期刊文献+

血管新生调节因子VEGF及其受体在恒河猴正常妊娠和药物流产胎盘中的表达 被引量:11

The Expression of VEGF, Flt-1 and KDR Proteins in the Placenta of Rhesus Monkey during Normal Pregnancy and Abortion
下载PDF
导出
摘要 目的:研究血管新生调节因子VEGF及其受体Flt-1、KDR在恒河猴正常妊娠和药物流产胎盘组织中的表达。方法:用免疫组化方法检测妊娠30天的恒河猴上述蛋白在胎盘中的表达。结果:VEGF蛋白主要表达于胎盘绒毛和子宫内膜,在母胎界面和子宫内膜血管中显著高表达;KDR蛋白的表达模式与VEGF类似;Flt-1蛋白在两组胎盘中的表达无显著差异。VEGF和KDR在药物流产胎盘中的表达量明显低于正常妊娠胎盘。结论:VEGF、Flt-1及KDR在恒河猴妊娠早期参与子宫内膜和胎盘发育过程中的血管新生,在胎盘绒毛的浸润以及腺上皮细胞分化及其分泌等过程中也发挥着重要作用;流产药物可能通过下调VEGF和KDR蛋白的表达,影响了血管发生和胎盘发育,增加了流产机会。 Objective: To further illuminate the role of vascular endothelial growth fator (VEGF), fms-like tyrosine kinase(Flt-1) and kinase-insert domain-containing receptor(KDR) proteins expressions in the placenta of rhesus monkey during early normal pregnancy and abortion induced by drugs, as well as the molecular mechanism of pharmacology during the abortion. Methods: a rhesus monkey pregnancy in 30 days model was employed and the expression of proteins of VEGF, Flt-1 and KDR in the endometrium and placenta was identified using immunostaining. Results: VEGF located in the placental villi and endometrium, and there was intensive expression on the fetal-maternal border and blood vessel of endometrium. The expressive mode of KDR was similar to that of VEGF. Flt-1 protein was expressed in the placenta of both groups having no significant difference. The expression of VEGF and KDR in treated group was significantly lower than that in normal group respectively. Conclusions: VEGF and KDR contribute to the angiogenesis in the process of development of endometrium and placenta. VEGF-VEGFR pairs are also involved in the process of trophoblast invasion and glandular epithelial cells differentiation and secretion during early pregnancy of rhesus monkey. Drugs might increase the danger for the abortion by downregulating the expression of VEGF and KDR, which influence the angiogenesis and development of placenta.
出处 《中国计划生育学杂志》 北大核心 2005年第6期356-359,共4页 Chinese Journal of Family Planning
基金 生殖生物学国家重点实验室开放基金资助
  • 相关文献

参考文献1

二级参考文献7

同被引文献187

引证文献11

二级引证文献58

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部