Apelin-induced vascular smooth muscle cell proliferation: The regulation of cyclin D1

Feng Li, Lanfang Li, Xuping Qin, Weinan Pan, Fen Feng, Feng Chen, Bingyan Zhu, Duanfang Liao, Herbert Tanowitz, Chris Albanese, Linxi Chen

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Vascular smooth muscle cells express both apelin and APJ, which are important regulatory factors in the cardiovascular and nervous systems. Importantly, APJ is also involved in the pathogenesis if HIV-1 infection. We investigated whether vascular smooth muscle cell proliferation was regulated through an apelin-pERK1/2-cyclin D1 signal transduction pathway. Apelin-13 significantly stimulated vascular smooth muscle cell proliferation and increased cell cycle progression. Apelin-13 a decreased the proportion of cell in the G0/G1 phase while increasing the number of cells in S phase. Apelin-13 also increased the levels of cyclin D1, cyclin E and pERK1/2. Treatment of cells with the MEK inhibitor PD98059 attenuated the apelin-3-induced pERK1/2 activation. Similarly, treatment with PD98059 partially diminished the apelin-13-induced expression of cyclin D1 and vascular smooth muscle cell proliferation. Taken together, these data established that apelin-13 stimulates vascular smooth muscle cell proliferation by promoting the G1-S phase transition, and that this effect is mediated in part by an apelin-pERKl/2-cyclin D1 signal cascade.

Original languageEnglish (US)
Pages (from-to)3786-3792
Number of pages7
JournalFrontiers in Bioscience
Issue number10
StatePublished - 2008


  • APJ
  • Apelin
  • Cell cycle
  • Cyclin d1
  • Vascular smooth muscle

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology


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