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血红素加氧酶-1 缺陷型小鼠胚胎胎盘内血管生成因子的表达。

Expression of angiogenic factors in the placenta of heme oxygenase-1 deficient mouse embryo.

机构信息

Department of Zoology, University of Delhi, India; Department of Zoology, Dyal Singh College, University of Delhi, India.

Department of Zoology, University of Delhi, India.

出版信息

Reprod Biol. 2023 Dec;23(4):100822. doi: 10.1016/j.repbio.2023.100822. Epub 2023 Nov 17.

Abstract

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.

摘要

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很重要。越来越多的证据表明 Hmox1 与血管生成有关,包括胎盘血管生成。在这项研究中,我们检查了 Hmox1 缺陷型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 Western blot 和免疫组织化学以及组织学分析,比较了 Hmox1 野生型和敲除型小鼠胚胎胎盘中 Hmoxs 和两种血管生成因子[Vegf 和 Prolactin 及其受体,以及 Cd31/Pecam1]的相对蛋白水平和定位。结果显示,敲除型胚胎胎盘组织排列紊乱,绒毛间隙面积减小,滋养层巨细胞核变小。敲除型胎盘的 Hmox2、催乳素和 Cd31/Pecam1 水平发生改变,而 Vegf 及其受体在我们的样本中似乎没有改变。总的来说,我们的发现表明,Hmox2 不太可能在敲除型胎盘代偿 Hmox1 的缺乏,催乳素和 Cd31/Pecam1 水平的改变提示这些胎盘中的血管生成受损。需要进一步研究来了解 Hmox1 敲除型小鼠胚胎胎盘血管生成缺陷的分子机制。

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