Static pressure drives proliferation of vascular smooth muscle cells via caveolin-1/ERK1/2 pathway
- Division of Pharmacoproteomics, Institute of Pharmacy and Pharmacology, Research Center of Life Science, University of South China, Hengyang, Hunan 421001 (China)
- Internal Medicine and SimmonsCooper Cancer Institute, Southern Illinois University School of Medicine, 911 N. Rutledge Street, Springfield, IL 62794-9626 (United States)
- Department of Pharmacology, School of Pharmaceutics, Central South University, Changsha, Hunan 410083 (China)
- Institute of Materia Medical, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730 (China)
Intimal hyperplasia plays an important role in various types of vascular remodeling. Mechanical forces derived from blood flow are associated with the proliferation of vascular smooth muscle cells (VSMC). This contributes to many vascular disorders such as hypertension, atherosclerosis and restenosis after percutaneous transluminal angioplasty (PTA). In this study, we show that static pressure induces the proliferation of VSMC and activates its related signal pathway. VSMC from a rat aorta were treated with different pressures (0, 60, 90, 120, 150 and 180 mm Hg) in a custom-made pressure incubator for 24 h. The most active proliferation of VSMC was detected at a pressure of 120 mm Hg. VSMC was also incubated under a static pressure of 120 mm Hg for different time intervals (0, 2, 4, 8, 12 and 24 h). We found that static pressure significantly stimulates VSMC proliferation. Extracellular signal-regulated kinases 1/2 (ERK1/2) activation showed a peak at the pressure of 120 mm Hg at 4-h time point. Moreover, caveolin-1 expression was significantly inhibited by rising static pressure. Downregulation of VSMC proliferation could be found after PD98059 (ERK1/2 phosphorylation inhibitor) treatment. Our data also showed that a siRNA-mediated caveolin-1 knock down increased ERK1/2 phosphorylation and VSMC proliferation. These results demonstrate that static pressure promotes VSMC proliferation via the Caveolin-1/ERK1/2 pathway.
- OSTI ID:
- 22202348
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 391, Issue 4; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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