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Objective: To observe the effects of thermal stress on proliferation of human vascular endothelial cells (VECs) and explore its significance. Methods: Changes of VECs proliferation were investigated with 3H TdR incorporation method after ECV304 was treated at 43℃ for 2 hours, while expressions of intercellular adhesion molecule 1 (ICAM 1), inhibitor of differentiation 1 (ID1), and P16 and P21 proteins were determined by Western Blotting. Results: The effect of inhibition of VECs growth after thermal stress was detected by 3H TdR incorporation experiment. Western blotting showed ICAM 1, a marker of activated endothelial cells, was increased markedly after thermal stress. Expression of ID1 protein declined gradually with increasing expressions of its downstream genes, P16 and P21 following the thermal stress. Conclusions: Thermal stress could strongly activate VECs and inhibit proliferation of VECs through ID1, thus down regulating cyclin dependent kinase inhibitors, P16 and P21, which might be an essential pathway for recovery of VECs after thermal stress.
Methods: Changes of VECs proliferation were investigated with 3H TdR incorporation method after ECV304 was treated at 43 ° C for 2 hours while while expressions Inhibitors of differentiation 1 (ID1), and P16 and P21 proteins were determined by Western Blotting. Results: The effect of inhibition of VECs growth after thermal stress was detected by 3H TdR incorporation experiment. Western blotting showed ICAM 1, a marker of activated endothelial cells, was increased markedly after thermal stress. Expression of ID1 protein declined gradually with increasing expressions of its downstream genes, P16 and P21 following the thermal stress. Conclusions: Thermal stress could strongly activate VECs and Inhibitory proliferation of VECs through ID1, thus down regulating cyclin dependent kinase inhibitors , P16 and P21, which might be an essential pathway for recovery of VECs after thermal stress.