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Monocyte chemoattractant protein-1 mediates angiotensin II-induced vascular smooth muscle cell proliferation via SAPK/JNK and ERK1/2

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Abstract

Abnormal vascular smooth muscle cells proliferation is the pathophysiological basis of cardiovascular diseases, such as hypertension, atherosclerosis, and restenosis after angioplasty. Angiotensin II can induce abnormal proliferation of vascular smooth muscle cells, but the molecular mechanisms of this process remain unclear. Here, we explored the role and molecular mechanism of monocyte chemotactic protein-1, which mediated angiotensin II-induced proliferation of rat aortic smooth muscle cells. 1,000 nM angiotensin II could stimulate rat aortic smooth muscle cells' proliferation by angiotensin II type 1 receptor (AT1R). Simultaneously, angiotensin II increased monocyte chemotactic protein-1 expression and secretion in a dose-and time-dependent manner through activation of its receptor AT1R. Then, monocyte chemotactic protein-1 contributed to angiotensin II-induced cells proliferation by CCR2. Furthermore, we found that intracellular ERK and JNK signaling molecules were implicated in angiotensin II-stimulated monocyte chemotactic protein-1 expression and proliferation mediated by monocyte chemotactic protein-1. These results contribute to a better understanding effect on angiotensin II-induced proliferation of rat smooth muscle cells.

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Acknowledgments

This project was supported by Research Grant 09JC1412300 from the Shanghai Science Committee, Shanghai, China.

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Authors and Affiliations

  1. Cardiac Vascular Unit, Shanghai First People’s Hospital Affiliated to Shanghai Jiao-Tong University, Shanghai, 200080, China

    Hua-Li Yao, Zong-Zhuang Li, Hong-Xian Wu, Meng-Dan Xu, Zhi Zhang & Qiu-Yan Dai

  2. No. 3 People’s Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, Shanghai, 201900, China

    Feng-Hou Gao

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  1. Hua-Li Yao
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Correspondence to Qiu-Yan Dai.

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Yao, HL., Gao, FH., Li, ZZ. et al. Monocyte chemoattractant protein-1 mediates angiotensin II-induced vascular smooth muscle cell proliferation via SAPK/JNK and ERK1/2. Mol Cell Biochem 366, 355–362 (2012). https://doi.org/10.1007/s11010-012-1315-x

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  • DOI: https://doi.org/10.1007/s11010-012-1315-x

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