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tsp 1  (MedChemExpress)


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    MedChemExpress tsp 1
    6‐month‐old ACSA‐2+ SAMP8 primary cultured astrocytes and differentiated astrocytes derived from SAMP8 neural stem cells display loss <t>in</t> <t>TSP‐1</t> levels. (A) RNA‐seq transcriptional profile of Thbs1 gene in astrocytes, neurons, endothelial cells, oligodendrocytes and microglia in P7 (postnatal day) mice. (B) RNA‐seq transcriptional profile of Thbs1 gene at different stages of development and aging in astrocytes from mouse hippocampus. (C) Representative images of GFAP (green) and TSP‐1 (red) immunostaining in ACSA‐2+ primary astrocytes cultures of the SAMP8 and SAMR1 strains (14 DIV) and in Diff‐Ast SAMP8 and SAMR1 strains (11 DIV). (D, E) Quantification of TSP‐1 protein shows lower levels in SAMP8 ACSA‐2+ astrocytes cultures ( p = 0.021) and in Diff‐Ast SAMP8 ( p = 0.011) than in the control SAMR1 strain. (F) RT‐qPCR of Thbs1 ( p = 0.001) demonstrates lower gene expression levels in Diff‐Ast SAMP8 compared to the control line SAMR1. Three independent experiments per cell type were analyzed ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed in (D, E). One‐sample t ‐test was done in (F). * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar: 50 μm. Data in (A) and (B) were obtained from databases produced by the Barres lab (Zhang et al. and Clarke et al. available at https://brainrnaseq.org/ ).
    Tsp 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tsp 1/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    tsp 1 - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss"

    Article Title: Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss

    Journal: Aging Cell

    doi: 10.1111/acel.70382

    6‐month‐old ACSA‐2+ SAMP8 primary cultured astrocytes and differentiated astrocytes derived from SAMP8 neural stem cells display loss in TSP‐1 levels. (A) RNA‐seq transcriptional profile of Thbs1 gene in astrocytes, neurons, endothelial cells, oligodendrocytes and microglia in P7 (postnatal day) mice. (B) RNA‐seq transcriptional profile of Thbs1 gene at different stages of development and aging in astrocytes from mouse hippocampus. (C) Representative images of GFAP (green) and TSP‐1 (red) immunostaining in ACSA‐2+ primary astrocytes cultures of the SAMP8 and SAMR1 strains (14 DIV) and in Diff‐Ast SAMP8 and SAMR1 strains (11 DIV). (D, E) Quantification of TSP‐1 protein shows lower levels in SAMP8 ACSA‐2+ astrocytes cultures ( p = 0.021) and in Diff‐Ast SAMP8 ( p = 0.011) than in the control SAMR1 strain. (F) RT‐qPCR of Thbs1 ( p = 0.001) demonstrates lower gene expression levels in Diff‐Ast SAMP8 compared to the control line SAMR1. Three independent experiments per cell type were analyzed ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed in (D, E). One‐sample t ‐test was done in (F). * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar: 50 μm. Data in (A) and (B) were obtained from databases produced by the Barres lab (Zhang et al. and Clarke et al. available at https://brainrnaseq.org/ ).
    Figure Legend Snippet: 6‐month‐old ACSA‐2+ SAMP8 primary cultured astrocytes and differentiated astrocytes derived from SAMP8 neural stem cells display loss in TSP‐1 levels. (A) RNA‐seq transcriptional profile of Thbs1 gene in astrocytes, neurons, endothelial cells, oligodendrocytes and microglia in P7 (postnatal day) mice. (B) RNA‐seq transcriptional profile of Thbs1 gene at different stages of development and aging in astrocytes from mouse hippocampus. (C) Representative images of GFAP (green) and TSP‐1 (red) immunostaining in ACSA‐2+ primary astrocytes cultures of the SAMP8 and SAMR1 strains (14 DIV) and in Diff‐Ast SAMP8 and SAMR1 strains (11 DIV). (D, E) Quantification of TSP‐1 protein shows lower levels in SAMP8 ACSA‐2+ astrocytes cultures ( p = 0.021) and in Diff‐Ast SAMP8 ( p = 0.011) than in the control SAMR1 strain. (F) RT‐qPCR of Thbs1 ( p = 0.001) demonstrates lower gene expression levels in Diff‐Ast SAMP8 compared to the control line SAMR1. Three independent experiments per cell type were analyzed ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed in (D, E). One‐sample t ‐test was done in (F). * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar: 50 μm. Data in (A) and (B) were obtained from databases produced by the Barres lab (Zhang et al. and Clarke et al. available at https://brainrnaseq.org/ ).

    Techniques Used: Cell Culture, Derivative Assay, RNA Sequencing, Immunostaining, Control, Quantitative RT-PCR, Gene Expression, Produced

    The hippocampus of 10‐month‐old SAMP8 mice shows deficiencies in TSP‐1 levels. (A) RT‐qPCR of Thbs1 ( p = 0.022) in SAMR1 ( n = 7 independent animals) and SAMP8 ( n = 8 independent animals). (B) TSP‐1 quantification by ELISA test in 10‐m SAMR1 ( n = 4 independent animals) and SAMP8 ( n = 3 independent animals) mice normalized to total protein levels. (C, D) Immunohistochemical analyses and TSP‐1 intensity quantification in 10‐m SAMR1 and SAMP8 hippocampus are shown. Representative astrocytes from the SLM layer in the hippocampus using GFAP (green) as an astroglial marker, and TSP‐1 (red) are depicted magnified. TSP‐1 signal intensity quantification was performed in each layer of the hippocampus and normalized to the quantification area (μm2). Three independent animals of each strain were analyzed for immunohistochemical analysis ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 100 μm; 10 μm (representative astrocyte).
    Figure Legend Snippet: The hippocampus of 10‐month‐old SAMP8 mice shows deficiencies in TSP‐1 levels. (A) RT‐qPCR of Thbs1 ( p = 0.022) in SAMR1 ( n = 7 independent animals) and SAMP8 ( n = 8 independent animals). (B) TSP‐1 quantification by ELISA test in 10‐m SAMR1 ( n = 4 independent animals) and SAMP8 ( n = 3 independent animals) mice normalized to total protein levels. (C, D) Immunohistochemical analyses and TSP‐1 intensity quantification in 10‐m SAMR1 and SAMP8 hippocampus are shown. Representative astrocytes from the SLM layer in the hippocampus using GFAP (green) as an astroglial marker, and TSP‐1 (red) are depicted magnified. TSP‐1 signal intensity quantification was performed in each layer of the hippocampus and normalized to the quantification area (μm2). Three independent animals of each strain were analyzed for immunohistochemical analysis ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 100 μm; 10 μm (representative astrocyte).

    Techniques Used: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Marker

    The competitive TSP‐1 receptor antagonist gabapentin (GBP) blocks the synaptogenic effect of SAMR1 ACMs. (A and C) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACMs from Diff‐Ast SAMR1 and SAMP8 with or without GBP 32 μM. (B and D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) colocalization vesicles in hippocampal neurons treated with ACMs from ACSA‐2 + SAMR1 and SAMP8 of 6‐m mice with or without GBP 32 μM. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05, ** p < 0.01, and *** p < 0.001. Scale bar: 50 μm.
    Figure Legend Snippet: The competitive TSP‐1 receptor antagonist gabapentin (GBP) blocks the synaptogenic effect of SAMR1 ACMs. (A and C) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACMs from Diff‐Ast SAMR1 and SAMP8 with or without GBP 32 μM. (B and D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) colocalization vesicles in hippocampal neurons treated with ACMs from ACSA‐2 + SAMR1 and SAMP8 of 6‐m mice with or without GBP 32 μM. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05, ** p < 0.01, and *** p < 0.001. Scale bar: 50 μm.

    Techniques Used: Immunostaining

    TSP‐1 rescues the synaptogenic function of Diff‐Ast SAMP8 ACM. (A, B) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from Diff‐Ast SAMP8 with or without TSP‐1 (250 ng/mL) supplementation. (C, D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from transfected Diff‐Ast SAMP8 overexpressing mThbs1 and GFP, or pcDNA3 and GFP as a control. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 50 μm.
    Figure Legend Snippet: TSP‐1 rescues the synaptogenic function of Diff‐Ast SAMP8 ACM. (A, B) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from Diff‐Ast SAMP8 with or without TSP‐1 (250 ng/mL) supplementation. (C, D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from transfected Diff‐Ast SAMP8 overexpressing mThbs1 and GFP, or pcDNA3 and GFP as a control. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 50 μm.

    Techniques Used: Immunostaining, Transfection, Control



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    6‐month‐old ACSA‐2+ SAMP8 primary cultured astrocytes and differentiated astrocytes derived from SAMP8 neural stem cells display loss <t>in</t> <t>TSP‐1</t> levels. (A) RNA‐seq transcriptional profile of Thbs1 gene in astrocytes, neurons, endothelial cells, oligodendrocytes and microglia in P7 (postnatal day) mice. (B) RNA‐seq transcriptional profile of Thbs1 gene at different stages of development and aging in astrocytes from mouse hippocampus. (C) Representative images of GFAP (green) and TSP‐1 (red) immunostaining in ACSA‐2+ primary astrocytes cultures of the SAMP8 and SAMR1 strains (14 DIV) and in Diff‐Ast SAMP8 and SAMR1 strains (11 DIV). (D, E) Quantification of TSP‐1 protein shows lower levels in SAMP8 ACSA‐2+ astrocytes cultures ( p = 0.021) and in Diff‐Ast SAMP8 ( p = 0.011) than in the control SAMR1 strain. (F) RT‐qPCR of Thbs1 ( p = 0.001) demonstrates lower gene expression levels in Diff‐Ast SAMP8 compared to the control line SAMR1. Three independent experiments per cell type were analyzed ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed in (D, E). One‐sample t ‐test was done in (F). * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar: 50 μm. Data in (A) and (B) were obtained from databases produced by the Barres lab (Zhang et al. and Clarke et al. available at https://brainrnaseq.org/ ).
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    Image Search Results


    6‐month‐old ACSA‐2+ SAMP8 primary cultured astrocytes and differentiated astrocytes derived from SAMP8 neural stem cells display loss in TSP‐1 levels. (A) RNA‐seq transcriptional profile of Thbs1 gene in astrocytes, neurons, endothelial cells, oligodendrocytes and microglia in P7 (postnatal day) mice. (B) RNA‐seq transcriptional profile of Thbs1 gene at different stages of development and aging in astrocytes from mouse hippocampus. (C) Representative images of GFAP (green) and TSP‐1 (red) immunostaining in ACSA‐2+ primary astrocytes cultures of the SAMP8 and SAMR1 strains (14 DIV) and in Diff‐Ast SAMP8 and SAMR1 strains (11 DIV). (D, E) Quantification of TSP‐1 protein shows lower levels in SAMP8 ACSA‐2+ astrocytes cultures ( p = 0.021) and in Diff‐Ast SAMP8 ( p = 0.011) than in the control SAMR1 strain. (F) RT‐qPCR of Thbs1 ( p = 0.001) demonstrates lower gene expression levels in Diff‐Ast SAMP8 compared to the control line SAMR1. Three independent experiments per cell type were analyzed ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed in (D, E). One‐sample t ‐test was done in (F). * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar: 50 μm. Data in (A) and (B) were obtained from databases produced by the Barres lab (Zhang et al. and Clarke et al. available at https://brainrnaseq.org/ ).

    Journal: Aging Cell

    Article Title: Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss

    doi: 10.1111/acel.70382

    Figure Lengend Snippet: 6‐month‐old ACSA‐2+ SAMP8 primary cultured astrocytes and differentiated astrocytes derived from SAMP8 neural stem cells display loss in TSP‐1 levels. (A) RNA‐seq transcriptional profile of Thbs1 gene in astrocytes, neurons, endothelial cells, oligodendrocytes and microglia in P7 (postnatal day) mice. (B) RNA‐seq transcriptional profile of Thbs1 gene at different stages of development and aging in astrocytes from mouse hippocampus. (C) Representative images of GFAP (green) and TSP‐1 (red) immunostaining in ACSA‐2+ primary astrocytes cultures of the SAMP8 and SAMR1 strains (14 DIV) and in Diff‐Ast SAMP8 and SAMR1 strains (11 DIV). (D, E) Quantification of TSP‐1 protein shows lower levels in SAMP8 ACSA‐2+ astrocytes cultures ( p = 0.021) and in Diff‐Ast SAMP8 ( p = 0.011) than in the control SAMR1 strain. (F) RT‐qPCR of Thbs1 ( p = 0.001) demonstrates lower gene expression levels in Diff‐Ast SAMP8 compared to the control line SAMR1. Three independent experiments per cell type were analyzed ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed in (D, E). One‐sample t ‐test was done in (F). * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar: 50 μm. Data in (A) and (B) were obtained from databases produced by the Barres lab (Zhang et al. and Clarke et al. available at https://brainrnaseq.org/ ).

    Article Snippet: At 11 DIV, neuron medium was totally replaced by ACM from Ast‐Diff or half replaced by ACSA‐2 + ACM during 3 h. Gabapentin (GBP, MedChemExpress, HY‐A0057) and TSP‐1 (MedChemExpress, HY‐P701325) dosages were based on Cheng et al. ( ) procedures.

    Techniques: Cell Culture, Derivative Assay, RNA Sequencing, Immunostaining, Control, Quantitative RT-PCR, Gene Expression, Produced

    The hippocampus of 10‐month‐old SAMP8 mice shows deficiencies in TSP‐1 levels. (A) RT‐qPCR of Thbs1 ( p = 0.022) in SAMR1 ( n = 7 independent animals) and SAMP8 ( n = 8 independent animals). (B) TSP‐1 quantification by ELISA test in 10‐m SAMR1 ( n = 4 independent animals) and SAMP8 ( n = 3 independent animals) mice normalized to total protein levels. (C, D) Immunohistochemical analyses and TSP‐1 intensity quantification in 10‐m SAMR1 and SAMP8 hippocampus are shown. Representative astrocytes from the SLM layer in the hippocampus using GFAP (green) as an astroglial marker, and TSP‐1 (red) are depicted magnified. TSP‐1 signal intensity quantification was performed in each layer of the hippocampus and normalized to the quantification area (μm2). Three independent animals of each strain were analyzed for immunohistochemical analysis ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 100 μm; 10 μm (representative astrocyte).

    Journal: Aging Cell

    Article Title: Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss

    doi: 10.1111/acel.70382

    Figure Lengend Snippet: The hippocampus of 10‐month‐old SAMP8 mice shows deficiencies in TSP‐1 levels. (A) RT‐qPCR of Thbs1 ( p = 0.022) in SAMR1 ( n = 7 independent animals) and SAMP8 ( n = 8 independent animals). (B) TSP‐1 quantification by ELISA test in 10‐m SAMR1 ( n = 4 independent animals) and SAMP8 ( n = 3 independent animals) mice normalized to total protein levels. (C, D) Immunohistochemical analyses and TSP‐1 intensity quantification in 10‐m SAMR1 and SAMP8 hippocampus are shown. Representative astrocytes from the SLM layer in the hippocampus using GFAP (green) as an astroglial marker, and TSP‐1 (red) are depicted magnified. TSP‐1 signal intensity quantification was performed in each layer of the hippocampus and normalized to the quantification area (μm2). Three independent animals of each strain were analyzed for immunohistochemical analysis ( n = 3). Data are presented as mean ± SEM. Unpaired t ‐test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 100 μm; 10 μm (representative astrocyte).

    Article Snippet: At 11 DIV, neuron medium was totally replaced by ACM from Ast‐Diff or half replaced by ACSA‐2 + ACM during 3 h. Gabapentin (GBP, MedChemExpress, HY‐A0057) and TSP‐1 (MedChemExpress, HY‐P701325) dosages were based on Cheng et al. ( ) procedures.

    Techniques: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Marker

    The competitive TSP‐1 receptor antagonist gabapentin (GBP) blocks the synaptogenic effect of SAMR1 ACMs. (A and C) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACMs from Diff‐Ast SAMR1 and SAMP8 with or without GBP 32 μM. (B and D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) colocalization vesicles in hippocampal neurons treated with ACMs from ACSA‐2 + SAMR1 and SAMP8 of 6‐m mice with or without GBP 32 μM. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05, ** p < 0.01, and *** p < 0.001. Scale bar: 50 μm.

    Journal: Aging Cell

    Article Title: Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss

    doi: 10.1111/acel.70382

    Figure Lengend Snippet: The competitive TSP‐1 receptor antagonist gabapentin (GBP) blocks the synaptogenic effect of SAMR1 ACMs. (A and C) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACMs from Diff‐Ast SAMR1 and SAMP8 with or without GBP 32 μM. (B and D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) colocalization vesicles in hippocampal neurons treated with ACMs from ACSA‐2 + SAMR1 and SAMP8 of 6‐m mice with or without GBP 32 μM. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05, ** p < 0.01, and *** p < 0.001. Scale bar: 50 μm.

    Article Snippet: At 11 DIV, neuron medium was totally replaced by ACM from Ast‐Diff or half replaced by ACSA‐2 + ACM during 3 h. Gabapentin (GBP, MedChemExpress, HY‐A0057) and TSP‐1 (MedChemExpress, HY‐P701325) dosages were based on Cheng et al. ( ) procedures.

    Techniques: Immunostaining

    TSP‐1 rescues the synaptogenic function of Diff‐Ast SAMP8 ACM. (A, B) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from Diff‐Ast SAMP8 with or without TSP‐1 (250 ng/mL) supplementation. (C, D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from transfected Diff‐Ast SAMP8 overexpressing mThbs1 and GFP, or pcDNA3 and GFP as a control. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 50 μm.

    Journal: Aging Cell

    Article Title: Astrocyte Senescence Impairs Synaptogenesis due to Thrombospondin‐1 Loss

    doi: 10.1111/acel.70382

    Figure Lengend Snippet: TSP‐1 rescues the synaptogenic function of Diff‐Ast SAMP8 ACM. (A, B) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from Diff‐Ast SAMP8 with or without TSP‐1 (250 ng/mL) supplementation. (C, D) Immunostaining of MAP2 (gray), VGLUT1 (red) and PSD95 (green), and quantification of excitatory pre‐ (VGLUT1) and postsynaptic (PSD95) vesicles colocalization in hippocampal neurons treated with ACM from transfected Diff‐Ast SAMP8 overexpressing mThbs1 and GFP, or pcDNA3 and GFP as a control. Three independent experiments were analyzed per cell type and experimental condition. Data are presented as mean ± SEM. One‐way ANOVA Tukey's multiple comparisons test was performed. * p < 0.05 and ** p < 0.01. Scale bar: 50 μm.

    Article Snippet: At 11 DIV, neuron medium was totally replaced by ACM from Ast‐Diff or half replaced by ACSA‐2 + ACM during 3 h. Gabapentin (GBP, MedChemExpress, HY‐A0057) and TSP‐1 (MedChemExpress, HY‐P701325) dosages were based on Cheng et al. ( ) procedures.

    Techniques: Immunostaining, Transfection, Control

    Figure 1. Proliferation- and apoptosis-related gene detection in CL23 cells and M60 cells. (a) Proliferation- and apoptosis-related genes were expressed at the mRNA level in CL23 cells and M60 cells. (b) Proliferation- and apopto sis-related genes were expressed at the protein level in CL23 cells and M60 cells. (c) THBS1 and EPHB2 protein level expression in CL23 cells and tu- mourigenic M60 cells. Differential grey value analysis. * indicates statistically significant difference (*** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 1. Proliferation- and apoptosis-related gene detection in CL23 cells and M60 cells. (a) Proliferation- and apoptosis-related genes were expressed at the mRNA level in CL23 cells and M60 cells. (b) Proliferation- and apopto sis-related genes were expressed at the protein level in CL23 cells and M60 cells. (c) THBS1 and EPHB2 protein level expression in CL23 cells and tu- mourigenic M60 cells. Differential grey value analysis. * indicates statistically significant difference (*** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Expressing

    Figure 3. Construction and characterisation of MDCK cell lines stably knocking down and overex- pressing THBS1. (a) Bright field and fluorescence expression of cells after puromycin screening of knockdown control cells THBS1-sh-con puromycin; bright field and fluorescence expression of cells after puromycin screening of knockdown cells THBS1-sh-122484 locus; knockdown cells THBS1-sh- 122485 locus puromycin screened for cell bright field and fluorescence expression; knockdown cells THBS1-sh-122486 locus puromycin screened for cell bright field and fluorescence expression; overex- pression of control cells THBS1-OE-con puromycin screened for cell bright field and fluorescence

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 3. Construction and characterisation of MDCK cell lines stably knocking down and overex- pressing THBS1. (a) Bright field and fluorescence expression of cells after puromycin screening of knockdown control cells THBS1-sh-con puromycin; bright field and fluorescence expression of cells after puromycin screening of knockdown cells THBS1-sh-122484 locus; knockdown cells THBS1-sh- 122485 locus puromycin screened for cell bright field and fluorescence expression; knockdown cells THBS1-sh-122486 locus puromycin screened for cell bright field and fluorescence expression; overex- pression of control cells THBS1-OE-con puromycin screened for cell bright field and fluorescence

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Stable Transfection, Fluorescence, Expressing, Knockdown, Control

    Figure 4. Effects of knockdown of THBS1 on proliferation, apoptosis, migration, and cell cycle of CL23 cells. (a) Growth curves of stably knocked down THBS1 cell lines. (b) Analysis of migratory ability of stably knocked down THBS1 cell lines. (c) Analysis of apoptotic ability of stably knocked down THBS1 cell lines. (d) Analysis of cell cycle of stably knocked down THBS1 cell lines. * denotes statistically significant difference (* p < 0.05; ** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 4. Effects of knockdown of THBS1 on proliferation, apoptosis, migration, and cell cycle of CL23 cells. (a) Growth curves of stably knocked down THBS1 cell lines. (b) Analysis of migratory ability of stably knocked down THBS1 cell lines. (c) Analysis of apoptotic ability of stably knocked down THBS1 cell lines. (d) Analysis of cell cycle of stably knocked down THBS1 cell lines. * denotes statistically significant difference (* p < 0.05; ** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Knockdown, Migration, Stable Transfection

    Figure 5. Effects of overexpression of THBS1 on proliferation, apoptosis, migration, and cell cycle of M60 cells. (a) Growth curves of stable overexpression of THBS1 cell lines. (b) Analysis of migration ability of stable overexpression of THBS1 cell lines. (c) Analysis of apoptosis ability of stable overexpression of THBS1 cell lines. (d) Analysis of cell cycle of stable overexpression of THBS1 cell lines. * denotes statistically significant difference (** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 5. Effects of overexpression of THBS1 on proliferation, apoptosis, migration, and cell cycle of M60 cells. (a) Growth curves of stable overexpression of THBS1 cell lines. (b) Analysis of migration ability of stable overexpression of THBS1 cell lines. (c) Analysis of apoptosis ability of stable overexpression of THBS1 cell lines. (d) Analysis of cell cycle of stable overexpression of THBS1 cell lines. * denotes statistically significant difference (** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Over Expression, Migration

    Figure 6. Effect of knockdown and overexpression of THBS1 on H1N1 influenza virus replication in MDCK cells. (a,b) Differences in expression of NP and NS1 mRNA levels across time of H1N1 influenza virus infection in stably knocked down THBS1 cell lines. (c,d) Differences in expression of NP protein levels across time of H1N1 influenza virus infection in stably knocked down THBS1 cell lines. (e,f) Stable overexpression of THBS1 cell lines infected with H1N1 influenza virus different time period NP and NS1 mRNA level expression differences. (g,h) Stable overexpression of THBS1 cell lines infected with H1N1 influenza virus different time period NP protein level expression differences. * indicates statistically significant difference (* p < 0.05; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 6. Effect of knockdown and overexpression of THBS1 on H1N1 influenza virus replication in MDCK cells. (a,b) Differences in expression of NP and NS1 mRNA levels across time of H1N1 influenza virus infection in stably knocked down THBS1 cell lines. (c,d) Differences in expression of NP protein levels across time of H1N1 influenza virus infection in stably knocked down THBS1 cell lines. (e,f) Stable overexpression of THBS1 cell lines infected with H1N1 influenza virus different time period NP and NS1 mRNA level expression differences. (g,h) Stable overexpression of THBS1 cell lines infected with H1N1 influenza virus different time period NP protein level expression differences. * indicates statistically significant difference (* p < 0.05; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Knockdown, Over Expression, Virus, Expressing, Infection, Stable Transfection

    Figure 7. Differential expression of target genes downstream of PI3K/Akt, P53, and TGF-β/Smad signalling pathways, as well as the predicted THBS1-interacting gene, SCARB2, in M60 and CL23 cells. (a,b) Differential expression of target genes downstream of the PI3K/Akt, P53, and TGF-β/Smad signalling pathways, as well as SCARB2 at mRNA level. (c,d) Differential expression of target genes downstream of the TGF-β/Smad signalling pathway and SCARB2 at the protein level. * indicates statistically significant difference (** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 7. Differential expression of target genes downstream of PI3K/Akt, P53, and TGF-β/Smad signalling pathways, as well as the predicted THBS1-interacting gene, SCARB2, in M60 and CL23 cells. (a,b) Differential expression of target genes downstream of the PI3K/Akt, P53, and TGF-β/Smad signalling pathways, as well as SCARB2 at mRNA level. (c,d) Differential expression of target genes downstream of the TGF-β/Smad signalling pathway and SCARB2 at the protein level. * indicates statistically significant difference (** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Quantitative Proteomics

    Figure 8. Effects of knockdown and overexpression of THBS1 on the differential expression of target genes downstream of TGF-β/Smad, PI3K/Akt, P53 signalling pathways, and SCARB2 in MDCK cells. (a,b) Effects of knockdown of THBS1 on the differential expression of target genes downstream of PI3K/Akt, P53, TGF-β/Smad signalling, and the SCARB2 mRNA level expression differences in CL23 cells. (c,d) Differential effects of overexpression of THBS1 on the expression of target genes downstream of PI3K/Akt, P53, TGF-β/Smad signalling, and SCARB2 at the mRNA level in M60 cells. (e) Differential effects of knockdown and overexpression of THBS1 on the expression of target genes downstream of the PI3K/Akt, P53, TGF-β/Smad signalling pathways in MDCK cells, and the SCARB2 protein level expression differences. (f,g) Grey value analysis of knockdown and overexpression of THBS1 on the expression of target genes downstream of the PI3K/Akt, P53, and TGF-β/Smad signalling pathways, as well as SCARB2 protein level in MDCK cells. * indicates statistically significant difference (* p < 0.05; ** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 8. Effects of knockdown and overexpression of THBS1 on the differential expression of target genes downstream of TGF-β/Smad, PI3K/Akt, P53 signalling pathways, and SCARB2 in MDCK cells. (a,b) Effects of knockdown of THBS1 on the differential expression of target genes downstream of PI3K/Akt, P53, TGF-β/Smad signalling, and the SCARB2 mRNA level expression differences in CL23 cells. (c,d) Differential effects of overexpression of THBS1 on the expression of target genes downstream of PI3K/Akt, P53, TGF-β/Smad signalling, and SCARB2 at the mRNA level in M60 cells. (e) Differential effects of knockdown and overexpression of THBS1 on the expression of target genes downstream of the PI3K/Akt, P53, TGF-β/Smad signalling pathways in MDCK cells, and the SCARB2 protein level expression differences. (f,g) Grey value analysis of knockdown and overexpression of THBS1 on the expression of target genes downstream of the PI3K/Akt, P53, and TGF-β/Smad signalling pathways, as well as SCARB2 protein level in MDCK cells. * indicates statistically significant difference (* p < 0.05; ** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Knockdown, Over Expression, Quantitative Proteomics, Expressing

    Figure 9. Determination of optimal concentration of TGF-β activator SRI-011381 on THBS1-sh-122484 cells and inhibitor LY2109761 on THBS1-OE cells, and its effect on the expression of target genes,

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 9. Determination of optimal concentration of TGF-β activator SRI-011381 on THBS1-sh-122484 cells and inhibitor LY2109761 on THBS1-OE cells, and its effect on the expression of target genes,

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Concentration Assay, Expressing

    Figure 10. Effect of SRI-011381 (5 µg/mL) on the expression of PI3K/Akt, target genes downstream of P53 signalling pathway, SCARB2 in knockdown THBS1 cells (THBS1-sh-122484), and LY2109761 (10 µg/mL) in overexpressing THBS1 (THBS1-OE) cells. (a) SRI-011381 (5 µg/mL) intervention in THBS1-sh-122484 cells showed differential expression of PI3K/Akt, target genes downstream of P53 signalling, and SCARB2 at the mRNA level. (b) LY2109761 (10 µg/mL) intervention in THBS1-OE cells showed differential expression of PI3K/Akt, target genes downstream of P53 signalling, and SCARB2 expression differences at the mRNA level. (c) PI3K/Akt, P53 signalling downstream target genes, and SCARB2 expression differences at the protein level after SRI-011381 (5 µg/mL) intervention in THBS1-sh-122484 cells and LY2109761 (10 µg/mL) intervention in THBS1-OE cells. (d) SRI- 011381 (5 µg/mL) intervention in THBS1-sh-122484 cells after PI3K/Akt, P53 signalling downstream target genes, and SCARB2 expression differences at protein level grey value analysis. (e) LY2109761 (10 µg/mL) intervention in THBS1-OE cells after PI3K/Akt, P53 signalling downstream target genes, and SCARB2 expression difference at protein level grey value analysis. * indicates statistically significant difference (* p < 0.05; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 10. Effect of SRI-011381 (5 µg/mL) on the expression of PI3K/Akt, target genes downstream of P53 signalling pathway, SCARB2 in knockdown THBS1 cells (THBS1-sh-122484), and LY2109761 (10 µg/mL) in overexpressing THBS1 (THBS1-OE) cells. (a) SRI-011381 (5 µg/mL) intervention in THBS1-sh-122484 cells showed differential expression of PI3K/Akt, target genes downstream of P53 signalling, and SCARB2 at the mRNA level. (b) LY2109761 (10 µg/mL) intervention in THBS1-OE cells showed differential expression of PI3K/Akt, target genes downstream of P53 signalling, and SCARB2 expression differences at the mRNA level. (c) PI3K/Akt, P53 signalling downstream target genes, and SCARB2 expression differences at the protein level after SRI-011381 (5 µg/mL) intervention in THBS1-sh-122484 cells and LY2109761 (10 µg/mL) intervention in THBS1-OE cells. (d) SRI- 011381 (5 µg/mL) intervention in THBS1-sh-122484 cells after PI3K/Akt, P53 signalling downstream target genes, and SCARB2 expression differences at protein level grey value analysis. (e) LY2109761 (10 µg/mL) intervention in THBS1-OE cells after PI3K/Akt, P53 signalling downstream target genes, and SCARB2 expression difference at protein level grey value analysis. * indicates statistically significant difference (* p < 0.05; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Expressing, Knockdown, Quantitative Proteomics

    Figure 11. Effects of SRI-011381 on knockdown THBS1 cells (THBS1-sh-122484) and LY2109761 on proliferation and migration ability of overexpressing THBS1 cells (THBS1-OE). (a) Growth curve of SRI-011381 intervention knockdown THBS1 cells (THBS1-sh-122484). (b,c) SRI-011381 intervention knockdown THBS1 cells (THBS1-sh-122484) migration ability assay. (d) SRI-011381 intervention knockdown THBS1 cells (THBS1-sh-122484) apoptosis ability assay. (e) LY2109761 intervention overexpression THBS1 cells (THBS1-OE) growth curve. (f,g) LY2109761 intervention overexpression THBS1 cells (THBS1-OE) migration ability assay. (h) LY2109761 intervention overexpression THBS1 cells (THBS1-OE) apoptosis ability assay. * indicates statistically significant difference (** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Journal: International journal of molecular sciences

    Article Title: Mechanism of THBS1 Regulation of MDCK Cell Proliferation and Apoptosis Through TGF-β/Smad Signalling.

    doi: 10.3390/ijms26010395

    Figure Lengend Snippet: Figure 11. Effects of SRI-011381 on knockdown THBS1 cells (THBS1-sh-122484) and LY2109761 on proliferation and migration ability of overexpressing THBS1 cells (THBS1-OE). (a) Growth curve of SRI-011381 intervention knockdown THBS1 cells (THBS1-sh-122484). (b,c) SRI-011381 intervention knockdown THBS1 cells (THBS1-sh-122484) migration ability assay. (d) SRI-011381 intervention knockdown THBS1 cells (THBS1-sh-122484) apoptosis ability assay. (e) LY2109761 intervention overexpression THBS1 cells (THBS1-OE) growth curve. (f,g) LY2109761 intervention overexpression THBS1 cells (THBS1-OE) migration ability assay. (h) LY2109761 intervention overexpression THBS1 cells (THBS1-OE) apoptosis ability assay. * indicates statistically significant difference (** p < 0.01; *** p < 0.001) and no * indicates no difference.

    Article Snippet: To further evaluate the mechanism by which THBS1 regulates MDCK cell proliferation and apoptosis through TGF-β/Smad signalling, we observed the cell growth status with different concentration gradients of the TGF-β/Smad signalling pathway activator SRI-011381 (MCE, Shanghai, China, HY-12075) of THBS1-knockdown cells (THBS1-sh122484) and the inhibitor LY2109761 (MCE, Shanghai, China, HY-100347) of THBS1-overexpressing cells (THBS1-OE).

    Techniques: Knockdown, Migration, Over Expression

    Selection of key genes based on protein–protein interaction analysis.

    Journal: PLOS ONE

    Article Title: miR-335-3p attenuates transforming growth factor beta 1-induced fibrosis by suppressing Thrombospondin 1

    doi: 10.1371/journal.pone.0311594

    Figure Lengend Snippet: Selection of key genes based on protein–protein interaction analysis.

    Article Snippet: Various TGF-β1 concentrations (0.1–10 ng/mL) were administered for 2 days after the cells stabilized for 24 h to construct the fibrosis model. For analysis, miRNA mimics and inhibitors were transfected into TGF-β1-treated and untreated groups for 48 h. A THBS1 inhibitor LSKL (MedChemExpress USA, Middlesex, NJ, USA) was simultaneously added at 20 μM in the TGF-β1-treated and untreated groups and cultured for 48 h.

    Techniques: Selection

    Transcriptome analysis on miRNA was conducted after treatment with 1 and 5 ng/mL TGF-β1 for 48 h. (A) miRNAs with significantly changed expression following TGF-β1 treatment were identified for each cell type. (B) Hierarchical clustering was performed on miRNAs targeting the core genes selected from those showing significant expression changes. (C) The expression of miR-335-3p decreased after TGF-β1 treatment in both cell lines. (D) The binding site of miR-335-3p is depicted on the 3ʹ-untranslated region of THBS1. Con: Control group (TGF-β1-untreated group); T1: 1 ng/mL TGF-β1-treated group; T5: 5 ng/mL TGF-β1-treated group.

    Journal: PLOS ONE

    Article Title: miR-335-3p attenuates transforming growth factor beta 1-induced fibrosis by suppressing Thrombospondin 1

    doi: 10.1371/journal.pone.0311594

    Figure Lengend Snippet: Transcriptome analysis on miRNA was conducted after treatment with 1 and 5 ng/mL TGF-β1 for 48 h. (A) miRNAs with significantly changed expression following TGF-β1 treatment were identified for each cell type. (B) Hierarchical clustering was performed on miRNAs targeting the core genes selected from those showing significant expression changes. (C) The expression of miR-335-3p decreased after TGF-β1 treatment in both cell lines. (D) The binding site of miR-335-3p is depicted on the 3ʹ-untranslated region of THBS1. Con: Control group (TGF-β1-untreated group); T1: 1 ng/mL TGF-β1-treated group; T5: 5 ng/mL TGF-β1-treated group.

    Article Snippet: Various TGF-β1 concentrations (0.1–10 ng/mL) were administered for 2 days after the cells stabilized for 24 h to construct the fibrosis model. For analysis, miRNA mimics and inhibitors were transfected into TGF-β1-treated and untreated groups for 48 h. A THBS1 inhibitor LSKL (MedChemExpress USA, Middlesex, NJ, USA) was simultaneously added at 20 μM in the TGF-β1-treated and untreated groups and cultured for 48 h.

    Techniques: Expressing, Binding Assay, Control

    The expression of miR-335-3p was altered in A549 and BEAS-2B cell lines to observe the regulatory effect of miR-335-3p on THBS1. (A, B) THBS1 expression and fibrosis markers were suppressed following transfection with miR-335-3p mimic. (C, D) The upregulation of TBHS1 and fibrotic marker expression were observed after the introduction of miR-335-3p inhibitor. Each experiment was conducted in triplicate. # p < 0.05; ## p < 0.01; ### p < 0.001 compared with the TGF-β1-only-treated group. C: Control group; T: 5 ng/mL TGF-β1-treated group; sc: scrambled RNA-treated group; mi:miR-335-3p mimic-treated group; in: mi:miR-335-3p inhibitor-treated group.

    Journal: PLOS ONE

    Article Title: miR-335-3p attenuates transforming growth factor beta 1-induced fibrosis by suppressing Thrombospondin 1

    doi: 10.1371/journal.pone.0311594

    Figure Lengend Snippet: The expression of miR-335-3p was altered in A549 and BEAS-2B cell lines to observe the regulatory effect of miR-335-3p on THBS1. (A, B) THBS1 expression and fibrosis markers were suppressed following transfection with miR-335-3p mimic. (C, D) The upregulation of TBHS1 and fibrotic marker expression were observed after the introduction of miR-335-3p inhibitor. Each experiment was conducted in triplicate. # p < 0.05; ## p < 0.01; ### p < 0.001 compared with the TGF-β1-only-treated group. C: Control group; T: 5 ng/mL TGF-β1-treated group; sc: scrambled RNA-treated group; mi:miR-335-3p mimic-treated group; in: mi:miR-335-3p inhibitor-treated group.

    Article Snippet: Various TGF-β1 concentrations (0.1–10 ng/mL) were administered for 2 days after the cells stabilized for 24 h to construct the fibrosis model. For analysis, miRNA mimics and inhibitors were transfected into TGF-β1-treated and untreated groups for 48 h. A THBS1 inhibitor LSKL (MedChemExpress USA, Middlesex, NJ, USA) was simultaneously added at 20 μM in the TGF-β1-treated and untreated groups and cultured for 48 h.

    Techniques: Expressing, Transfection, Marker, Control