Detection of mitochondrial coupling factor 6 in placental tissues from preeclamptic pregnancies and its influence on biological behavior of trophoblast cells

xlomafota13 shared this article with you from Inoreader Detection of mitochondrial coupling factor 6 in placental tissues from preeclamptic pregnancies and its influence on biological behavior of trophoblast cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1185. doi: 10.3892/etm.2021.10619. Epub 2021 Aug 16. ABSTRACT Increased levels of mitochondrial coupling factor 6 (CF6) are present in the peripheral blood of patients with preeclamptic pregnancies, and are particularly evident in cases of early-onset or severe preeclampsia. The present study examined the location and expression levels of CF6 in the placental tissue and its effect on the biological behavior of trophoblast cells. Placental tissue microarrays, including placental villous cytotrophoblast and extravillous cytotrophoblast microarrays, were used to detect the location and relative expression levels of CF6 in the placenta using immunohistochemistry. It was found that CF6 was expressed in both the normal and preeclamptic placenta, but its levels were higher in the preeclamptic tissues. In addition, the effects of the hypoxic environment on the biological behaviors of trophoblast cells were investig ated in the JAR and JEG-3 cell lines. Following induction of hypoxia, the expression levels of CF6 were increased. Moreover, exogenous addition of human recombinant CF6 attenuated cell invasion, but exerted no effect on cell proliferation. At the molecular level, the expression levels of MMP-2 were decreased and were accompanied with a reduction in cell invasion following addition of exogenous CF6. In conclusion, the increased expression levels of CF6 and its effects in reducing the invasive abilities of trophoblast cells may be involved in the pathogenesis of severe preeclampsia. PMID:34475975 | PMC:PMC8406808 | DOI:10.3892/etm.2021.10619 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.