Expression of Retinoid Acid Receptor-Responsive Genes in Rodent Models of Placental Pathology

Abstract

In humans, retinoic acid receptor responders (RARRES) have been shown to be altered in third trimester placentas complicated by the pathologies preeclampsia (PE) and PE with intrauterine growth restriction (IUGR). Currently, little is known about the role of placental Rarres in rodents. Therefore, we examined the localization and expression of Rarres1 and 2 in placentas obtained from a Wistar rat model of isocaloric maternal protein restriction (E18.5, IUGR-like features) and from an eNOS-knockout mouse model (E15 and E18.5, PE-like features). In both rodent models, Rarres1 and 2 were mainly localized in the placental spongiotrophoblast and giant cells. Their placental expression, as well as the expression of the Rarres2 receptor chemokine-like receptor 1 (CmklR1), was largely unaltered at the examined gestational ages in both animal models. Our results have shown that RARRES1 and 2 may have different expression and roles in human and rodent placentas, thereby underlining immanent limitations of comparative interspecies placentology. Further functional studies are required to elucidate the potential involvement of these proteins in early placentogenesis.

Chemerin: A Functional Adipokine in Reproductive Health and Diseases

“…Chemerin was predominantly located in the spongiotrophoblast and giant cells of the placenta-derived from the intrauterine growth restriction (IUGR)-like rat model and PE-like mouse model [ 117 ]. Increased chemerin and CMKLR1 protein levels were also found in the placenta derived from the PE-like rat model [ 118 ] and human patients [ 119 ].…”

Special Issue “Molecular and Cellular Mechanisms of Preeclampsia”

“…It is a fascinating journey through the complex world of science, all meant to add another piece to the picture. The original papers range from new technologies for identifying changes in the maternal system to putative new therapies, the effect of the syndrome on the placenta, rodent models of preeclampsia, effects of the syndrome on the cardiovascular system, sex-specific differences and the effect on the children born from a preeclamptic pregnancy [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ]. The reviews of this Special Issue range from immunoregulation and macrophages during preeclampsia and molecular targets of therapeutics to trophoblast invasion, uterine blood flow and angiogenesis, they touch on specific protein families and oxidative stress related to preeclampsia, and finally deal with autophagy in preeclampsia and the role of epigenetics in the etiology of the syndrome [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ].…”