G alpha(12/13) Induction of CYR61 in Association With Arteriosclerotic Intimal Hyperplasia Effect of Sphingosine-1-Phosphate
- Authors
- Kim, Young Mi; Lim, Sung-Chul; Han, Chang Yeob; Kay, Hee Yeon; Cho, Il Je; Ki, Sung Hwan; Lee, Moo Yeol; Kwon, Hyuck Moon; Lee, Chang Ho; Kim, Sang Geon
- Issue Date
- Apr-2011
- Publisher
- LIPPINCOTT WILLIAMS & WILKINS
- Keywords
- atherosclerosis; G proteins; oncogenes; signal transduction; vascular biology; G alpha(12/13); cysteine-rich protein 61; sphingosine-1-phosphate; vascular smooth muscle cell
- Citation
- ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, v.31, no.4, pp.861 - U328
- Indexed
- SCIE
SCOPUS
- Journal Title
- ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
- Volume
- 31
- Number
- 4
- Start Page
- 861
- End Page
- U328
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/38173
- DOI
- 10.1161/ATVBAHA.110.218552
- ISSN
- 1079-5642
- Abstract
- Objective-G alpha(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 G alpha(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 G alpha(12) or G alpha(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 G alpha(12/13). JunD/activator protein-1 (AP-1) was identified as a transcription factor required for CYR61 transactivation by S1P. Deficiencies in G alpha(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 G alpha(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 G alpha(12/13) were increased within thickened intimas and medias in wire-injured mouse femoral arteries, which was accompanied by simultaneous CYR61 induction. Moreover, G alpha(12/13) and CYR61 were costained in the arteriosclerotic lesions immediately adjacent to human tumor tissues. Conclusion-G alpha(12/13) regulate AP-1-dependent CYR61 induction in VSMCs and promote VSMC migration, and they are upregulated with CYR61 in arteriosclerotic lesions. (Arterioscler Thromb Vasc Biol. 2011;31:861-869.)
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