2016
DOI: 10.1016/j.biopha.2016.07.007
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Periostin mediates cigarette smoke extract-induced proliferation and migration in pulmonary arterial smooth muscle cells

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Cited by 13 publications
(8 citation statements)
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“…Recent evidence points to an important role of components of the ECM from both a biomarker and a therapeutic prospective in PAH . The most upregulated gene in severe PAH was indeed periostin, another matricellular protein involved in response to vascular injury and regulation of SMC proliferation . Chronic normobaric hypoxic exposure for 2 weeks significantly increased the mRNA level of periostin in the rat lung and hypoxia‐induced periostin expression was localized to PA‐SMC of hypertrophic PA.…”
Section: Discussionmentioning
confidence: 99%
“…Recent evidence points to an important role of components of the ECM from both a biomarker and a therapeutic prospective in PAH . The most upregulated gene in severe PAH was indeed periostin, another matricellular protein involved in response to vascular injury and regulation of SMC proliferation . Chronic normobaric hypoxic exposure for 2 weeks significantly increased the mRNA level of periostin in the rat lung and hypoxia‐induced periostin expression was localized to PA‐SMC of hypertrophic PA.…”
Section: Discussionmentioning
confidence: 99%
“…It has been reported that Pn is secreted not only from fibrocytes or fibroblasts but also from PASMCs in the lung under stressed condition[9,30,34,35]. Given that Pn is a marker for proliferation in these cells[36,37,38], Pn-positive cells would be responded cells for the pathological stress and have a pivotal role on perivascular cellular proliferation and vascular remodeling in the lung with PAH. Pn-expressing cell-targeted inhibition of TGF-β signaling (Pn-Cre/ Tgfbr1 fl/fl mice) effectively attenuated the development of PAH under hypoxic condition, suggesting that Pn-positive cells are crucial for TGF-β-mediated vascular remodeling in PAH.…”
Section: Discussionmentioning
confidence: 99%
“…In myocardial infarction model rats, ERK1/2 phosphorylation mediates TGF-β1-induced cardiac fibrosis via Rho-kinase 1 activation but not the JNK or p38 MAPK pathway [44]. ERK1/2 also mediates cigarette smoke extract-induced periostin expression in pulmonary arterial smooth muscle cells [45]. In a dilated cardiomyopathy mouse model overexpressing the Fas ligand (an inducer of apoptosis via caspase 3 activation), Fas ligand-activated periostin expression is mediated by the ERK1/2 pathway [46,47].…”
Section: Roles Of Erk1/2 and P38 Mapk In Periostin Production In Cmentioning
confidence: 99%