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Cited by 17Protein Kinase Regulation and GTPase SignalingSphingolipid Metabolism and SignalingCardiovascular, Neuropeptides, and Oxidative Stress Research

Gα 12/13 Induction of CYR61 in Association With Arteriosclerotic Intimal Hyperplasia: Effect of Sphingosine-1-Phosphate

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Kim, Young Mi, Lim, Sung-Chul, Han, Chang Yeob, Kay, Hee Yeon, Cho, Il Je, Ki, Sung Hwan, Lee, Moo Yeol, Kwon, Hyuck Moon +2 more·2011·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/atvbaha.110.218552
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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. Conclusion—: Gα 12/13 regulate AP-1-dependent CYR61 induction in VSMCs and promote VSMC migration, and they are upregulated with CYR61 in arteriosclerotic lesions.

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  • CCN1 is activated by agonists of G protein-coupled receptors such as thrombin, prostaglandins E2 and F2α, and sphingosine-1-phosphate.

    “CCN1 is activated by agonists of G protein-coupled receptors (GPCRs) such as thrombin [34,35], prostaglandins E2 and F2α [33,36], and sphinogosine-1-phosphate [37].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [37]

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Authors
Kim, Y. M., Lim, S.-C., Han, C. Y., Kay, H. Y., Cho, I. J., Ki, S. H., Lee, M. Y., Kwon, H. M., Lee, C. H., & Kim, S. G.
Affiliations
  • Chonnam National University (KR)
  • Seoul National University (KR)
ORCID
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2011-04
Volume
31
Issue
4
Pages
861-869
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/atvbaha.110.218552
OpenAlex
W1991785185
Cited by
17
References
43
Citations by year
2026: 1 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 1 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 2 · 2012: 1
FWCI
0.26
Type
journal article
Language
en
Open access
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
  • YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
  • The Royal Society of Chemistry’s Journals, Books and Databases (The Royal Society of Chemistry) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
Keywords
Gα12/13, CYR61, cysteine-rich protein 61, sphingosine-1-phosphate, arteriosclerosis, intimal hyperplasia, vascular smooth muscle cells, AP-1, c-Jun N-terminal kinase, reactive oxygen species, NADPH oxidase, N-acetylcysteine, smooth muscle cell migration
MeSH terms
Aged, Animals, Arteriosclerosis, Cell Movement, Disease Models, Animal, Enzyme Activation, Female, Humans, Hyperplasia, Lysophospholipids, Male, Mice, Inbred ICR, Middle Aged, Muscle, Smooth, Vascular, Mutation, Promoter Regions, Genetic, Sphingosine, Transfection, Signal Transduction, Up-Regulation, Proto-Oncogene Proteins c-jun, Rats, Sprague-Dawley, Reactive Oxygen Species, Tunica Intima, Mice, Knockout, Transcription Factor AP-1, NADPH Oxidases, RNA Interference, GTP-Binding Protein alpha Subunits, G12-G13, JNK Mitogen-Activated Protein Kinases, Mice, Rats, Cysteine-Rich Protein 61, HEK293 Cells

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