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|本期目录/Table of Contents|

17β-雌二醇对大鼠心肌的促血管新生作用：促进微血管内皮细胞分泌VEGF

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第6期
页码:
790-794
栏目:
基础研究
出版日期:
2009-11-05

文章信息/Info

Title:
Role of estrogen in angiogenic activity in rat myocardium in vitro: promoting microvascular endothelial cells to secrete VEGF
作者:
郝媛媛; 王海昌; 刘海涛; 刘毅; 尹智勇
第四军医大学西京医院心血管内科，陕西 西安 710032
Author(s):
HAO Yuan-yuan;  WANG Hai-chang;  LIU Hai-tao;  LIU yi;  YIN Zhi-yong
Department of Cardiology, Xijing Hospital, Forth Military University, Shaanxi, Xi’an 710032, China
关键词:
心肌微血管内皮细胞; 雌二醇; 血管新生
Keywords:
cardiac microvascular endothelial cells;  angiogenesis;  17β-estradiol
分类号:
Q579.13
DOI:
-
文献标识码:
A
摘要:
目的: 研究17β-雌二醇（17β-E2）对大鼠心肌微血管内皮细胞(CMEC)的促血管新生作用。方法: 以体外培养的CMECs为模型，用免疫荧光染色法检测雌激素受体(ER)的表达。用MTT比色法检测不同剂量的17β-E2对细胞增殖的影响。用细胞划痕法检测加入17β-E2后细胞的迁移能力。用Millicell小室测定法检测17β-E2对细胞侵入能力的影响。用管样结构形成实验观察加入17β-E2后细胞分化的情况。用ELISA法检测17β-E2对细胞分泌血管内皮生长因子（VEGF）的影响。结果: 免疫荧光染色法检测显示，心肌微血管内皮细胞内存在ER。MTT比色法检测表明，17β-E2可明显促进CMECs的增殖，在其浓度为0.01 μmol/L时，可产生最大的增殖效应；而雌激素的拮抗剂三苯氧胺（TMF）则可阻断此效应。同时发现，17β-E2处理组CMECs的迁移能力和管样结构形成的能力，均明显强于对照组及17β-E2+TMF处理组。与对照组及17β-E2+TMF处理组相比，17β-E2处理组可明显促进大鼠CMESs分泌VEGF（P<0.01）。结论: 在体外环境中，17β-E2可刺激CMECs自分泌VEGF，提高CMECs血管新生的活性。
Abstract:
AIM: To examine the pro-angiogenesis effect of 17β-estradiol (E2) on rat cardiac microvascular endothelial cells (CMECs) in vitro. METHODS: Rat CMECs were primarily cultured in vitro and the expression of estrogen receptor (ER) protein was observed by immunofluorescence. Cell proliferation was determined with MTT method after cells were treated with increasing concentrations of 17β-estradiol (E2). Cell migration ability was evaluated by wound scraping. CMEC invasion was measured using transwell chamber and the differentiated ability of CMECs was examined by tube formation assay. VEGF secretion was detected by enzyme-linked immunosorbent assay. RESULTS: ER protein was expressed in CMECs. 17β-E2 obviously promoted cell proliferation and the highest proliferation rate was determined at a concentration of 0.01 μmol/L. At the concentration of 0.01 μmol/L, 17β-E2 significantly enhanced the migration and tube-like formation of CMECs (P<0.01 vs. control group). The secretion of VEGF significantly increased at the concentration of 0.01 μmol/L (P<0.01 vs. control group). The pro-angiogenesis effect of 17β-estradiol (E2) was blocked by estrogen antagonist tamoxifen. CONCLUSION: In vitro, estradiol enhances CMEC biological activities and has some pro-angiogenesis effects.

参考文献/References

［1］ Nishida M, Carley WW, Gerritsen ME, et al. Isolation and characterization of human and rat cardiac micr ovascular endothelial cells［J］. Am J Physiol, 1993, 264(2Pt 2):H639-H652.

［2］ Syed I S, Sanb orn TA, Rosengart TK. The rapeutic angiogenesis: a biologic bypass［J］. Cardiology, 2004, 101(1-3):131-143.

［3］ van Royen N, Piek JJ, Buschmann I, et al. Stimulation of arteriogensis;a new concept for treatment of arterial occlusive disease ［J］. Cardiovasc Res, 2001, 49(3):543-553．

［4］ 冯建章，尹瑞兴，姚震. 急性心肌梗死大鼠血清血管内皮生长因子含量的变化［J］ . 中国病理生理杂志， 2000， 16(1)：30-32.

［5］ Kalka C, Tehrani H, Laudedberg B, et al. VEGF gene transfer mobilizes endothelial progenitor cell in patients with inoperable coronary disease［J］. Ann Thorac Surg, 2000,70(3):829-834.

［6］ Watanahe E, Smith DM, Sun J, et al. Effect of basic fibroblast growth factor on angiogenesis in the infarcted porcine heart［J］. Basic Res Cardiol,1998, 93(1):30-37.

［7］ Zheng W, Brown MD, Brock TA, et al. Brady cardia induced coron-ary angiogenesis is dependent on vascular endothelial growth factor［J］. Circ Res, 1999, 85(2):192-198.

［8］ Pieano E, Michelassi C. Chronic oral dipyridamole as a novel anti anginal drug, the collateral hypothesis［J］. Cardiovasc Res, 1997, 33(3):666-670．

［9］ Murohara T, Asahara T, Silver M, et al. Nitric oxide synthase modulates angiogenesis in respon-se to tissue ischemia［J］. J Clin Invest, 1998, 101(11):2567-2578．

［10］Somjen D, Kohen F, Jaffe A, et al. Effects of gonadal steroids and their antagonists on DNA synthesis in human vascular cells［J］. Hypertension,1998, 32(1):39-45.

［11］Caulin-Glaser T, Garcia-Cardena G, Sarrel P, et al. 17 beta-estradiol regulation of human endothelial cell basal nitric oxide release, independent of cytosolic Ca2+ mobilization［J］. Cire Res, 1997, 81(5):885-892.

［12］Akishita M, Kozzki K, Eto M, et al. Estrogen attenuates endothelin-1 production by bovine endothelial cells via estrogen receptor［J］. Biochem Biophys Res Commun, 1998, 251(1):17-21.

［13］Shushan A, Schenker JG. The use of oocytes obtained from aborted fetuses in egg donation programs［J］. Fertil Steril, 1994, 62(3):449-451.

备注/Memo

备注/Memo:
收稿日期：2008-12-11.通讯作者：王海昌，教授，主要从事冠心病基础与临床研究Email:wanghc@fmmu.edu.cn 作者简介：郝媛媛，住院医师，硕士Email:chinahaoyuan@21cn.com
更新日期/Last Update: 2009-09-30