Reduces sFlt-1 and sENG secretion from primary human tissues; reduces endothelial dysfunction
WEDNESDAY, Dec. 30, 2015 (HealthDay News) — Metformin reduces soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sENG) secretion from primary human tissues, and reduces endothelial dysfunction, according to a study published online Dec. 21 in the American Journal of Obstetrics & Gynecology.
Fiona C. Brownfoot, M.B.B.S., from the University of Melbourne in Australia, and colleagues examined the effects of metformin in preeclampsia. They performed functional experiments to examine the effects of metformin on sFlt-1 and sENG secretion from placenta, endothelial cells, and placental villous explants, and assessed whether the effects of metformin were mediated through mitochondria. Mitochondrial electron transport chain activity was assessed in mitochondria isolated from preterm preeclamptic placentas and gestation-matched controls.
The researchers observed a reduction in sFlt-1 and sENG secretion from primary endothelial cells, villous cytotrophoblast cells, and preterm preeclamptic placental villous explants. This reduction was rescued by co-administration of succinate; sFlt-1 secretion was reduced by the mitochondrial electron transport chain inhibitors rotenone and antimycin. In preterm preeclamptic placentas, mitochondrial electron transport chain activity was increased versus gestation-matched controls. Metformin was also associated with improvement in features of endothelial dysfunction relevant to preeclampsia, including reduction in endothelial cell mRNA expression of vascular cell adhesion molecule 1 induced by tumor necrosis factor-α.
“Metformin reduced endothelial dysfunction, enhanced vasodilation in omental arteries, and induced angiogenesis,” the authors write. “Metformin has potential to prevent or treat preeclampsia.”
Abstract
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