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Effects of endothelial cell growth states on the proliferation and migration of vascular smooth muscle cells in vitro

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Author:
No author available
Journal Title:
ACTA PHYSIOLOGICA SINICA
Issue:
5
DOI:
10.3321/j.issn:0371-0874.2003.05.010
Key Word:
内皮细胞;平滑肌细胞;增生;迁移;endothelial cell;smooth muscle cell;proliferation;migration

Abstract: Endothelial injury, smooth muscle cells (SMCs) proliferation and migration are the same common pathophysiological processes of many cardiovascular diseases, such as atherosclerosis, hypertension, diabetes and restenosis. It is important to determine the functional interactions between endothelial cells (ECs) and SMCs under pathologic conditions. This work was to study the effects of ECs growth states on the proliferation and migration of vascular SMCs in cell coculture system. 3 HTdR incorporation and flow cytometry were used to determine the effects of ECs growth states on the proliferation of SMCs. The number of migrating SMCs was counted. RT-PCR was used to analyze the expression of α-SM-actin mRNA. The results showed that 3H-TdR incorporation decreased significantly from 14900 ± 1035 cpm/well in the control group to 8575 + 749cpm/well in the confluent ECs group (n=6, P<0.01), and increased to 27268±2310 cpm/well in the proliferative ECs group (n = 6, P<0.01). The transition of SMCs from G0/G1 phase to G2/M and S phases was blocked in the confluent ECs group but promoted in the proliferative ECs group. Compared with the control group, the number of migrating cells was about 4 times higher in the proliferative ECs group(n=6, P<0. 01 ), while it in the confluent ECs group was only the half of the number of the control ( n = 6, P< 0. 05 ). The expression of α-SM-actin mRNA was increased significantly in the confluent ECs group(2. 3±0. 11vs 1.4±0. 12,P<0. 05), but decreased significantly in the proliferative ECs group(0. 92±0. 08 vs 1.4 ± 0.12, P< 0.05 ). The results suggest that the biologic features of SMCs are influenced by ECs growth states. The proliferative ECs promote SMCs proliferation, migration and downregulate ot-SM-actin mRNA expression significantly.

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