Journal
MOLECULAR MEDICINE REPORTS
Volume 9, Issue 5, Pages 1590-1596Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.1984
Keywords
apelin-13; AMP-activated protein kinase; Akt; endothelial nitric oxide synthase; angiogenesis
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Funding
- Natural Science Foundation of Shanghai Science and Technology Commission [10ZR1422900]
- National Natural Science Foundation of China [81070110]
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Currently, there is major interest in the functions of apelin-13, an endogenous ligand for the orphan G-protein coupled receptor APJ, a receptor that closely resembles the angiotensin receptor AT1.. In the present study, the role of apelin-13 in angiogenesis and its mechanism as a novel angiogenic factor in myocardial microvascular endothelial cells (MMVECs) was investigated. It was revealed that apelin-13 can promote proliferation, migration and tube formation in MMVECs. In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively. The treatment with the AMPK (compound C) and protein kinase Akt/protein kinase B (Akt; LY294002) inhibitor significantly suppressed the apelin13-induced AMPK, Akt and eNOS phosphorylation. They also inhibited the apelin13-stimulated endothelial cell migration and tube formation. Therefore, we hypothesize that apelin-13 promotes angiogenesis through the modulation of AMPK and Akt signaling in MMVECs.
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