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The PDE1A-PKCα Signaling Pathway Is Involved in the Upregulation of α-Smooth Muscle Actin by TGF-β<sub>1</sub> in Adventitial Fibroblasts
Author(s) -
Haiyan Zhou,
Wen-Dong Chen,
Dingliang Zhu,
LinSheng Wu,
Jia Zhang,
Weiqing Han,
Jiandong Li,
Chen Yan,
Pingjin Gao
Publication year - 2009
Publication title -
journal of vascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.58
H-Index - 74
eISSN - 1423-0135
pISSN - 1018-1172
DOI - 10.1159/000231716
Subject(s) - myofibroblast , downregulation and upregulation , protein kinase c , calphostin c , transforming growth factor beta , microbiology and biotechnology , transforming growth factor , signal transduction , phorbol , immunocytochemistry , activator (genetics) , actin , chemistry , biology , endocrinology , medicine , receptor , fibrosis , biochemistry , gene
Increasing evidence has suggested that differentiation of adventitial fibroblasts (AFs) to myofibroblasts plays an important role in arterial remodeling. The molecular mechanisms by which myofibroblast formation is regulated still remain largely unknown. This study aimed to evaluate the role of cyclic nucleotide phosphodiesterase 1A (PDE1A) in the formation of adventitial myofibroblasts induced by transforming growth factor (TGF)-beta(1).

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