Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (46): 8603-8608.doi: 10.3969/j.issn.1673-8225.2011.46.013

Previous Articles     Next Articles

apelin-13 promotes proliferation of vascular smooth muscle cells by downregulating caveolae expression

Mao Xiao-huan1, 2, Li Lan-fang1, Gao Jing1, Yang Li1, Liu Wei1, Qin Xu-ping1, Chen Lin-xi1   

  1. 1Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, Hunan Province, China
    2Hunan Polytechnic College of Environment and Biology, Hengyang 421005, Hunan Province, China
  • Received:2011-05-10 Revised:2011-07-06 Online:2011-11-12 Published:2011-11-12
  • Contact: Chen Lin-xi, Doctor, Professor, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China chenlinxi@tom.com
  • About author:Mao Xiao-huan★, Studying for master’s degree, Lecturer, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China; Hunan Polytechnic College of Environment and Biology, Hengyang 420001, Hunan Province, China csumxh@sina.com Li Lan-fang☆, Doctor, Lecturer, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China 149083488@qq.com Ma Xiao-huan and Li Lan-fang contributed equally to this paper and were considered as co-first authors.
  • Supported by:

    the National Natural Science Foundation of China, No.30901577*; the Scientific Research Foundation for Returned Overseas Chinese Scholars, State Education Ministry, No. 20091590*

PDF

646

Abstract:

BACKGROUND: Previous results have shown that caveolae is likely to participate in apelin-13 promotion of vascular smooth muscle cell proliferation.
OBJECTIVE: APJ is a G-protein coupled receptor, and its ligand is apelin peptide. Previously, we reported PI3K and ERK1/2 signal pathway mediated proliferation of vascular smooth muscle cells (VSMCs) induced by apelin-13. This study is to observe caveolae involved in rat VSMCs proliferation induced by apelin-13 and to determine whether caveolin-1 protein binds to signal molecules PI3K, ERK1/2 to mediate VSMC proliferation induced by apelin-13.
METHODS: VSMCs were prepared from male Sprague-Dawley rat thoracic aorta by the primary-explant method. The effect of β- cyclodextrin on cell proliferation induced by apelin-13 was measured by MTT assay. VSMCs were incubated with apelin-13 and β-cyclodextrin (β-CD), caveolin-1 expression was detected by western blot assay. Formation of high molecular weight polyprotein component including caveolin-1 and PI3K /ERK1/2 was detected by immunoprecipitation.
RESULTS AND CONCLUSION: β-CD (5 mmol/L, 25 hours) significantly enhanced VSMCs proliferation induced by apelin-13   (P< 0.05). Treating VSMCs with apelin-13 (0, 1, 2, 4, 8 µmol/L) downregulated apelin-13-induced expression of caveolin-1 and the effect was distinct at 1µmol/L (P < 0.05). Pretreatment of the cells with 5 mmol/L β-CD could strength the downregulation of apelin-13-induced caveolin-1 expression (P < 0.05). Apelin-13 may induce dissociation of PI3K (ERK1/2) with caveolin-1 in VSMCs compared with the control group. These findings suggest that caveolae is involved in apelin-13-induced VSMCs proliferation.

CLC Number: