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[肿瘤坏死因子-α对人脐静脉内皮细胞内皮增殖及细胞内游离钙浓度的影响]

[Effects of tumor necrosis factor-alpha on proliferation and intracellular free calcium concentration in endothelium of human umbilical vein endothelial cells].

作者信息

Jin Z, Pei L, Wang D

机构信息

Department of Obstetric and Gynecology, Second Hospital, China Medical University, Shenyang 110003, China.

出版信息

Zhonghua Fu Chan Ke Za Zhi. 2000 Nov;35(11):657-9.

Abstract

OBJECTIVE

To Observe the effects of tumor necrosis factor-alpha (TNF-alpha) on cell proliferation and Intracellular free calcium concentration ([Ca2+]i) in endothelium of human umbilical vein endothelial cells (HUVEC) and investigate the pathogenesis of pregnancy induced hypertension syndrome (PIH).

METHODS

Confluent monolayer of HUVEC was directly incubated with TNF-alpha at following final concentrations: 500, 1,000, 2,000 U/ml for 24 hours. The percentages of different cellcycles and [Ca2+]i were measured by flow cytometry and fluorospectrophotmetry.

RESULTS

Incubated with TNF-alpha, the endothelial cells were elongated and transformed into fibroblast-like cells. Border of nucleus was sharp, clarity, and cells were in regular shape. But there were abnormal granules in cytoplasma and some cells detached at the concentrotion of 2,000 U/ml of TNF-alpha. Stimulated by TNF-alpha, the percentage of cellcycles from phase G0 + G1 to S and G2 + M decreased significantly and it was dose-dependent [Ca2+]i increased significantly and dose-dependent as well.

CONCLUSION

TNF-alpha may injure endothelium directly and inhibit its proliferation and repair through the changes of [Ca2+]i level. It may play an important role in the pathogenesis of PIH.

摘要

目的

观察肿瘤坏死因子-α(TNF-α)对人脐静脉内皮细胞(HUVEC)内皮细胞增殖及细胞内游离钙浓度([Ca2+]i)的影响,探讨妊娠高血压综合征(PIH)的发病机制。

方法

将融合的HUVEC单层细胞分别用终浓度为500、1000、2000 U/ml的TNF-α直接孵育24小时。采用流式细胞术和荧光分光光度法检测不同细胞周期的百分比及[Ca2+]i。

结果

用TNF-α孵育后,内皮细胞拉长并转化为成纤维细胞样细胞。细胞核边界清晰、规整,细胞形态正常。但在TNF-α浓度为2000 U/ml时,细胞质中有异常颗粒,部分细胞脱落。TNF-α刺激后,细胞周期从G0+G1期向S期和G2+M期转化的百分比显著降低,且呈剂量依赖性;[Ca2+]i显著升高,也呈剂量依赖性。

结论

TNF-α可能直接损伤内皮细胞,通过改变[Ca2+]i水平抑制其增殖和修复。它可能在PIH的发病机制中起重要作用。

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