Gestational exposure of bisphenol-A limits decidual ECM organization via S100a10-Annexin A2 axis in murine placenta
Environmental exposure to endocrine disrupting chemicals, like bisphenol-A (BPA), can impart detrimental effects on developing feto-placental unit, during pregnancy. Placenta remains a central player maintaining this feto-placental homeostasis for sustenance of a healthy pregnancy. Thus, the bisphenol-A mediated endocrine disruption affects the healthy functioning of placenta by altering key…
A recent study investigates the effects of bisphenol-A (BPA) exposure during pregnancy on placental tissue remodeling. BPA, an endocrine-disrupting chemical, can negatively impact the developing feto-placental unit. The researchers used a mouse model to examine the impact of BPA on the placenta, which plays a crucial role in maintaining fetal health during pregnancy.
The findings indicate that BPA exposure leads to altered phenotypic changes in the feto-placental interface, along with a perturbed placental proteome. Further analysis reveals an S100a10-Annexin A2 axis that is responsible for upregulation of tissue plasminogen activator (tPA). This upregulation drives altered ECM degradation in the placental decidua, resulting in functional dysregulation of the feto-placental axis.
The impaired ECM remodeling due to BPA exposure leads to a reduced size of both the fetus and placenta, which may ultimately result in adverse pregnancy outcomes related to toxicity. This study provides valuable insights into a novel mechanism that contributes to BPA-induced alterations in ECM remodeling within the placental decidua.
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