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• W147841794 abstract "Introduction I n the pathogenesis of pulmonary fibrosis in general and systemic sclerosis {SSc, scleroderma) in particular, lung fibroblasts undergo specific phenotypic modulation and develop cytoskeletal features similar to those of smooth muscle cells. These phenotypically altered, activated fibroblasts, or myofibroblasts, express a contractile isoform of actin (a-smooth muscle actin) and promote contractility of lung parenchyma. Constitutively activated SSc fibroblasts produce an over abundance of collagen, fibronectin, and other extracellular matrix (ECM) proteins. They also overexpress several profibrotic receptors, including receptors for the dominant fibrogenic cytokine TGF-p. Recently, we found that the main receptor for thrombin on lung fibroblasts, Protease-Activated Receptor (PAR)-1, is also abundantly expressed in scleroderma lung tissue and, furthermore, its expression is observed in association with myofibroblasts. Moreover, thrombin itself is capable of differentiating normal lung fibroblasts to a myofibroblast phenotype. Such diff^erentiation occurs via protein kinase C and a RhoA-dependent pathway. Additionally, thrombin induces several potent fibrogenic cytokines. CTGF, whose expression is constitutively upregulated in scleroderma fibroblasts and correlates well with the severity of lung fibrosis, is one such potent fibrogenic cytokine induced by thrombin. This study was undertaken to establish the link between the expression of CTGF and the contractile activity observed in scleroderma lung fibroblasts." @default.
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• W147841794 date "2013-01-01" @default.
• W147841794 modified "2023-09-23" @default.
• W147841794 title "Scleroderma Lung Fibroblasts: Contractility and Connective Tissue Growth Factor" @default.
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