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Regulation of uterus and placenta remodeling under high estradiol levels in gestational diabetes mellitus models†. | LitMetric

AI Article Synopsis

  • The study explored how gestational diabetes mellitus (GDM) affects the remodeling of the placenta and uterus, specifically focusing on the role of estradiol.
  • In vitro and in vivo models were created using human placental cells and pregnant rats treated with streptozotocin to simulate GDM conditions.
  • Results showed increased levels of anti-angiogenic factors and disrupted angiogenesis in placentas, alongside decreased factors in the uterus, suggesting that GDM hampers both placental blood vessel formation and uterine remodeling, while also raising estradiol levels to possibly help maintain pregnancy.

Article Abstract

The present study aimed to investigate the regulation of placentas and uterus remodeling and involvement of estradiol in gestational diabetes mellitus. To achieve this, we established in vitro and in vivo models for gestational diabetes mellitus placentas by culturing human placental choriocarcinoma cells (BeWo) under hyperglycemic concentration and treating pregnant rats with streptozotocin. We evaluated the expression of angiogenesis-related proteins. The expression of the anti-angiogenic factor, excess placental soluble fms-like tyrosine kinase 1 was increased in our in vitro gestational diabetes mellitus model compared with the control. Moreover, the expressions of placental soluble fms-like tyrosine kinase 1 and the von Willebrand factor were also significantly elevated in the placenta of streptozotocin-treated rats. These data indicate the disruption of angiogenesis in the gestational diabetes mellitus placentas. The expression levels of connexin 43, a component of the gap junction and collagen type I alpha 2 chain, a component of the extracellular matrix, were decreased in the gestational diabetes mellitus uterus. These results suggest that uterus decidualization and placental angiogenesis are inhibited in gestational diabetes mellitus rats. Our results also showed upregulation of the expression of genes regulating estradiol synthesis as well as estrogen receptors in vivo models. Accordingly, the concentration of estradiol measured in the culture medium under hyperglycemic conditions, as well as in the serum and placenta of the streptozotocin-treated rats, was significantly elevated compared with the control groups. These results suggest that the dysregulated remodeling of the placenta and uterus may result in the elevation of estradiol and its signaling pathway in the gestational diabetes mellitus animal model to maintain pregnancy.

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Source
http://dx.doi.org/10.1093/biolre/ioad059DOI Listing

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