Journal
INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS
Volume 17, Issue 4, Pages 307-315Publisher
SPRINGER
DOI: 10.1007/s10989-011-9269-5
Keywords
G protein coupled receptor; Reactive oxygen species; NADPH oxidase; Vascular smooth muscle cell; Proliferation
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Funding
- National Natural Science Foundation of China [30901577, 81070634]
- Hengyang Municipal Bureau of Science and Technology [2009 kJ 14]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry [20091590]
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Apelin is the endogenous ligand of the G-protein-coupled receptor, apelin-angiotensin receptor-like 1 (APJ). Vascular smooth muscle cells express both apelin and APJ, which are important regulatory factors in the cardiovascular system. Apelin-13 significantly stimulated vascular smooth muscle cell proliferation. However, little is known about the precise cellular mechanisms responsible for vascular smooth muscle cell proliferation induced by apelin-13. Here, we present novel data that indicate the key role of NADPH oxidase 4-derived reactive oxygen species in proliferation of vascular smooth muscle cells treated with apelin-13. Apelin-13 stimulated reactive oxygen species production in a concentration-and time-dependent manner. Furthermore, DPI impaired apelin-13-induced reactive oxygen species generation and vascular smooth muscle cell proliferation. Apelin-13-treatment increased the expression of NADPH oxidase 4 in a dose-dependent manner. Down-regulation of NADPH oxidase 4 using siRNA prevented apelin-13-induced reactive oxygen species generation and vascular smooth muscle cell proliferation. An increase in reactive molecules can trigger the activation of ERK stress-sensitive signaling pathways. Additionally, siRNA-NOX4 and DPI reversed the phosphorylation of ERK induced by apelin-13. Apelin-13 induced vascular smooth muscle cell proliferation by NOX4-derived ROS via the ERK signaling pathway.
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