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作 者:Fen Huang Xiaofang Xiong Huabin Wang Sha You Hesong Zeng
机构地区:[1]Department of Cardiology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China [2]Department of Cardiology, Third Hospital of Wuhan, Wuhan 430060, China
出 处:《Acta Biochimica et Biophysica Sinica》2010年第5期325-331,共7页生物化学与生物物理学报(英文版)
基 金:This work was supported by a grant from the National Natural Science Foundation of China (30470713).
摘 要:Leptin is a peptide hormone primarily involved in the regulation of food intake and energy expenditure. Recent studies have suggested that leptin is one of the risk factors for cardiovascular diseases including atherosclerosis and hypertension. Vascular smooth muscle cells (VSMCs) play a vital role in arterial intimai thickening and vascular remodeling. In this study, we investigated the effect of leptin on VSMC cell-cycle regulation and the possible pathway. We found that leptin stimulated VSMC proliferation and increased cell progression to S and G2/M phases. The expression of cyclinD1, phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), and nuclear factor (NF)-KBp65 was increased. Treatment of the cells with leptin antagonist triple mutant attenuated the leptininduced ERK1/2 and NF-KB activation. These results suggested that leptin stimulated VSMC proliferation by promoting transition from G1 to S phase and ERK1/2 and NF-κB pathway might contribute to this procession.Leptin is a peptide hormone primarily involved in the regulation of food intake and energy expenditure. Recent studies have suggested that leptin is one of the risk factors for cardiovascular diseases including atherosclerosis and hypertension. Vascular smooth muscle cells (VSMCs) play a vital role in arterial intimai thickening and vascular remodeling. In this study, we investigated the effect of leptin on VSMC cell-cycle regulation and the possible pathway. We found that leptin stimulated VSMC proliferation and increased cell progression to S and G2/M phases. The expression of cyclinD1, phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), and nuclear factor (NF)-KBp65 was increased. Treatment of the cells with leptin antagonist triple mutant attenuated the leptininduced ERK1/2 and NF-KB activation. These results suggested that leptin stimulated VSMC proliferation by promoting transition from G1 to S phase and ERK1/2 and NF-κB pathway might contribute to this procession.
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