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The present study aimed to investigate the regulation of placentas and uterus remodeling and involvement of E2 in gestational diabetes mellitus (GDM). To achieve this, we established in vitro and in vivo models for GDM placentas by culturing BeWo cells under hyperglycemic concentration, and treating pregnant rats with streptozotocin (STZ). We evaluated the expression of angiogenesis-related proteins. The expression of the anti-angiogenic factor, excess placental soluble fms-like tyrosine kinase 1 (sFLT1) was increased in our in vitro GDM model compared to the control. Moreover, the expressions of placental sFLT1 and the von willebrand factor (VWF) were also significantly elevated in the placenta of STZ-treated rats. These data indicate the disruption of angiogenesis in the GDM placentas. The expression levels of connexin 43 (Cx43), a component of the gap junction and collagen type I alpha 2 chain (Col1a2), a component of the extracellular matrix, were decreased in the GDM uterus. These results suggest that uterus decidualization and placental angiogenesis are inhibited in GDM rats. Our results also showed upregulation of the expression of genes regulating E2 synthesis as well as estrogen receptors (ER) in vivo models. Accordingly, the concentration of E2 measured in the culture medium under hyperglycemic conditions, as well as in the serum and placenta of the STZ-treated rats, was significantly elevated compared to the control groups. These results suggest that the dysregulated remodeling of the placenta and uterus may result in the elevation of E2 and its signaling pathway in the GDM animal model to maintain pregnancy.

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