Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 24, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/ijms24087124
Keywords
chromogranin A; catestatin; pregnancy; preeclampsia; hypertension
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Preeclampsia is a dangerous complication of pregnancy, with high risks of mortality and morbidity for both mother and fetus. The placenta, which produces hormones such as chromogranin A (CgA), is believed to play a central role in this condition. This study investigated the influence of the preeclamptic environment on CgA production in trophoblastic cell lines and tested the secretion of CgA-derived peptide catestatin (CST) as well as its correlation with apoptosis. The findings suggest that both CgA and CST may have roles in the complex pathogenesis of preeclampsia.
One of the most dangerous complications of pregnancy is preeclampsia (PE), a disease associated with a high risk of maternal and fetal mortality and morbidity. Although its etiology remains unknown, the placenta is believed to be at the center of ongoing changes. One of the hormones produced by the placenta is chromogranin A (CgA). Thus far, its role in pregnancy and pregnancy-related disorders is enigmatic, yet it is known that both CgA and its derived peptide catestatin (CST) are involved in the majority of the processes that are disturbed in PE, such as blood pressure regulation or apoptosis. Therefore, in this study, the influence of the preeclamptic environment on the production of CgA using two cell lines, HTR-8/SVneo and BeWo, was investigated. Furthermore, the capacity of trophoblastic cells to secrete CST to the environment was tested, as well as the correlation between CST and apoptosis. This study provided the first evidence that CgA and CST proteins are produced by trophoblastic cell lines and that the PE environment has an impact on CST protein production. Furthermore, a strong negative correlation between CST protein level and apoptosis induction was found. Hence, both CgA and its derived peptide CST may play roles in the complex process of PE pathogenesis.
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