Reactive oxygen species from mitochondria impacts trophoblast fusion and the production of endocrine hormones by syncytiotrophoblasts

• DOI: 10.1371/journal.pone.0229332
• Publication Date: 2020-02-24T13:28:21Z
• Authors: O’Llenecia S. Walker; Rehginald Ragos; Michael K. Wong; Mohamed Adam; Anson Cheung; Sandeep Raha
• Keywords: MFN2; Mitochondrial ROS

The placenta, a tissue that is metabolically active and rich in mitochondria, forms critical interface between the mother developing fetus. Oxidative stress within this tissue, derived from dysregulation of reactive oxygen species (ROS), has been linked to number adverse fetal outcomes. While such outcomes have associated with mitochondrial dysfunction, causal role dysfunction mitochondrially generated ROS altering process placentation remains unclear. In study, complex I activity was attenuated using 10 nM rotenone induce cellular oxidative by increasing production BeWo choriocarcinoma cell line. Increased resulted significant decrease transcripts which encode for proteins fusion (GCM1, ERVW-1, ERVFRD-1) resulting 5-fold percentage fusion. This outcome increased indicators fragmentation, as determined decreased expression MFN2 OPA1 along an increase marker fission (DRP1). Importantly, also 5.0-fold reduction human placental lactogen (PL) 4.4-fold insulin like growth factor 2 (IGF2) transcripts; hormones play important regulating growth. pre-treatment rotenone-exposed cells 5 mM N-acetyl cysteine (NAC) prevention these mediated changes function supports central signaling maintenance materno-fetal interface.