|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
CTRP3/cartducin is induced by transforming growth factor-β1 and promotes vascular smooth muscle cell proliferation
Takashi Maeda1 and Satoshi Wakisaka
Department of Anatomy and Cell Biology, Graduate School of Dentistry, Osaka University, 18 Yamadaoka, Suita, Osaka 5650871, Japan
CTRP3 (C1q and tumour necrosis factor-related protein 3)/cartducin, a novel serum protein, is a member of the CTRP superfamily. Although the CTRP3/cartducin gene is markedly up-regulated in rat carotid arteries after balloon injury, little is known about its biological roles in arterial remodelling and neointima formation in injured blood vessels. We have investigated the mechanisms underlying CTRP3/cartducin up-regulation and the in vitro effects of CTRP3/cartducin on vascular smooth muscle cells. CTRP3/cartducin expression in cultured p53LMAC01 vascular smooth muscle cells was induced by TGF-β1 (transforming growth factor-β1), but not by bFGF (basic fibroblast growth factor) or PDGF-BB (platelet-derived growth factor-BB). Exogenous CTRP3/cartducin promoted the proliferation of p53LMAC01 cells in a dose-dependent manner via ERK1/2 (extracellular signal-regulated kinase 1/2)- and MAPK (p38 mitogen-activated protein kinase)-signalling pathways. In contrast, CTRP3/cartducin exhibited no effect on the migration of p53LMAC01 cells. Taken together, the results of the present study demonstrate a novel biological role of CTRP3/cartducin in promoting vascular smooth muscle cell proliferation in blood vessel walls after injury.
Key words: CTRP3/cartducin, mitogen-activated protein kinase (MAPK), p53LMAC01 cell, proliferation
Abbreviations: bFGF, basic fibroblast growth factor, BrdU, bromodeoxyuridine, CTRP3, C1q and tumour necrosis factor-related protein 3, DMEM, Dulbecco's modified Eagle's medium, ERK1/2, extracellular signal-regulated kinase 1/2, GAPDH, glyceraldehyde-3-phosphate dehydrogenase, JNK, c-Jun N-terminal kinase, MAPK, p38 mitogen-activated protein kinase, PDGF-BB, platelet-derived growth factor-BB, RT, reverse transcription, TGF-β1, transforming growth factor-β1, VSMC, vascular smooth muscle cell
1To whom correspondence should be addressed (email firstname.lastname@example.org).
Received 9 June 2009/1 September 2009; accepted 26 October 2009
Published as Cell Biology International Immediate Publication 26 October 2009, doi:10.1042/CBI20090043
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