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vitro myofibroblast culture methods early passage  (ATCC)


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    ATCC vitro myofibroblast culture methods early passage
    (A) Spironolactone inhibits TGFβ induction of αSMA protein expression in colonic <t>myofibroblasts.</t> A representative Western blot of αSMA expression in protein extracts from <t>CCD-18co</t> colonic myofibroblasts stimulated for 24 h with TGFβ is shown. Increasing amounts of spironolactone (SPIR) from 10 μM to 100 μM reduce αSMA expression to levels comparable to unstimulated cells (no Tx). GAPDH expression serves as the loading control for the amount of protein. (B) Treatment of TGFβ stimulated CCD-18co cells with spironolactone (SPIR) represses expression of Acta2, Col1a1, and Ctgf. A metabolite of spironolactone, canrenone (CAN) partially represses pro-fibrotic gene expression. (C) The role of the RAAS pathway in fibrosis and the relationship of pathway inhibitors. (D) Inhibitors of the RAAS pathway aliskiren (ALK), enalaprilat (ENT), and losartan (LOR) partially repress TGFβ induction of fibrotic genes with partial repression of Acta2 expression but have minimal effect on Col1a1 expression (E). Results are from 9 independent experiments. Asterisks denote statistically significant comparisons between untreated control cells (no Tx) and the treatment groups. Brackets denote comparisons between TGFβ treated and other treatment groups. * P <0.05, *** P <0.001
    Vitro Myofibroblast Culture Methods Early Passage, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 975 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vitro+myofibroblast+culture+methods+early+passage/pmc03288762-76-1-17?v=ATCC
    Average 97 stars, based on 975 article reviews
    vitro myofibroblast culture methods early passage - by Bioz Stars, 2026-07
    97/100 stars

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    1) Product Images from "Spironolactone and colitis: Increased mortality in rodents and in humans"

    Article Title: Spironolactone and colitis: Increased mortality in rodents and in humans

    Journal: Inflammatory Bowel Diseases

    doi: 10.1002/ibd.21929

    (A) Spironolactone inhibits TGFβ induction of αSMA protein expression in colonic myofibroblasts. A representative Western blot of αSMA expression in protein extracts from CCD-18co colonic myofibroblasts stimulated for 24 h with TGFβ is shown. Increasing amounts of spironolactone (SPIR) from 10 μM to 100 μM reduce αSMA expression to levels comparable to unstimulated cells (no Tx). GAPDH expression serves as the loading control for the amount of protein. (B) Treatment of TGFβ stimulated CCD-18co cells with spironolactone (SPIR) represses expression of Acta2, Col1a1, and Ctgf. A metabolite of spironolactone, canrenone (CAN) partially represses pro-fibrotic gene expression. (C) The role of the RAAS pathway in fibrosis and the relationship of pathway inhibitors. (D) Inhibitors of the RAAS pathway aliskiren (ALK), enalaprilat (ENT), and losartan (LOR) partially repress TGFβ induction of fibrotic genes with partial repression of Acta2 expression but have minimal effect on Col1a1 expression (E). Results are from 9 independent experiments. Asterisks denote statistically significant comparisons between untreated control cells (no Tx) and the treatment groups. Brackets denote comparisons between TGFβ treated and other treatment groups. * P <0.05, *** P <0.001
    Figure Legend Snippet: (A) Spironolactone inhibits TGFβ induction of αSMA protein expression in colonic myofibroblasts. A representative Western blot of αSMA expression in protein extracts from CCD-18co colonic myofibroblasts stimulated for 24 h with TGFβ is shown. Increasing amounts of spironolactone (SPIR) from 10 μM to 100 μM reduce αSMA expression to levels comparable to unstimulated cells (no Tx). GAPDH expression serves as the loading control for the amount of protein. (B) Treatment of TGFβ stimulated CCD-18co cells with spironolactone (SPIR) represses expression of Acta2, Col1a1, and Ctgf. A metabolite of spironolactone, canrenone (CAN) partially represses pro-fibrotic gene expression. (C) The role of the RAAS pathway in fibrosis and the relationship of pathway inhibitors. (D) Inhibitors of the RAAS pathway aliskiren (ALK), enalaprilat (ENT), and losartan (LOR) partially repress TGFβ induction of fibrotic genes with partial repression of Acta2 expression but have minimal effect on Col1a1 expression (E). Results are from 9 independent experiments. Asterisks denote statistically significant comparisons between untreated control cells (no Tx) and the treatment groups. Brackets denote comparisons between TGFβ treated and other treatment groups. * P <0.05, *** P <0.001

    Techniques Used: Expressing, Western Blot, Control, Gene Expression



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    vitro myofibroblast culture methods early passage  (ATCC)
    97
    ATCC vitro myofibroblast culture methods early passage
    (A) Spironolactone inhibits TGFβ induction of αSMA protein expression in colonic <t>myofibroblasts.</t> A representative Western blot of αSMA expression in protein extracts from <t>CCD-18co</t> colonic myofibroblasts stimulated for 24 h with TGFβ is shown. Increasing amounts of spironolactone (SPIR) from 10 μM to 100 μM reduce αSMA expression to levels comparable to unstimulated cells (no Tx). GAPDH expression serves as the loading control for the amount of protein. (B) Treatment of TGFβ stimulated CCD-18co cells with spironolactone (SPIR) represses expression of Acta2, Col1a1, and Ctgf. A metabolite of spironolactone, canrenone (CAN) partially represses pro-fibrotic gene expression. (C) The role of the RAAS pathway in fibrosis and the relationship of pathway inhibitors. (D) Inhibitors of the RAAS pathway aliskiren (ALK), enalaprilat (ENT), and losartan (LOR) partially repress TGFβ induction of fibrotic genes with partial repression of Acta2 expression but have minimal effect on Col1a1 expression (E). Results are from 9 independent experiments. Asterisks denote statistically significant comparisons between untreated control cells (no Tx) and the treatment groups. Brackets denote comparisons between TGFβ treated and other treatment groups. * P <0.05, *** P <0.001
    Vitro Myofibroblast Culture Methods Early Passage, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vitro+myofibroblast+culture+methods+early+passage/pmc03288762-76-1-17?v=ATCC
    Average 97 stars, based on 1 article reviews
    vitro myofibroblast culture methods early passage - by Bioz Stars, 2026-07
    97/100 stars
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    (A) Spironolactone inhibits TGFβ induction of αSMA protein expression in colonic myofibroblasts. A representative Western blot of αSMA expression in protein extracts from CCD-18co colonic myofibroblasts stimulated for 24 h with TGFβ is shown. Increasing amounts of spironolactone (SPIR) from 10 μM to 100 μM reduce αSMA expression to levels comparable to unstimulated cells (no Tx). GAPDH expression serves as the loading control for the amount of protein. (B) Treatment of TGFβ stimulated CCD-18co cells with spironolactone (SPIR) represses expression of Acta2, Col1a1, and Ctgf. A metabolite of spironolactone, canrenone (CAN) partially represses pro-fibrotic gene expression. (C) The role of the RAAS pathway in fibrosis and the relationship of pathway inhibitors. (D) Inhibitors of the RAAS pathway aliskiren (ALK), enalaprilat (ENT), and losartan (LOR) partially repress TGFβ induction of fibrotic genes with partial repression of Acta2 expression but have minimal effect on Col1a1 expression (E). Results are from 9 independent experiments. Asterisks denote statistically significant comparisons between untreated control cells (no Tx) and the treatment groups. Brackets denote comparisons between TGFβ treated and other treatment groups. * P <0.05, *** P <0.001

    Journal: Inflammatory Bowel Diseases

    Article Title: Spironolactone and colitis: Increased mortality in rodents and in humans

    doi: 10.1002/ibd.21929

    Figure Lengend Snippet: (A) Spironolactone inhibits TGFβ induction of αSMA protein expression in colonic myofibroblasts. A representative Western blot of αSMA expression in protein extracts from CCD-18co colonic myofibroblasts stimulated for 24 h with TGFβ is shown. Increasing amounts of spironolactone (SPIR) from 10 μM to 100 μM reduce αSMA expression to levels comparable to unstimulated cells (no Tx). GAPDH expression serves as the loading control for the amount of protein. (B) Treatment of TGFβ stimulated CCD-18co cells with spironolactone (SPIR) represses expression of Acta2, Col1a1, and Ctgf. A metabolite of spironolactone, canrenone (CAN) partially represses pro-fibrotic gene expression. (C) The role of the RAAS pathway in fibrosis and the relationship of pathway inhibitors. (D) Inhibitors of the RAAS pathway aliskiren (ALK), enalaprilat (ENT), and losartan (LOR) partially repress TGFβ induction of fibrotic genes with partial repression of Acta2 expression but have minimal effect on Col1a1 expression (E). Results are from 9 independent experiments. Asterisks denote statistically significant comparisons between untreated control cells (no Tx) and the treatment groups. Brackets denote comparisons between TGFβ treated and other treatment groups. * P <0.05, *** P <0.001

    Article Snippet: In vitro myofibroblast culture methods Early passage (3 to 12) colonic human fibroblast CCD-18Co cells (CRL-1459 from ATCC) were cultured in alpha-MEM (Invitrogen, Carlsbad, CA) supplemented with 10% fetal bovine serum and sub-cultured weekly.

    Techniques: Expressing, Western Blot, Control, Gene Expression