Du Junbao, Hui Yan, Cheung Yiufai, Bin Geng, Jiang Hongfeng, Chen Xiaobo, Tang Chaoshu
Department of Pediatrics, Peking University, First Hospital, Xi-An Men Str. No. 1, West District, 100034, Beijing, PR China.
Heart Vessels. 2004 Mar;19(2):75-80. doi: 10.1007/s00380-003-0743-7.
Hydrogen sulfide (H(2)S) was recently suggested to be a possible endogenous gasotransmitter in physiological concentration. For the purpose of understanding its possible role in the regulation of the cardiovascular system, we explored the potential effect of H(2)S on the proliferation of cultured aortic vascular smooth muscle cells (VSMCs) of rats and mitrogen-activated protein kinase (MAPK) as a signaling transduction pathway. Vascular smooth muscle cells were cultured in vitro and the cells were divided into six groups: (1). control group, (2). serum group, (3). endothelin group, (4). NaHS group, (5). serum + NaHS group, and (6). endothelin + NaHS group. VSMC proliferation was measured by [(3)H]thymidine ([(3)H]TdR) incorporation and MAPK activity in the VSMCs was determined by radioactivity assay. The results showed that endothelin-1 increased VSMC [(3)H]TdR incorporation 2.39-fold ( P << 0.01) and MAPK activity 1.62-fold ( P << 0.01), as compared with controls. Hydrogen sulfide at 5 x 10(-5) mol/l, 1 x 10(-4) mol/l, and 5 x 10(-4) mol/l decreased VSMC [(3)H]TdR incorporation by 16.8%, 26.60%, and 37.40%, respectively, and reduced MAPK activity by 7.37% ( P >> 0.05), 23.39%, and 33.57%, respectively ( P << 0.01). The results demonstrated that H(2)S could dose-dependently suppress the proliferation of VSMCs through the MAPK pathway.
