PI3K/Akt signaling transduction pathway is involved in rat vascular smooth muscle cell proliferation induced by apelin-13

Liu, Changhui
Su, Tao
Li, Fang
Li, Lanfang
Qin, Xuping
Pan, Weinan
Feng, Fen
Chen, Feng
Liao, Duanfang
Chen, Linxi

¹Department of Cardiology, The First Affiliated Hospital, Guangzhou, China
²Key Laboratory for Arteriosclerology of Hunan Province, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China

† These authors contributed equally to this work.

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Received October 24, 2009

Accepted March 31, 2010

Acta Biochimica et Biophysica Sinica 42(6):p 396-402, June 2010. | DOI: 10.1093/abbs/gmq035

Vascular smooth muscle cells (VSMCs) were prepared from thoracic aortas of male Sprague–Dawley rats by the explant method to observe VSMC proliferation via phosphoinositide 3 kinase (PI3K)/Akt signaling transduction pathway induced by apelin-13. Expression of PI3K, phospho-PI3K, phospho-Akt, ERK1/2, phospho-ERK1/2 and cyclin D1 was detected by western blot analysis. Results showed that apelin-13 promoted the expression of phospho-PI3K and phospho-Akt in dose- and time-dependent manner. PI3K inhibitor LY294002 significantly decreased the expression of phospho-PI3K, phospho-Akt, phospho-ERK1/2, and cyclin D1 induced by apelin-13. The Akt inhibitor 1701-1 significantly diminished the expression of phospho-Akt, phospho-ERK1/2, and cyclin D1 stimulated by apelin-13. MTT assay results showed that PI3K inhibitor LY294002 and Akt inhibitor 1701-1 significantly inhibited the VSMC proliferation induced by apelin-13. Apelin-13 promoted VSMC proliferation through PI3K/Akt signaling transduction pathway.