We are analyzing https://link.springer.com/article/10.1007/s12079-020-00596-x.

Title:
Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts | Journal of Cell Communication and Signaling
Description:
Fibrosis is perpetuated by an autocrine, pro-adhesive signaling loop maintained by the synthetic and contractile abilities of myofibroblasts and the stiff, highly-crosslinked extracellular matrix. Transcriptional complexes that are exquisitely responsive to mechanotransduction include the co-activator YAP1, which regulates the expression of members of the CCN family of matricellular proteins such as CCN2 and CCN1. Although selective YAP1 inhibitors exist, the effect of these inhibitors on profibrotic gene expression in fibroblasts is largely unknown, and is the subject of our current study. Herein, we use genome-wide expression profiling, real-time polymerase chain reaction and Western blot analyses, cell migration and collagen gel contraction assays to assess the ability of a selective YAP inhibitor verteporfin (VP) to block fibrogenic activities in dermal fibroblasts from healthy individual human controls and those from isolated from fibrotic lesions of patients with diffuse cutaneous systemic sclerosis (dcSSc). In control fibroblasts, VP selectively reduced expression of fibrogenic genes and also blocked the ability of TGFbeta to induce actin stress fibers in dermal fibroblasts. VP also reduced the persistent profibrotic phenotype of dermal fibroblasts cultured from fibrotic lesions of patients with dcSSc. Our results are consistent with the notion that, in the future, YAP1 inhibitors may represent a novel, valuable method of treating fibrosis as seen in dcSSc.
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Keywords {🔍}

article, google, scholar, cas, fibroblasts, leask, fibrosis, ccn, expression, cell, dermal, yap, sclerosis, liu, verteporfin, systemic, tissue, fibrotic, phenotype, shiwen, growth, arthritis, access, skin, cancer, abraham, biol, privacy, cookies, content, journal, research, signaling, scleroderma, quesnel, denton, factor, london, information, publish, search, persistent, matrix, myofibroblast, wound, carter, plos, inhibition, adhesion, rheum,

Topics {✒️}

month download article/chapter cytokine-mediated tissue fibrosis systemic sclerosis fibrosis transforming growth factor-beta1 bleomycin-induced skin fibrosis tgfbeta-induced jnk phosphorylation signaling xu shi-wen genome-wide expression profiling connective tissue deposition connective tissue remodelling triple-negative breast cancer highly-crosslinked extracellular matrix systemic sclerosis tead-yap complex suppresses lesional scleroderma fibroblasts focal adhesion kinase article shi-wen related subjects cutaneous tissue repair improves skin fibrosis full article pdf privacy choices/manage cookies molecular mechanisms cancer cells profibrotic gene expression mechanotransduction include check access ccn2/ctgf ctgf/ccn2 instant access yap–tead complex xu sw photoinduced biological properties skin scleroderma mechanosignaling sensor essential rac inhibition reverses european economic area chinese herbal decoction taxol-based chemoresistance ovarian cortex autotransplantation synergic glioblastoma treatment rheumatism collaborative initiative royal free campus rowland hill st human dermal fibroblasts α-sma expression yin/yang expression skin fibrosis conditions privacy policy persistent profibrotic phenotype

Questions {❓}

Chaqour B (2020) Caught between a “Rho” and a hard place: Are CCN1/CYR61 and CCN2/CTGF the arbiters of microvascular stiffness?
Leask A (2020) Conjunction junction, what’s the function?

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         headline:Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts
         description:Fibrosis is perpetuated by an autocrine, pro-adhesive signaling loop maintained by the synthetic and contractile abilities of myofibroblasts and the stiff, highly-crosslinked extracellular matrix. Transcriptional complexes that are exquisitely responsive to mechanotransduction include the co-activator YAP1, which regulates the expression of members of the CCN family of matricellular proteins such as CCN2 and CCN1. Although selective YAP1 inhibitors exist, the effect of these inhibitors on profibrotic gene expression in fibroblasts is largely unknown, and is the subject of our current study. Herein, we use genome-wide expression profiling, real-time polymerase chain reaction and Western blot analyses, cell migration and collagen gel contraction assays to assess the ability of a selective YAP inhibitor verteporfin (VP) to block fibrogenic activities in dermal fibroblasts from healthy individual human controls and those from isolated from fibrotic lesions of patients with diffuse cutaneous systemic sclerosis (dcSSc). In control fibroblasts, VP selectively reduced expression of fibrogenic genes and also blocked the ability of TGFbeta to induce actin stress fibers in dermal fibroblasts. VP also reduced the persistent profibrotic phenotype of dermal fibroblasts cultured from fibrotic lesions of patients with dcSSc. Our results are consistent with the notion that, in the future, YAP1 inhibitors may represent a novel, valuable method of treating fibrosis as seen in dcSSc.
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      headline:Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts
      description:Fibrosis is perpetuated by an autocrine, pro-adhesive signaling loop maintained by the synthetic and contractile abilities of myofibroblasts and the stiff, highly-crosslinked extracellular matrix. Transcriptional complexes that are exquisitely responsive to mechanotransduction include the co-activator YAP1, which regulates the expression of members of the CCN family of matricellular proteins such as CCN2 and CCN1. Although selective YAP1 inhibitors exist, the effect of these inhibitors on profibrotic gene expression in fibroblasts is largely unknown, and is the subject of our current study. Herein, we use genome-wide expression profiling, real-time polymerase chain reaction and Western blot analyses, cell migration and collagen gel contraction assays to assess the ability of a selective YAP inhibitor verteporfin (VP) to block fibrogenic activities in dermal fibroblasts from healthy individual human controls and those from isolated from fibrotic lesions of patients with diffuse cutaneous systemic sclerosis (dcSSc). In control fibroblasts, VP selectively reduced expression of fibrogenic genes and also blocked the ability of TGFbeta to induce actin stress fibers in dermal fibroblasts. VP also reduced the persistent profibrotic phenotype of dermal fibroblasts cultured from fibrotic lesions of patients with dcSSc. Our results are consistent with the notion that, in the future, YAP1 inhibitors may represent a novel, valuable method of treating fibrosis as seen in dcSSc.
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      dateModified:2021-01-04T00:00:00Z
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