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G(alpha)12/13 induction of CYR61 in association with arteriosclerotic intimal hyperplasia: effect of sphingosine-1-phosphate.

Authors
 Young Mi Kim  ;  Sung-Chul Lim  ;  Chang Yeob Han  ;  Hee Yeon Kay  ;  Il Je Cho  ;  Sung Hwan Ki  ;  Moo Yeol Lee  ;  Hyuck Moon Kwon  ;  Chang Ho Lee  ;  Sang Geon Kim 
Citation
 ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol.31(4) : 861-869, 2011 
Journal Title
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
ISSN
 1079-5642 
Issue Date
2011
Keywords
atherosclerosis ; G proteins ; oncogenes ; signal transduction ; vascular biology ; G 12/13 ; cysteine-rich protein 61 ; sphingosine-1-phosphate ; vascular smooth muscle cell
Abstract
OBJECTIVE: Gα(12/13) play a role in oncogenic transformation and tumor growth. Cysteine-rich protein 61 (CYR61) is a growth-factor-inducible angiogenic factor. In view of potential overlapping functions between Gα(12/13) and CYR61, this study investigated the role of these G proteins in CYR61 induction in association with hyperplastic vascular abnormality.

METHODS AND RESULTS: Overexpression of activated Gα(12) or Gα(13) induced CYR61 expression in vascular smooth muscle cells (VSMCs). Gene knockdown and knockout experiments revealed that sphingosine-1-phosphate (S1P) treatment induced CYR61 via Gα(12/13). JunD/activator protein-1 (AP-1) was identified as a transcription factor required for CYR61 transactivation by S1P. Deficiencies in Gα(12/13) abrogated AP-1 activation and AP-1-mediated CYR61 induction. c-Jun N-terminal kinase was responsible for CYR61 induction. Moreover, deficiencies of Gα(12/13) abolished c-Jun N-terminal kinase-dependent CYR61 induction by S1P. N-acetyl-l-cysteine or NADPH oxidase inhibitor treatment reversed CYR61 induction by S1P, indicating that reactive oxygen species are responsible for this process. The levels of Gα(12/13) were increased within thickened intimas and medias in wire-injured mouse femoral arteries, which was accompanied by simultaneous CYR61 induction. Moreover, Gα(12/13) and CYR61 were costained in the arteriosclerotic lesions immediately adjacent to human tumor tissues.

CONCLUSIONS: Gα(12/13) regulate AP-1-dependent CYR61 induction in VSMCs and promote VSMC migration, and they are upregulated with CYR61 in arteriosclerotic lesions.
Files in This Item:
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DOI
10.1161/ATVBAHA.110.218552
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kwon, Hyuck Moon(권혁문) ORCID logo https://orcid.org/0000-0001-9901-5015
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/93087
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