Liu N, Ren X, Cen L
Institute of Cardiovascular Research, Beijing Medical University.
Zhonghua Yi Xue Za Zhi. 1996 Apr;76(4):297-300.
To investigate the changes of calcium homeostasis in smooth muscle cells (VSMC) and the role of disturbance of calcium homeostasis in VSMC proliferation after balloon denudation.
Assay of the cellular incorporation of 3H-leucine and measurement of 45Ca transport were done on the model of balloon-denuded aorta in rat.
Endothelial injury induced VSMC proliferation, intimal thickening. After balloon denudation, VSMC calcium influx increased (3 days after balloon denudation, 3.28 +/- 0.14 vs 4.12 +/- 0.28, P < 0.05; 10 days 3.31 +/- 0.09 vs 4.09 +/- 0.21 nmol/10(6) cells, P < 0.01), and calcium efflux decreased, and calcium content increased (3 days after balloon denudation 695 +/- 33 vs 995 +/- 54, P < 0.01; 10 days 709 +/- 32 vs 1022 +/- 94 nmol/10(6) cell, P < 0.01). SR and mitochondria calcium uptake increased. Calcium antagonist, verapamil not only regulated the disturbance of calcium homeostasis, but also inhibited endothelium injury-induced VSMC proliferation.
The disturbance of calcium homeostasis is probably one of the underlying mechanisms of VSMC proliferation induced by balloon denudation.
探讨平滑肌细胞(VSMC)钙稳态的变化以及钙稳态紊乱在球囊剥脱术后VSMC增殖中的作用。
在大鼠球囊剥脱主动脉模型上进行3H-亮氨酸细胞掺入测定和45Ca转运测量。
内皮损伤诱导VSMC增殖、内膜增厚。球囊剥脱后,VSMC钙内流增加(球囊剥脱后3天,3.28±0.14对4.12±0.28,P<0.05;10天,3.31±0.09对4.09±0.21 nmol/10(6)细胞,P<0.01),钙外流减少,钙含量增加(球囊剥脱后3天,695±33对995±54,P<0.01;10天,709±32对1022±94 nmol/10(6)细胞,P<0.01)。肌浆网和线粒体钙摄取增加。钙拮抗剂维拉帕米不仅调节钙稳态紊乱,还抑制内皮损伤诱导的VSMC增殖。
钙稳态紊乱可能是球囊剥脱诱导VSMC增殖的潜在机制之一。