Rafia Aziz, Afak Sherwani and Sameer Mohammad
Background and Objective: Preeclampsia is one of the most dangerous hypertensive disorders that may arise during pregnancy and it is a major cause of maternal and fetal morbidity and mortality. Despite being a prominent topic of scientific inquiry, the fundamental pathways that contribute to the pathophysiology of preeclampsia remain little understood. Recent research suggested that G Protein-Coupled Receptors (GPCRs) may play a role in the etiology of preeclampsia, certain of these receptors have been observed to be elevated during a healthy pregnancy and decreased in preeclamptic people. However, the expression and functional importance of the great majority of GPCRs in the preeclamptic placenta are unclear. The goal of this study was to find highly expressed GPCRs that might play key roles in the physiology and pathology of the placenta. Materials and Methods: Dataset GSE148241 contained RNA sequencing data of 41 placentae in total, including from 9 patients with early-onset severe preeclampsia (EOSPE) and 32 normal controls. The RNA sequencing data were re-analyzed to evaluate the mRNA expression of the whole set of non-visual GPCRs in normal and preeclamptic human placenta. Results: The RNA sequencing identified more than 200 GPCRs in the healthy human placenta. Adhesion receptors (ADRGRG6 and ADGRG1), Atypical Chemokine Receptor 2 (ACKR2), Melanocortin Receptor 1 (MC1R), GPR107 and GPR78 are among the most abundant GPCRs. The expression of several GPCRs is significantly altered in the preeclamptic placenta. The list of GPCRs that are upregulated includes CCR5, HCAR2, GPR32, ADORA2A and GPR17 and those that are downregulated include ACKR1, SSTR1,OPRK1, FPR3 and CX3CR1. Conclusion: The GPCRs with altered expression in the preeclamptic may have substantial physiological importance in the placenta and may bring novel therapeutic options.
Rafia Aziz, Afak Sherwani and Sameer Mohammad, 2023. Analyzing Expression of GPCRs in Healthy and Preeclamptic Human Placenta. Journal of Biological Sciences, 23: 1-9.