The mitochondrial Na+/Ca2+ exchanger enables mitochondrial calcium balance in placental vessel from preeclampsia

Abstract

Placental ischaemia and hypoxia accelerate the development of preeclampsia. Although mitochondria could actively regulate Ca2+ signals and involves in sarcoendoplasmic reticulum (SR) Ca2+ release in smooth muscle. AIM: To investigate mitochondrial calcium responses to caffeine-induced Ca2+ release via ryanodine receptor (RyR) in placental vessels from preeclampsia. METHODS: Placenta was collected from normal pregnancy (N = 40) or preeclampsia (N = 30). Vascular tension was recorded using Power-Lab system. Total internal reflection fluorescent microscope (TIRFM) was used to recorded and analyzed the [Ca2+]m uptake and efflux. RESULTS: Caffeine-induced contraction was decreased both in placental artery and placental vascular smooth muscle cells (VSMCs) from preeclampsia, which was related to the mitochondrial dysfunction. Mitochondria in placental vessels from preeclampsia showed impaired [Ca2+]m efflux function. To understand the role of NCLX in preeclampsia, studies about on vascular smooth muscle cells under ischaemia and hypoxia was performed in the absence of overexpression NCLX or not. Cells under ischaemia and hypoxia showed mitochondrial dyfunction similar to placental vessel from preeclampsia.