期刊论文详细信息
Nutrients
Folate Deficiency Could Restrain Decidual Angiogenesis in Pregnant Mice
Yanli Li1  Rufei Gao1  Xueqing Liu2  Xuemei Chen2  Xinggui Liao2  Yanqing Geng2  Yubin Ding2  Yingxiong Wang2 
[1] Laboratory of Reproductive Biology, School of Public Health, Chongqing Medical University, Chongqing 400016, China;
关键词: folate deficiency;    decidual angiogenesis;    reproductive hormone;   
DOI  :  10.3390/nu7085284
来源: mdpi
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【 摘 要 】

The mechanism of birth defects induced by folate deficiency was focused on mainly in fetal development. Little is known about the effect of folate deficiency on the maternal uterus, especially on decidual angiogenesis after implantation which establishes vessel networks to support embryo development. The aim of this study was to investigate the effects of folate deficiency on decidual angiogenesis. Serum folate levels were measured by electrochemiluminescence. The status of decidual angiogenesis was examined by cluster designation 34 (CD34) immunohistochemistry and the expression of angiogenic factors, including vascular endothelial growth factor A (VEGFA), placental growth factor (PLGF), and VEGF receptor 2 (VEGFR2) were also tested. Serum levels of homocysteine (Hcy), follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), progesterone (P4), and estradiol (E2) were detected by Enzyme-linked immunosorbent assay. The folate-deficient mice had a lower folate level and a higher Hcy level. Folate deficiency restrained decidual angiogenesis with significant abnormalities in vascular density and the enlargement and elongation of the vascular sinus. It also showed a reduction in the expressions of VEGFA, VEGFR2, and PLGF. In addition, the serum levels of P4, E2, LH, and PRL were reduced in folate-deficient mice, and the expression of progesterone receptor (PR) and estrogen receptor α (ERα) were abnormal. These results indicated that folate deficiency could impaire decidual angiogenesis and it may be related to the vasculotoxic properties of Hcy and the imbalance of the reproductive hormone.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.

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