Comparison of the effects of recombinant human endostatin and docetaxel on human umbilical vein endothelial cells in different growth states
Comparison of the effects of recombinant human endostatin and docetaxel on human umbilical vein endothelial cells in different growth states作者机构：Department of Thoracic Oncology Tianjin Medical University Cancer Institute and Hospital Tianjin Key Laboratory of Cancer Prevention and Therapy Tianjin 300060 China Department of Oncology Xinghua People's Hospital Xinghua Jiangsu 225700. China
出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)
年 卷 期：2011年第000卷第18期
页 面：2883-2889页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)]
基 金：This study was supported by a grant from Tianjin Science & Technology Project (No.09ZCZDSF04400)
主 题：recombinant humanedostatin CD105 CD146 CD62E
摘 要：Background Recombinant human endostatin （rh-endostatin, Endostar） has been proved to be an inhibitor of angiogenesis. Docetaxel has been also considered as a common chemotherapeutic agent with inhibition of angiogenesis of malignancies. However, their function has been seldom compared and a best synergism protocol is not determined. This study aimed to compare the effects of two drugs, investigate their combined impact on human umbilical vein endothelial cells （HUVECs）, a molecular basis and find ideal protocols to inhibit endothelial cell proliferation. Methods HUVECs on confluent growth or activated by vascular endothelial growth factor （VEGF） were treated by rh-endostatin or/and docetaxel at respective gradient concentration in following operations as cell proliferation determined by MTT assay, cell cycle distribution, apoptosis and markers of CD146, CD62E and CD105 detected by flow cytometery, the structure of the channel formed by HUVECs measured by tube formation count. Results Rh-endostatin exhibited time dependent inhibition of proliferation while docetaxel showed both time and dose dependent inhibition. HUVECs accumulated in G0-G1 with decreased numbers of cells in G2 after a single treatment of rh-endostatin or that followed by docetaxel treatment. Cells accumulated in G2 after both a single docetaxel and simultaneous administration. Both the number of cells in Go-G1 and apoptotic cells were increased by docetaxel followed by rh-endostatin treatment. The number of non-apoptotic cells at Go-G1 was increased by first administering rh-endostatin then docetaxet. Sequential treatment of docetaxel followed by rh-endostatin resulted in the greatest increase in apoptosis （34.7%） and the second highest apoptosis was seen with simultaneous administration （18.2%）. Expression of CD146 and CD105 on confluent HUVECs was reduced at certain doses of rh-endostatin and/or docetaxel. However, rh-endostatin reduced CD105 without any apparent impact on either CD146 or CD62E ex
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