC42 treatment. Unpaired Student’s t -test, n = 3/group. (B) Enzyme-linked immunosorbent assay (ELISA) shows the secretory CDC42 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (C) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. (D) The inclined plane angles were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-CDC42 group was compared with SCI + Vehicle group, * P < 0.05, ** P < 0.01, *** P < 0.001; when SCI + ML141 group was compared with SCI + Vehicle group, ## P < 0.01, ### P < 0.001. (E,F) Detection of the protein expression level of galectin-3 (GAL3) (E) and CDC42 (F) in serum of healthy volunteers and SCI patients by ELISA. Unpaired Student’s t -test, n = 8/group. *** P < 0.001.

    Article Snippet: SCI + GAL3 , 8 , SCI + GAL3 (400 mg/kg, No. HY- P77684 , MedChemExpress).

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing

    Infarct size correlations with peri‐infarct immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 in a standard environment (SE) mouse at peri‐infarct area (at ×20 magnification). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at peri‐infarct area (at ×20 magnification). (C) Quantification of indirect infarct area measurements. (D) Correlation of infarct area with Neuroscore per group. (E) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (H) Correlation of infarct area with Gal3 coverage. (I) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (J) Correlation of infarct area with P2RY12 coverage. Peri‐infarct area is shown as dashed red lines in A and B. In (C, E, G, and I), values are expressed as individual experimental replicates with mean ± SEM. In (D, F, H, and J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C, E, G, and I), unpaired t ‐test was performed. n = 4/6 mice in SE and n = 7 mice in EE (2 mice in SE were not behaviorally characterized). P ‐values and r values are expressed with 3 decimals. P ‐values were not corrected for multiple comparisons.

    Journal: Neuroprotection

    Article Title: Environmental enrichment modulates chronic poststroke inflammation and links white matter TREM2‐positive microglia in recovery in mice

    doi: 10.1002/nep3.70028

    Figure Lengend Snippet: Infarct size correlations with peri‐infarct immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 in a standard environment (SE) mouse at peri‐infarct area (at ×20 magnification). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at peri‐infarct area (at ×20 magnification). (C) Quantification of indirect infarct area measurements. (D) Correlation of infarct area with Neuroscore per group. (E) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (H) Correlation of infarct area with Gal3 coverage. (I) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (J) Correlation of infarct area with P2RY12 coverage. Peri‐infarct area is shown as dashed red lines in A and B. In (C, E, G, and I), values are expressed as individual experimental replicates with mean ± SEM. In (D, F, H, and J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C, E, G, and I), unpaired t ‐test was performed. n = 4/6 mice in SE and n = 7 mice in EE (2 mice in SE were not behaviorally characterized). P ‐values and r values are expressed with 3 decimals. P ‐values were not corrected for multiple comparisons.

    Article Snippet: They were then incubated at 4°C overnight with one of the following antibodies: Iba1 (1:500, rabbit, Cat# 016‐26721; Wako), Gal3 (1:750, goat, Cat# AF1197; R&D Systems) P2RY12 (1:200, rat, Cat# S16007D; Biolegend).

    Techniques: Immunofluorescence, Binding Assay, Immunostaining

    Infarct size correlations with white matter immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 (at ×20 magnification) in a standard environment (SE) mouse at white matter area (corpus callosum + external capsule). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at white matter area (at ×20 magnification). (C) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (D) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (E) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Correlation of infarct area with Gal3 coverage. (H) Correlation of infarct area with P2RY12 coverage. White matter area is shown as dashed red lines in (A, B). In (C–E) values are expressed as individual experimental replicates with mean ± SEM. In (F–H) values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C–E) unpaired t ‐test was performed n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.

    Journal: Neuroprotection

    Article Title: Environmental enrichment modulates chronic poststroke inflammation and links white matter TREM2‐positive microglia in recovery in mice

    doi: 10.1002/nep3.70028

    Figure Lengend Snippet: Infarct size correlations with white matter immunofluorescence analysis of ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), and purinergic receptor P2Y12 (P2RY12). (A) Representative immunostaining of 4′,6‐diamidino‐2‐phenylindole (DAPI), Iba1, P2RY12, and Gal3 (at ×20 magnification) in a standard environment (SE) mouse at white matter area (corpus callosum + external capsule). (B) Representative immunostaining of DAPI, Iba1, P2RY12, and Gal3 in an enriched environment (EE) mouse at white matter area (at ×20 magnification). (C) Iba1 coverage quantification measured as the percentage of image covered by Iba1 area (%area). (D) Gal3 coverage quantification measured as the percentage of image covered by Iba1 + Gal3 + area (%area). (E) P2RY12 coverage quantification measured as the percentage of image covered by Iba1 + P2RY12 + area (%area). (F) Correlation of infarct area with Iba1 coverage. (G) Correlation of infarct area with Gal3 coverage. (H) Correlation of infarct area with P2RY12 coverage. White matter area is shown as dashed red lines in (A, B). In (C–E) values are expressed as individual experimental replicates with mean ± SEM. In (F–H) values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (C–E) unpaired t ‐test was performed n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.

    Article Snippet: They were then incubated at 4°C overnight with one of the following antibodies: Iba1 (1:500, rabbit, Cat# 016‐26721; Wako), Gal3 (1:750, goat, Cat# AF1197; R&D Systems) P2RY12 (1:200, rat, Cat# S16007D; Biolegend).

    Techniques: Immunofluorescence, Binding Assay, Immunostaining

    Quantification of peri‐infarct myelin debris, white matter myelin loss, and their correlations with microglial markers. (A) Representative myelin staining in a standard environment mouse (at ×20 magnification). (B) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in a standard environment (SE) mouse. (C) Representative myelin staining in an enriched environment mouse (at ×20 magnification). (D) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in an enriched environment (EE) mouse. (E) Myelin debris coverage quantification measured as the percentage of peri‐infarct image covered by Black Gold Myelin dark debris area (%area). (F) Correlation of infarct area with myelin debris coverage. (G) Myelin loss quantification measured as the percentage of myelin lost at corpus callosum in ipsilateral versus contralateral infarct. (H) Correlation of infarct area with myelin loss. (I) Correlations of myelin debris with ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), purinergic receptor P2Y12 (P2RY12), cluster of differentiation 68 (CD68), and triggering receptor expressed on myeloid cells 2 (TREM2) coverages at peri‐infarct. (J) Correlations of myelin loss with Iba1, Gal3, P2RY12, CD68, and TREM2 coverages at white matter. In (E, G) values are expressed as individual experimental replicates with mean ± SEM. In (F, H, I, J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (E, G) unpaired t‐test was performed. n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.

    Journal: Neuroprotection

    Article Title: Environmental enrichment modulates chronic poststroke inflammation and links white matter TREM2‐positive microglia in recovery in mice

    doi: 10.1002/nep3.70028

    Figure Lengend Snippet: Quantification of peri‐infarct myelin debris, white matter myelin loss, and their correlations with microglial markers. (A) Representative myelin staining in a standard environment mouse (at ×20 magnification). (B) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in a standard environment (SE) mouse. (C) Representative myelin staining in an enriched environment mouse (at ×20 magnification). (D) Enlarged views of infarct contralateral cortical (green square) and peri‐infarct (red square) myelin in an enriched environment (EE) mouse. (E) Myelin debris coverage quantification measured as the percentage of peri‐infarct image covered by Black Gold Myelin dark debris area (%area). (F) Correlation of infarct area with myelin debris coverage. (G) Myelin loss quantification measured as the percentage of myelin lost at corpus callosum in ipsilateral versus contralateral infarct. (H) Correlation of infarct area with myelin loss. (I) Correlations of myelin debris with ionized calcium binding adaptor molecule 1 (Iba1), galectin‐3 (Gal3), purinergic receptor P2Y12 (P2RY12), cluster of differentiation 68 (CD68), and triggering receptor expressed on myeloid cells 2 (TREM2) coverages at peri‐infarct. (J) Correlations of myelin loss with Iba1, Gal3, P2RY12, CD68, and TREM2 coverages at white matter. In (E, G) values are expressed as individual experimental replicates with mean ± SEM. In (F, H, I, J), values are expressed as individual experimental replicates with simple linear regression lines; Pearson correlation's r value with p ‐value are also shown. In (E, G) unpaired t‐test was performed. n = 6 mice in SE and n = 7 mice in EE. p ‐Values and r values are expressed with 3 decimals. p ‐Values were not corrected for multiple comparisons.

    Article Snippet: They were then incubated at 4°C overnight with one of the following antibodies: Iba1 (1:500, rabbit, Cat# 016‐26721; Wako), Gal3 (1:750, goat, Cat# AF1197; R&D Systems) P2RY12 (1:200, rat, Cat# S16007D; Biolegend).

    Techniques: Staining, Binding Assay

    Spinal cord injury (SCI) increases galectin-3 (GAL3) expression in spinal neurons. (A) Relative GAL3 mRNA expression in the spinal cord after SCI. One-way ANOVA, n = 3/group. (B) Western blot analysis of GAL3 protein after SCI. (C) Statistical data show relative GAL3 protein expression after SCI. One-way ANOVA, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) detection of GAL3 protein levels in rat serum after SCI. One-way ANOVA, n = 6/group. (E) Immunofluorescence microscopy reveals GAL3 co-localization with NeuN post-SCI. (F) Fluorescence intensity of GAL3 after SCI. One-way ANOVA, n = 3/group. (G,H) Immunofluorescence double staining of GAL3 and GFAP (G) or IBA1 (H) after SCI. (I) Determination of optimal glutamate concentration and duration using CCK8 assay. (J) Relative GAL3 mRNA expression in the glutamate-stimulated spinal cord neurons. Unpaired Student’s t -test, n = 3/group. (K) Western blot analysis of GAL3 protein in neuronal injury model. (L) Relative GAL3 protein expression in neuronal injury model. Unpaired Student’s t -test, n = 3/group. (M) ELISA detection of GAL3 in cell supernatant of neuronal injury model. Unpaired Student’s t -test, n = 3/group. (N) Immunofluorescence microscopy showing GAL3 expression in neuronal injury model. (O) Quantification of GAL3 fluorescence intensity in neuronal injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Spinal cord injury (SCI) increases galectin-3 (GAL3) expression in spinal neurons. (A) Relative GAL3 mRNA expression in the spinal cord after SCI. One-way ANOVA, n = 3/group. (B) Western blot analysis of GAL3 protein after SCI. (C) Statistical data show relative GAL3 protein expression after SCI. One-way ANOVA, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) detection of GAL3 protein levels in rat serum after SCI. One-way ANOVA, n = 6/group. (E) Immunofluorescence microscopy reveals GAL3 co-localization with NeuN post-SCI. (F) Fluorescence intensity of GAL3 after SCI. One-way ANOVA, n = 3/group. (G,H) Immunofluorescence double staining of GAL3 and GFAP (G) or IBA1 (H) after SCI. (I) Determination of optimal glutamate concentration and duration using CCK8 assay. (J) Relative GAL3 mRNA expression in the glutamate-stimulated spinal cord neurons. Unpaired Student’s t -test, n = 3/group. (K) Western blot analysis of GAL3 protein in neuronal injury model. (L) Relative GAL3 protein expression in neuronal injury model. Unpaired Student’s t -test, n = 3/group. (M) ELISA detection of GAL3 in cell supernatant of neuronal injury model. Unpaired Student’s t -test, n = 3/group. (N) Immunofluorescence microscopy showing GAL3 expression in neuronal injury model. (O) Quantification of GAL3 fluorescence intensity in neuronal injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Microscopy, Fluorescence, Double Staining, Concentration Assay, CCK-8 Assay

    Galectin-3 (GAL3) contributes to spinal cord injury (SCI)-induced motor impairment. (A) The mRNA level of GAL3 after siR-GAL3 treatment. Unpaired Student’s t -test, n = 3/group. (B) Western blot shows the protein level of GAL3 after siR-GAL3 treatment. (C) Statistical data show the knockdown of GAL3 by siRNA. Unpaired Student’s t -test, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) shows the secretory GAL3 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (E) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. (F) The inclined plane angles were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-GAL3 group was compared with SCI + Vehicle group, ** P < 0.01, *** P < 0.001; when SCI + TD139 group was compared with SCI + Vehicle group, # P < 0.05, ### P < 0.001; when SCI + GAL3 group was compared with SCI + Vehicle group, + P < 0.05,++ P < 0.01.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) contributes to spinal cord injury (SCI)-induced motor impairment. (A) The mRNA level of GAL3 after siR-GAL3 treatment. Unpaired Student’s t -test, n = 3/group. (B) Western blot shows the protein level of GAL3 after siR-GAL3 treatment. (C) Statistical data show the knockdown of GAL3 by siRNA. Unpaired Student’s t -test, n = 3/group. (D) Enzyme-linked immunosorbent assay (ELISA) shows the secretory GAL3 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (E) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. (F) The inclined plane angles were increased after siR-GAL3 or inhibitor treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-GAL3 group was compared with SCI + Vehicle group, ** P < 0.01, *** P < 0.001; when SCI + TD139 group was compared with SCI + Vehicle group, # P < 0.05, ### P < 0.001; when SCI + GAL3 group was compared with SCI + Vehicle group, + P < 0.05,++ P < 0.01.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Western Blot, Knockdown, Enzyme-linked Immunosorbent Assay

    Galectin-3 (GAL3) is closely related to programmed cell death after spinal cord injury (SCI). (A) The four datasets before the batch effect were removed. (B) The four datasets after the batch effect were removed. (C) Volcano map shows DEGs in the SCI dataset. (D) Biological Process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the SCI dataset. Each column represents the P -value score of the pathway between the Sham group and the SCI group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (E) Protein-Protein Interaction Networks (PPI) analysis of differentially expressed genes (DEGs) in SCI dataset. In the PPI nodes, red signifies an increase in expression level, while blue indicates a decrease. The intensity of the color corresponds to the magnitude of the differential expression, with darker shades representing a higher differential expression multiple.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) is closely related to programmed cell death after spinal cord injury (SCI). (A) The four datasets before the batch effect were removed. (B) The four datasets after the batch effect were removed. (C) Volcano map shows DEGs in the SCI dataset. (D) Biological Process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the SCI dataset. Each column represents the P -value score of the pathway between the Sham group and the SCI group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (E) Protein-Protein Interaction Networks (PPI) analysis of differentially expressed genes (DEGs) in SCI dataset. In the PPI nodes, red signifies an increase in expression level, while blue indicates a decrease. The intensity of the color corresponds to the magnitude of the differential expression, with darker shades representing a higher differential expression multiple.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Expressing, Quantitative Proteomics

    Galectin-3 (GAL3) regulates neuronal autophagy. (A) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in neurons. (B-E) Quantification of western blot detection of GAL3 (B) , ATG7 (C) , P62 (D) , and LC3 II/I (E) in neurons. One-way ANOVA, n = 3/group. (F) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in the spinal cord of rats. (G–I) Quantification of western blot detection of ATG7 (G) , P62 (H) , and LC3 II/I (I) in the spinal cord of rats. One-way ANOVA, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) regulates neuronal autophagy. (A) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in neurons. (B-E) Quantification of western blot detection of GAL3 (B) , ATG7 (C) , P62 (D) , and LC3 II/I (E) in neurons. One-way ANOVA, n = 3/group. (F) Western blot analysis of GAL3 and neuronal autophagy markers ATG7, P62, and LC3 II/I in the spinal cord of rats. (G–I) Quantification of western blot detection of ATG7 (G) , P62 (H) , and LC3 II/I (I) in the spinal cord of rats. One-way ANOVA, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Western Blot

    Sequencing analysis of spinal cord neurons with galectin-3 (GAL3) knocked down. (A) Volcano map shows differential expression genes (DEGs) in the neuron dataset. (B) Biological process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the neuron dataset. Each column represents the P -value score of the pathway between the Sham group and the spinal cord injury (SCI) group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (C) The Protein-Protein Interaction Networks (PPI) analysis of DEGs in the neuron dataset. In the PPI nodes, red indicates that the expression level increases and blue indicates that the expression level decreases. The darker the color, the greater the differential expression multiple.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Sequencing analysis of spinal cord neurons with galectin-3 (GAL3) knocked down. (A) Volcano map shows differential expression genes (DEGs) in the neuron dataset. (B) Biological process (BP) analysis of Gene Set Enrichment Analysis (GSEA) in the neuron dataset. Each column represents the P -value score of the pathway between the Sham group and the spinal cord injury (SCI) group, with red indicating upregulation of the pathway in the SCI group, and blue indicating downregulation. (C) The Protein-Protein Interaction Networks (PPI) analysis of DEGs in the neuron dataset. In the PPI nodes, red indicates that the expression level increases and blue indicates that the expression level decreases. The darker the color, the greater the differential expression multiple.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Sequencing, Quantitative Proteomics, Expressing

    Galectin-3 (GAL3) interacts with Cell-division-cycle-42 (CDC42) to regulate neuronal autophagy. (A) Intersected 29 core nodes from the neuron dataset with 22 core nodes from the spinal cord injury (SCI) dataset by the Venn diagram. (B) Correlation analysis between GAL3 and CDC42 expression level in SCI dataset. (C) Correlation analysis between GAL3 and CDC42 expression level in the neuron dataset. (D) Co-immunoprecipitation (Co-IP) shows a direct interaction between GAL3 and CDC42 in the glutamate-induced neuronal damage model. (E) Western blot shows the expression of CDC42, ATG7, P62, and LC3 II/I. (F–I) Quantification of western blot detection of CDC42 (F) , ATG7 (G) , P62 (H) , and LC3 II/I (I) . One-way ANOVA, n = 3/group. (J) Enzyme-linked immunosorbent assay (ELISA) detection of CDC42 in cell supernatant of GAL3-injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Galectin-3 (GAL3) interacts with Cell-division-cycle-42 (CDC42) to regulate neuronal autophagy. (A) Intersected 29 core nodes from the neuron dataset with 22 core nodes from the spinal cord injury (SCI) dataset by the Venn diagram. (B) Correlation analysis between GAL3 and CDC42 expression level in SCI dataset. (C) Correlation analysis between GAL3 and CDC42 expression level in the neuron dataset. (D) Co-immunoprecipitation (Co-IP) shows a direct interaction between GAL3 and CDC42 in the glutamate-induced neuronal damage model. (E) Western blot shows the expression of CDC42, ATG7, P62, and LC3 II/I. (F–I) Quantification of western blot detection of CDC42 (F) , ATG7 (G) , P62 (H) , and LC3 II/I (I) . One-way ANOVA, n = 3/group. (J) Enzyme-linked immunosorbent assay (ELISA) detection of CDC42 in cell supernatant of GAL3-injury model. Unpaired Student’s t -test, n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Expressing, Immunoprecipitation, Co-Immunoprecipitation Assay, Western Blot, Enzyme-linked Immunosorbent Assay

    Cell-division-cycle-42 (CDC42) contributes to spinal cord injury (SCI)-induced motor function impairment. (A) The mRNA level after siR-CDC42 treatment. Unpaired Student’s t -test, n = 3/group. (B) Enzyme-linked immunosorbent assay (ELISA) shows the secretory CDC42 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (C) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. (D) The inclined plane angles were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-CDC42 group was compared with SCI + Vehicle group, * P < 0.05, ** P < 0.01, *** P < 0.001; when SCI + ML141 group was compared with SCI + Vehicle group, ## P < 0.01, ### P < 0.001. (E,F) Detection of the protein expression level of galectin-3 (GAL3) (E) and CDC42 (F) in serum of healthy volunteers and SCI patients by ELISA. Unpaired Student’s t -test, n = 8/group. *** P < 0.001.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

    doi: 10.3389/fncel.2025.1622825

    Figure Lengend Snippet: Cell-division-cycle-42 (CDC42) contributes to spinal cord injury (SCI)-induced motor function impairment. (A) The mRNA level after siR-CDC42 treatment. Unpaired Student’s t -test, n = 3/group. (B) Enzyme-linked immunosorbent assay (ELISA) shows the secretory CDC42 in the supernatant of neurons after siRNA treatment. Unpaired Student’s t -test, n = 3/group. (C) The Basso-Beattie-Bresnahan (BBB) locomotor scores were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. (D) The inclined plane angles were increased after siR-CDC42 and ML141 treatment. Two-way Repeated Measures ANOVA, n = 8/group. When SCI + siR-CDC42 group was compared with SCI + Vehicle group, * P < 0.05, ** P < 0.01, *** P < 0.001; when SCI + ML141 group was compared with SCI + Vehicle group, ## P < 0.01, ### P < 0.001. (E,F) Detection of the protein expression level of galectin-3 (GAL3) (E) and CDC42 (F) in serum of healthy volunteers and SCI patients by ELISA. Unpaired Student’s t -test, n = 8/group. *** P < 0.001.

    Article Snippet: The primary antibody used targeted the following proteins: NeuN (1:500, mouse IgG; No.26975, Proteintech), GAL3 (1:200, mouse IgG; No. 60207, Proteintech), and CDC42 (1:200, rabbit IgG; No.10155, Proteintech).

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing