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Expression of angiogenic factors in the placenta of heme oxygenase-1 deficient mouse embryo
Reproductive Biology ( IF 2.1 ) Pub Date : 2023-11-17 , DOI: 10.1016/j.repbio.2023.100822
Meenakshi Rana 1 , Pooja Choubey 2 , Gouri Nandi 3 , Sidhant Jain 4 , Divya Bajaj 5 , Sonika Sharma 6 , Sharmila Basu-Modak 2
Affiliation  

Heme oxygenase 1 (Hmox1), the inducible form of heme degrading enzymes Hmoxs, is important for establishment and maintenance of pregnancy. A growing body of evidence suggests an association between Hmox1 and angiogenesis, including placental angiogenesis. In this study, we examined the expression of two angiogenic factors in the placentas of Hmox1 deficient mouse embryos, whose expression was found to be related to that of Hmox1. Relative protein levels and localization of Hmoxs and two angiogenic factors [Vegf and Prolactin along with their receptors, and Cd31/Pecam1] were compared in the placentas of Hmox1 wildtype and knockout mouse embryos using western blotting and immunohistochemistry along with histological analysis. The results revealed tissue disorganisation, reduced area of labyrinth and smaller nuclear size of trophoblast giant cell in the placentas of knockout embryos. The levels of Hmox2, prolactin, and Cd31/Pecam1 were found to be altered in knockout placentas, whereas Vegf and its receptors seem to be unaltered in our samples. Overall, our findings imply that Hmox2 is unlikely to compensate for Hmox1 deficiency in knockout placentas, and altered levels of prolactin and Cd31/Pecam1 hint towards impaired angiogenesis in these placentas. Further investigation would be needed to understand the molecular mechanism of defective angiogenesis in the placentas of Hmox1 knockout mouse embryos.



中文翻译:

血红素加氧酶1缺陷小鼠胚胎胎盘中血管生成因子的表达

血红素加氧酶1 (Hmox1) 是血红素降解酶 Hmoxs 的诱导形式,对于妊娠的建立和维持非常重要。越来越多的证据表明 Hmox1 与血管生成(包括胎盘血管生成)之间存在关联。在本研究中,我们检测了Hmox1缺陷小鼠胚胎胎盘中两种血管生成因子的表达,发现其表达与Hmox1相关。使用蛋白质印迹和免疫组织化学以及组织学分析,比较 Hmox1 野生型和敲除小鼠胚胎胎盘中 Hmox 和两种血管生成因子 [Vegf 和催乳素及其受体,以及 Cd31/Pecam1] 的相对蛋白质水平和定位。结果显示,敲除胚胎胎盘组织混乱,迷路面积缩小,滋养层巨细胞核尺寸变小。我们发现敲除胎盘中 Hmox2、催乳素和 Cd31/Pecam1 的水平发生了改变,而 Vegf 及其受体在我们的样本中似乎没有改变。总体而言,我们的研究结果表明,Hmox2 不太可能补偿敲除胎盘中 Hmox1 的缺陷,并且催乳素和 Cd31/Pecam1 水平的改变暗示这些胎盘中血管生成受损。需要进一步研究以了解 Hmox1 敲除小鼠胚胎胎盘中缺陷血管生成的分子机制。

更新日期:2023-11-20
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