[No authors listed]
Preeclampsia (PE) is a pathological condition that manifests during pregnancy as the occurrence of an abnormal urine protein level and increased blood pressure due to inadequate cytotrophoblast invasion. To elucidate the mechanism underlying PE, the present study primarily focused on the regulatory effects and mechanism of the G protein γ 7 (GNG7) on placental cytotrophoblasts in a rat PE model. Initially, the PE model was established with 45 specific pathogenâfree SpragueâDawley rats (30 females and 15 males). The expression patterns of GNG7, 4Eâbinding protein 1 (4EâBP1), phosphoprotein 70 ribosomal protein S6 kinase (p70S6K) and mammalian target of rapamycin (mTOR) were examined in the PE rats. Placental cytotrophoblasts isolated from normal and PE rats were treated with a small interfering RNA against GNG7, mTOR signaling pathway activator (HIVâ1 Tat) or inhibitor (rapamycin). Following treatment, cell proliferation, differentiation and apoptosis were evaluated, and mTOR signaling pathwayârelated factors (4EâBP1, p70S6K and mTOR), cell proliferationârelated factors (vascular endothelial growth factor and transforming growth factorâβ1), differentiationârelated factors [activator proteinâ2 (APâ2)α and APâ2γ], and apoptosisârelated factors [Bâcell lymphoma 2 (Bclâ2) and Bclâ2âassociated X protein] were determined. Finally, soluble fmsâlike tyrosine kinase 1 (sFltâ1) and soluble endoglin (sEng) levels were measured via enzymeâlinked immunosorbent assay. Initially, the mTOR signaling pathway was inactivated in the placental tissues and cytotrophoblasts in the PE rats. Silencing GNG7 reduced the levels of sFltâ1 and sEng and activated the mTOR signaling pathway. Silencing of GNG7 or activation of the mTOR signaling pathway enhanced cell proliferation and differentiation, but inhibited the apoptosis of placental cytotrophoblasts in the PE rats. Taken together, the results showed that GNG7 silencing repressed apoptosis and enhanced the proliferation and differentiation of placental cytotrophoblasts in PE rats through activation of the mTOR signaling pathway.
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