目的:流产是最常见的妊娠并发症之一。尽管胚胎的染色体异常是众所周知的流产原因,很多案件仍然无法解释,免疫和血管生长改变被认为是可能的原因。趋化因子由多种细胞产生,并表现出几种功能,包括促血管生成特性和抗血管生成特性。在这项研究中,我们研究了自然流产和诱导流产的胎盘和蜕膜组织中血管生成和血管抑制趋化因子的作用。
方法:从胎盘和蜕膜组织中提取总RNA,然后将其纯化并转化为cDNA。然后对血管生成CCL2、CCL5、CCL20、CXCL1、CXCL2、CXCL3、CXCL5、CXCL6、CXCL7、CXCL8和CXCL4的表达进行实时PCR,并对血管抑制CXCL9、CXCL10、CXCL11、CXCL12和CXCL14的表达进行统计分析。
结果:关于胎盘,CXCL7(2.29倍,2.16-2.38,p<0.05),CXCL4(1.01倍,0.74-4.447,p<0.05),CXCL9(0.87倍,0.43-1.34,p<0.05)和CXCL11(0.31倍,0.22-0.45,p<0.05)在自然流产中发生了变化。CCL2、CCL5、CXCL2-3、CXCL8、CXCL10、CXCL12和CXCL14均无统计学意义的变更。关于decidua,CXCL7(7.13倍,6.32-7.54,p<0.01),CXCL8(11.02倍,8.58-13.45,p<0.05),CCL20(1.21倍,0.29-1.89,p<0.05)和CXCL9(5.49倍,3.67-6.39,p<0.05)在自然流产中过表达。CXCL2-4、CCL2、CCL5、CXCL10-12和CXCL14没有显示任何差异。趋化因子CXCL1、CXCL5-6的表达在组织或组中均不存在。
结论:我们的结果表明,在自然流产的胎盘和蜕膜中发生血管生成趋化因子的过度表达和减少表达,提示血管生成失调可能是流产发病的一个因素。
OBJECTIVE: Miscarriage is one of the most common complications of pregnancy. Although chromosomal abnormalities of the embryo is a well-known cause of miscarriage, a lot of cases remain unexplained, with immunologic and vascular growth alterations being considered as probable causes. Chemokines are produced by a variety of cells and exhibit several functions including both pro and anti-angiogenic properties. In this study, we investigated the role of the angiogenic and angiostatic chemokines in placenta and decidua tissues from spontaneous and induced abortions.
METHODS: Total RNA was extracted from the placenta and decidua tissues, which was then purified and converted into cDNA. Real-time PCR was then performed for the expression of the angiogenic CCL2, CCL5, CCL20, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, CXCL8 and CXCL4, and the angiostatic CXCL9, CXCL10, CXCL11, CXCL12 and CXCL14 and results were then statistically analyzed.
RESULTS: Regarding the placenta, CXCL7 (2.29-fold, 2.16-2.38, p < 0.05), CXCL4 (1.01-fold, 0.74-4.447, p < 0.05), CXCL9 (0.87-fold, 0.43-1.34, p < 0.05) and CXCL11 (0.31-fold, 0.22-0.45, p < 0.05) were altered in spontaneous abortions. CCL2, CCL5, CXCL2-3, CXCL8, CXCL10, CXCL12 and CXCL14 were not statistically significant altered. Regarding the decidua, CXCL7 (7.13-fold, 6.32-7.54, p < 0.01), CXCL8 (11.02-fold, 8.58-13.45, p < 0.05), CCL20 (1.21-fold, 0.29-1.89, p < 0.05) and CXCL9 (5.49-fold, 3.67-6.39, p < 0.05) were overexpressed in spontaneous abortions. CXCL2-4, CCL2, CCL5, CXCL10-12 and CXCL14 did not show any differences. The expression of the chemokines CXCL1, CXCL5-6 was absent in either tissue or group.
CONCLUSIONS: Our results show that the overexpression of angiostatic and diminished expression of angiogenic chemokines takes place in the placenta and decidua of spontaneous abortions, suggesting that dysregulation of angiogenesis could be a contributive factor to the pathogenesis of miscarriage.