recombinant human tgf β1 protein  (R&D Systems)

Journal: IBRO Neuroscience Reports

Article Title: TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury

doi: 10.1016/j.ibneur.2026.03.009

Figure Lengend Snippet: Exercise modulates TGF-β1 expression in the prefrontal cortex (PFC) of mice 24 days after spared nerve injury (SNI). (a) Representative Western blot images of TGF-β receptor I (TGF-βR1) and TGF-β1 in the PFC. Tissue lysates from all experimental groups (SHAM, SHAME, SNI, SNIE) and recombinant human TGF-β1 (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody under identical exposure conditions. The recombinant protein (250 ng per lane) served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (b-d) Quantitative Western blot analyses of (b) TGF-βR1, (c) dimeric TGF-β1 (25 kDa), and (d) monomeric TGF-β1 (12.5 kDa) expression levels in tissue lysates. Data are presented as mean ± SEM (n = 3). ** P < 0.01 vs. SHAM group; ## P < 0.01 vs. SNI group.

Article Snippet: To validate the specificity of the TGF-β1 antibody, Recombinant human TGF-β1 protein (Catalog # 240-B, R&D Systems, USA) was used as a positive control.

Techniques: Expressing, Western Blot, Recombinant, SDS Page, Membrane, Positive Control, Control

Journal: IBRO Neuroscience Reports

Article Title: TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury

doi: 10.1016/j.ibneur.2026.03.009

Figure Lengend Snippet: At 24 d after SNI, mouse PFC astrocytes were activated and microglia were unchanged. (a)Western blotting analysis of changes in GFAP and Iba1 expression in PFC (n = 3); (b) Quantification of GFAP in PFC; (c) Quantification of Iba1 in PFC; (d) MFI representative images of GFAP in PFC; (e) MFI representative image of Iba1 in PFC; (f) Quantification of GFAP in PFC. Values represent mean ± SEM (Scale bar =75μm, 9 PFC sections from 3 mice per group); (g) Quantification of Iba1 in PFC. Values represent mean ±SEM (Scale bar = 75μm, 9 PFC sections from 3 mice per group). Values represent the mean ±SEM. * P < 0.05, ** P < 0.01, compared with SHAM group; # P < 0.05, ## P < 0.01, compared with SNI group, the difference was statistically significant; (h) Representative MFI images of changes in the colocalization of TGF-β1(red) and astrocytes (green) in the PFC; (i) Quantification of TGF-β1 and astrocytes in PFC. Values represent the mean ± SEM (Scale bar =100μm, nine PFC sections from three mice per group). * P < 0.05 versus the SHAM group; # P < 0.05 versus the SNI group.

Article Snippet: To validate the specificity of the TGF-β1 antibody, Recombinant human TGF-β1 protein (Catalog # 240-B, R&D Systems, USA) was used as a positive control.

Techniques: Western Blot, Expressing

Journal: IBRO Neuroscience Reports

Article Title: TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury

doi: 10.1016/j.ibneur.2026.03.009

Figure Lengend Snippet: TGF-βRI inhibition reverses exercise-induced analgesia and modulates glial activation in the PFC. (a, b) Time course of mechanical and cold hyperalgesia tests (n = 9). The green shading indicates the duration of the exercise intervention, and the green vertical lines denote the timing of intrathecal injections. Data are presented as mean ± SEM. ** P < 0.01 versus the SNIE group, # P < 0.05, ## P < 0.01 vs. SC group. (c) Representative Western blot images of TGF-βR1 and TGF-β1 in the PFC. Tissue lysates from SC and SA groups and recombinant human TGF-β1 (100 ng per lane) (non-reduced and reduced) were loaded on the same SDS–PAGE gel, transferred to a single membrane, and probed with the same TGF-β1 antibody in a single exposure without splicing. The recombinant protein served as a positive control to verify the molecular weights of the dimeric (25 kDa) and monomeric (12.5 kDa) forms of TGF-β1. GAPDH was used as the loading control. (d-f) Quantitative analysis of (d) TGF-βR1, (e) dimeric TGF-β1 (25 kDa), and (f) monomeric TGF-β1 (12.5 kDa) expression levels (n = 3). (g-i) Western blot analysis of glial markers. (g) Representative images of GFAP and Iba1 with GAPDH control. Quantitative analysis of (h) GFAP and (i) Iba1 expression levels (n = 3). (j, k) Representative immunofluorescence images showing the expression of (j) GFAP and (k) Iba1 in the PFC. Scale bar = 75 μm. (l, m) Quantification of the mean fluorescence intensity (MFI) for (l) GFAP and (m) Iba1 (n = 9 sections from 3 mice per group). Data in bar graphs are presented as mean ± SEM. * P < 0.05, ** P < 0.01 vs. SC group. SC: Spared nerve injury with exercise training followed by intrathecal (i.t.) injection of saline; SA: Spared nerve injury with exercise training followed by i.t. injection of the TGF-βRI inhibitor.

Article Snippet: To validate the specificity of the TGF-β1 antibody, Recombinant human TGF-β1 protein (Catalog # 240-B, R&D Systems, USA) was used as a positive control.

Techniques: Inhibition, Activation Assay, Western Blot, Recombinant, SDS Page, Membrane, Positive Control, Control, Expressing, Immunofluorescence, Fluorescence, Injection, Saline

Journal: Molecular and Clinical Oncology

Article Title: Long non-coding RNAs affect the metastasis of hepatocellular carcinoma cells by regulating the epithelial-to-mesenchymal transition

doi: 10.3892/mco.2026.2940

Figure Lengend Snippet: Validation of the epithelial-to-mesenchymal transition model. (A) Micrographs of Huh7 cells treated with or without 10 ng/ml TGF-β for 4 days. (B) Relative mRNA levels of E-cadherin, N-cadherin, Snail and Slug in Huh7 cells treated with or without 10 ng/ml TGF-β for 4 days. (C) In vitro migration of Huh7 cells treated with or without 10 ng/ml TGF-β for 4 days. * P<0.05 vs. the control group. TGF-β, transforming growth factor-β.

Article Snippet: To induce the in vitro EMT cell model, Huh7 cells were cultured at 37 ̊C in DMEM with 2.5% FBS and 10 ng/ml TGF-β (cat. no. HY-P7118; MedChemExpress) for 4 days.

Techniques: Biomarker Discovery, In Vitro, Migration, Control

Journal: Molecular and Clinical Oncology

Article Title: Long non-coding RNAs affect the metastasis of hepatocellular carcinoma cells by regulating the epithelial-to-mesenchymal transition

doi: 10.3892/mco.2026.2940

Figure Lengend Snippet: DE lncRNAs and mRNAs in TGF-β treated Huh7 cells. (A) Volcano plot demonstrating DE lncRNAs and mRNAs. Red points represent upregulated RNAs, blue points represent downregulated RNAs and black points represent RNAs with no significant differences. (B) Hierarchical clustering analysis based on the significantly DE lncRNAs and mRNAs. Red indicates high relative expression levels, blue indicates low relative expression levels and white indicates no change in the gene expression levels. The color brightness indicates the extent of the upregulation or downregulation of the gene expression. TGF-β, transforming growth factor-β; DE, differentially expressed; lncRNA, long non-coding RNA; FC, fold-change; FDR, false-discovery rate.

Article Snippet: To induce the in vitro EMT cell model, Huh7 cells were cultured at 37 ̊C in DMEM with 2.5% FBS and 10 ng/ml TGF-β (cat. no. HY-P7118; MedChemExpress) for 4 days.

Techniques: Expressing, Gene Expression

Journal: Molecular and Clinical Oncology

Article Title: Long non-coding RNAs affect the metastasis of hepatocellular carcinoma cells by regulating the epithelial-to-mesenchymal transition

doi: 10.3892/mco.2026.2940

Figure Lengend Snippet: GO and KEGG enrichment analysis. GO term enrichment categories, including (A) molecular function, (B) cellular component and (C) biological process. (D) KEGG pathway enrichment analysis. GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; ECM, extracellular matrix; TGF-β, transforming growth factor-β; PPAR, peroxisome proliferator-activated receptor; AGE-RAGE, advanced glycation end-products-receptor for advanced glycation end-products.

Article Snippet: To induce the in vitro EMT cell model, Huh7 cells were cultured at 37 ̊C in DMEM with 2.5% FBS and 10 ng/ml TGF-β (cat. no. HY-P7118; MedChemExpress) for 4 days.

Techniques:

Journal: Molecular and Clinical Oncology

Article Title: Long non-coding RNAs affect the metastasis of hepatocellular carcinoma cells by regulating the epithelial-to-mesenchymal transition

doi: 10.3892/mco.2026.2940

Figure Lengend Snippet: Validation of the sequencing data using reverse transcription-quantitative PCR. (A) Relative mRNA levels of COL1A1, BMP6, TUBA1A, ATP2B2 and F2 in Huh7 cells treated with or without 10 ng/ml TGF-β for 4 days. (B) Relative lncRNA levels of NNMT-205, CASC15-204, UBASH3B-202, CAPN2-206, CAV2-214 and ZSWIM8-210 in Huh7 cells treated with or without 10 ng/ml TGF-β for 4 days. * P<0.05 vs. the control group. lncRNA, long non-coding RNA; TGF-β, transforming growth factor-β.

Article Snippet: To induce the in vitro EMT cell model, Huh7 cells were cultured at 37 ̊C in DMEM with 2.5% FBS and 10 ng/ml TGF-β (cat. no. HY-P7118; MedChemExpress) for 4 days.

Techniques: Biomarker Discovery, Sequencing, Reverse Transcription, Real-time Polymerase Chain Reaction, Control

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Proteomic analysis showed that expressions of TXNDC5 and ECM proteins were upregulated in TGFβ2-treated HTM cells. HTM cells were starved with serum-free DMEM/F12 medium for 24 hours and then treated with TGFβ2 (5 ng/mL) for 48 hours. (A) Changes of protein expression after TGFβ2 treatment in HTM cells were represented by volcano plots (≥1.2-fold difference: upregulated genes [ red ] and downregulated genes [ blue ]). Violin plots showed the TGFβ2-induced significant changes in TXNDC5 (B) , LN (C) , FN (D) , COL4A1 (E) , and COL4A2 (F) . ** P < 0.01; *** P < 0.001. (G) KEGG analysis indicated multiple metabolic and signal pathways, including ECM-receptor interaction, were changed markedly.

Article Snippet: Both control and TGFβ2-treated groups were induced with 100 mg/mL CHX (MedChemExpress, Monmouth Junction, NJ, USA) to inhibit protein translation.

Techniques: Expressing

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Western blot, qRT-PCR, and immunocytochemistry showed that expressions of TXNDC5 and ECM proteins were upregulated in TGFβ2-treated HTM cells. (A) Concentration of TXNDC5 in the non-POAG ( n = 10) and POAG patients ( n = 7) in aqueous humor detected by ELISA. (B, C) TXNDC5 levels were not correlated with age and IOP in the non-POAG group and in POAG patients ( n = 7–8). (D) Representative images of Western blot analysis showing TGFβ2-induced changes in expressions of TXNDC5 and ECM proteins in HTM cells. (E–H) Quantitative analyses of Western blot of individual protein ( n = 4–6): TXNDC5 ( E ) , LN (F) , FN (G) , Col-IV (H) . Data are presented as mean ± SEM. (A) * P < 0.05 by unpaired, two-tailed t -test compared to non-POAG. (E–H) * P < 0.05; ** P < 0.01; *** P < 0.001 by unpaired, two-tailed t -test compared to control. (I) Representative images of immunofluorescence staining of TXNDC5, LN, FN, and COL-IV proteins in untreated control and TGFβ2-treated groups. Scale bars : 50 µm.

Article Snippet: Both control and TGFβ2-treated groups were induced with 100 mg/mL CHX (MedChemExpress, Monmouth Junction, NJ, USA) to inhibit protein translation.

Techniques: Western Blot, Quantitative RT-PCR, Immunocytochemistry, Concentration Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Control, Immunofluorescence, Staining

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Proteomic analysis showed that expressions of TXNDC5 and ECM proteins were upregulated in TGFβ2-treated HTM cells. HTM cells were starved with serum-free DMEM/F12 medium for 24 hours and then treated with TGFβ2 (5 ng/mL) for 48 hours. (A) Changes of protein expression after TGFβ2 treatment in HTM cells were represented by volcano plots (≥1.2-fold difference: upregulated genes [ red ] and downregulated genes [ blue ]). Violin plots showed the TGFβ2-induced significant changes in TXNDC5 (B) , LN (C) , FN (D) , COL4A1 (E) , and COL4A2 (F) . ** P < 0.01; *** P < 0.001. (G) KEGG analysis indicated multiple metabolic and signal pathways, including ECM-receptor interaction, were changed markedly.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Expressing

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Western blot, qRT-PCR, and immunocytochemistry showed that expressions of TXNDC5 and ECM proteins were upregulated in TGFβ2-treated HTM cells. (A) Concentration of TXNDC5 in the non-POAG ( n = 10) and POAG patients ( n = 7) in aqueous humor detected by ELISA. (B, C) TXNDC5 levels were not correlated with age and IOP in the non-POAG group and in POAG patients ( n = 7–8). (D) Representative images of Western blot analysis showing TGFβ2-induced changes in expressions of TXNDC5 and ECM proteins in HTM cells. (E–H) Quantitative analyses of Western blot of individual protein ( n = 4–6): TXNDC5 ( E ) , LN (F) , FN (G) , Col-IV (H) . Data are presented as mean ± SEM. (A) * P < 0.05 by unpaired, two-tailed t -test compared to non-POAG. (E–H) * P < 0.05; ** P < 0.01; *** P < 0.001 by unpaired, two-tailed t -test compared to control. (I) Representative images of immunofluorescence staining of TXNDC5, LN, FN, and COL-IV proteins in untreated control and TGFβ2-treated groups. Scale bars : 50 µm.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Western Blot, Quantitative RT-PCR, Immunocytochemistry, Concentration Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Control, Immunofluorescence, Staining

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Knockdown or overexpression of TXNDC5 regulated TGFβ2-induced ECM aggregation in HTM cells. HTM cells were pre-transfected with si-TXNDC5 for eight hours and then treated with or without TGFβ2 for 48 hours. (A) Western blot assessment of the knockdown efficiency of three different tested siRNA sequences of si-TXNDC5. The most effective of them (no. 3) was used for the following knockdown studies. (B–G) Western blot and immunocytochemical staining analyses for TXNDC5 and ECM proteins by si-TXNDC5 transfection with or without TGFβ2 induction. (H–J) Western blot was assayed for ECM (FN) expression by overexpressing TXNDC5. Data are presented as mean ± SEM; * P < 0.05; ** P < 0.01; *** P < 0.001 compared with control; # P < 0.05; ## P < 0.01; ### P < 0.001 compared with TGFβ2 group by one-way ANOVA followed by Tukey's multiple comparisons test. Scale bar : 50 µm.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Knockdown, Over Expression, Transfection, Western Blot, Staining, Expressing, Control

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: TXNDC5 knockdown reduced the TGFβ2-induced TGFβR2 expression, whereas TGFβR2 knockdown did not affect TXNDC5 expression. HTM cells were pre-transfected with si-TXNDC5 or si-TGFβR2 for eight hours with or without TGFβ2 treatment for 48 hours. (A) Representative images showing protein levels of TXNDC5, TGFβR1 and TGFβR2 after si-TXNDC5 with or without TGFβ2 treatment in the HTM cells. (B, C) Quantitative analyses of TGFβR1 and TGFβR2 levels after si-TXNDC5 with or without TGFβ2 treatment. (D) Three different siRNA sequences were tested for their knockdown efficiency of TGFβR2. The most effective of them (no. 3) was used for the following knockdown studies. (E–H) The effect of TGFβR2 knockdown on the expression of TGFβR2, TXNDC5 and FN proteins with or without TGFβR2 treatment. Error bars : mean ± SEM ( n = 3-6); * P < 0.05; ** P < 0.01; *** P < 0.001 compared with control; # P < 0.05; ### P < 0.001 compare with TGFβ2. One-way ANOVA followed by Tukey's multiple comparisons test. Scale bar : 50 µm.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Knockdown, Expressing, Transfection, Control

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: TXNDC5 is degraded via the lysosomal pathway. (A–D) Quantitative analyses qRT-PCR of individual mRNA ( n = 3–6): TXNDC5 (A) , LN (B) , FN (C) , COL-IV (D) . (E, F) After TGFβ2 treatment for 24 hours, CHX (100 µg/mL) was added to the HTM cells to inhibit the synthesis of new proteins. Cells were harvested at the indicated time points (0, 12, or 24 hours after CHX treatment) and immunoblotted to evaluate TXNDC5 protein levels. (E) Representative images of the immunoblot. (F) The slope of decline of TXNDC5 protein in TGFβ2 and Control groups. (G) Quantitative analysis, the level of TXNDC5 relative to GAPDH at time 0 of each group defines 1. (H, I) Effects of 24 hours treatment with lysosomal inhibitor CQ (10 µM) or proteasome inhibitor MG132 (5 µM) on TXNDC5 accumulation in HTM cells. The level of TXNDC5 relative to GAPDH of the control group (DMSO only) defines 1. (J, K) Effects of CQ and TGFβ2 on TXNDC5 accumulation in HTM cells. (L) Appropriate amount of cell lysate was taken for input group, TXNDC5 was immunoprecipitated with Hsc70, and TXNDC5 and Hsc70 protein expression was detected by Western blot. The level of TXNDC5 relative to GAPDH of the control group defines 1. All quantitative data are shown as mean and SEM. (A–F) * P < 0.05; ** P < 0.01; *** P < 0.001 by unpaired, two-tailed t -test compared to control. (G–J) * P < 0.05; ** P < 0.01; *** P < 0.001 vs. Control; # P < 0.05 between the indicated groups by one-way ANOVA followed with Tukey's multiple comparisons test.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Quantitative RT-PCR, Western Blot, Control, Immunoprecipitation, Expressing, Two Tailed Test

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Involvement of CMA influences TXNDC5 protein levels induced by TGFβ2. (A) The amino acid sequence of TXNDC5 has a "KFERQ" -like pentapeptide motif. (B) Three different siRNA sequences of LAMP2A were used to test their knockdown efficiency of LAMP2A, the most effective of which (No. 2) was used for following knockdown studies. (C, D) Silencing of LAMP2A aggravated upregulation of TXNDC5 by TGFβ2 induction. (E, F) Treatment with AR7 (40 µM) at HTM for 24 hours reduced accumulation of TXNDC5 by siLAMP2A. (G, H) AR7 treatment for 24 hours reversed TGFβ2-induced upregulation of TXNDC5. All quantitative data are shown as mean and SEM ( n = 3–6). * P < 0.05; ** P < 0.01; *** P < 0.001 vs. Control; # P < 0.05; ## P < 0.01; ### P < 0.001 between the indicated groups by one-way ANOVA followed with Tukey's multiple comparisons test.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Sequencing, Knockdown, Control

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Knockdown of TXNDC5 attenuated ECM protein accumulation and high IOP induced by Ad.hTGFβ2 226/228 in mouse TM. (A) Illustration of experimental design: si-TXNDC5 or si-negative control (si-NC) was injected intravitreally on day 0 and day 7, and Ad.hTGFβ2 226/228 was injected intravitreally once on day 2. Mice were euthanized on day 14. (B) Changes in IOP treated by Ad.hTGFβ2 226/228 with or without si-TXNDC5 treatment. (C) Statistical analysis of mouse IOP on day 10. (D–G) Expression of TXNDC5 (D) , FN (E) , COL-IV (F) , LN (G) mRNA in TM tissues from the study groups. (H) Representative immunofluorescence stainings of TXNDC5, LN, FN, and COL-IV in mouse ocular tissue are shown. Blue fluorescence = DAPI; red fluorescence = TXNDC5 or indicated ECM protein. Data are represented as means ± SEM ( n ≥ 4 mice for each group). * P < 0.05; ** P < 0.01; *** P < 0.001 compared with control; # P < 0.05; ## P < 0.01; ### P < 0.001 compared with TGFβ2 group; & P < 0.05; && P < 0.01 compared with TGFβ2 + si-TXNDC5 group. One-way ANOVA followed by Tukey's multiple comparisons test. Scale bar : 50 µm (H) .

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Knockdown, Negative Control, Injection, Expressing, Immunofluorescence, Fluorescence, Control

Journal: Investigative Ophthalmology & Visual Science

Article Title: TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure

doi: 10.1167/iovs.67.4.46

Figure Lengend Snippet: Schematic representation of the involvement of CMA lysosomal degradation pathway of TXNDC5 in TM ECM protein accumulation. Treatment with TGFβ2 increased the expression of TXNDC5 and further promoted the expression of TGFβR2, which in turn promoted the increase of ECM protein. Intracellularlly, mutual recognition of the molecular chaperone Hsc70 with TXNDC5 protein and synergism with LAMP2A molecule promotes the entry of TXNDC5 protein into lysosomal degradation, and activation of CMA activity by AR7 leads to the entry of more TXNDC5 into lysosomal degradation, thereby reducing ECM accumulation. The expression of TXNDC5 in the aqueous humor of POAG patients was significantly higher than that of non-POAG patients. In the Ad.hTGFβ 226/228 -mediated high IOP mouse model, injection of si-TXNDC5 significantly improved Ad.hTGFβ 226/228 -mediated high IOP and ECM accumulation in TM tissue.

Article Snippet: HTM cells were starved in serum-free medium, treated with TGFβ2 (5 ng/mL; Med Chem Express, Monmouth Junction, NJ, USA) for 48 hours, and then subjected to subsequent assays.

Techniques: Expressing, Activation Assay, Activity Assay, Injection