Abstract
CTRP3/cartducin, a novel secretory protein, is a member of the C1q and tumor necrosis factor (TNF)-related protein (CTRP) superfamily. CTRP3/cartducin gene is transiently up-regulated in a balloon-injured rat carotid artery tissue. In this study, we report a new function of CTRP3/cartducin as a regulator of angiogenic processes. CTRP3/cartducin promoted proliferation and migration of mouse endothelial MSS31 cells in a dose-dependent manner. Further, stimulation of MSS31 by CTRP3/cartducin led to activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK). MAPK/ERK kinase 1/2 (MEK1/2) inhibitor, U0126, and p38 MAPK inhibitor, SB203580, blocked the CTRP3/cartducin-induced cell proliferation, and migration was blocked by U0126, but not the SB203580. Taken together, these results suggest that CTRP3/cartducin may be involved as a novel angiogenic factor in the formation of neointima following angioplasty.
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Acknowledgements
This work was supported by Grants-in-aid for Scientific Research (No. 18592062) and the 21st Century Center of Excellence Program from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
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Akiyama, H., Furukawa, S., Wakisaka, S. et al. CTRP3/cartducin promotes proliferation and migration of endothelial cells. Mol Cell Biochem 304, 243–248 (2007). https://doi.org/10.1007/s11010-007-9506-6
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DOI: https://doi.org/10.1007/s11010-007-9506-6