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Cigarette smoke extract induced rat pulmonary artery smooth muscle cells proliferation via PKCα‐mediated cyclin D1 expression
Author(s) -
Zeng Daxiong,
Xu Yongjian,
Liu Xiansheng,
Wang Ran,
Xiang Min
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23131
Subject(s) - cyclin d1 , protein kinase c , activator (genetics) , cancer research , cell growth , microbiology and biotechnology , cyclin , cell cycle , chemistry , cyclin d , dna synthesis , kinase , biology , apoptosis , dna , biochemistry , gene
Cigarette smoke could induce pulmonary smooth muscle cells (PASMCs) proliferation. Although our previous study had implied the involvement of protein kinase Cα (PKCα), the molecular mechanism underlying PKCα pathway in this process is still unknown. In this study, rat PASMCs were stimulated by cigarette smoke extract (CSE) or PMA (a special activator to PKCα). Two percent CSE and PMA significantly enhanced cyclin D1 expression and cells proliferation. But cyclin D1‐specific siRNA successfully inhibited DNA synthesis in CSE‐treated or PMA‐treated cells. On the other hand, PKCα‐specific siRNA significantly suppressed cyclin D1 expression in CSE‐treated cells. Moreover, PKCα‐specific siRNA resulted in a cell‐cycle arrest in G0/G1 and decreased cells number significantly. We conclude that CSE induced rat PASMCs proliferation at least partly via PKCα‐mediated cyclin D1 expression. J. Cell. Biochem. 112: 2082–2088, 2011. © 2011 Wiley‐Liss, Inc.