Investigation of Aquaporin Molecules in the Placentas of Pregnant Women with Premature Rupture of Membranes

Abstract

Aim: This study aimed to investigate the immunohistochemical expression of Aquaporin 3 (AQP3) in placentas of pregnant women with premature rupture of membrane (PROM) and to explore AQP3-related interactors and signaling pathways using in silico approaches. Material and Method: Placental samples from 21 healthy (control) pregnant women and 21 pregnant women diagnosed with PROM were processed for routine histological tissue preparation. Sections were immunostained with AQP3 and analyzed under light microscope via ImageJ software. Protein-protein interaction (PPI) network of AQP3 was constructed with Cytoscape (version 3.10.2). Nodal centrality indexes (degree, closeness and betweenness) were computed through CentiScaPe plugin. The Enrichr tool was utilized to perform pathway enrichment analysis for 15 central genes. Results: AQP3 immune activity was significantly decreased in the plasma membrane of the trophoblastic cell layer of the PROM group compared to control group. According to network centrality analysis, AQP subfamily proteins predominantly play central roles in the AQP3 network; Major Intrinsic Protein of Lens Fiber (MIP), Glycerol-3-Phosphate Dehydrogenase 2 (GPD2), Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH), Glycerol Kinase 2 (GK2), GK, and Actin Beta (ACTB) with additional central interactors including proteins. Peroxisome proliferator-activated receptors (PPAR) signaling pathway was obtained as the most significantly enriched pathway. Conclusion: Alterations in AQP3 expression level in the PROM group compared with the control group may contribute to disturbances in water transport and cellular homeostasis in placental tissues and in silico potential interaction between AQP3 expression and PPAR signaling suggest the role of AQP3 in cell metabolism in PROM.

Keywords

• Premature rupture of membranes
• aquaporin 3
• placenta
• immunohistochemistry

Kaynakça

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