Gestasyonel Diyabetli Gebe Plasentalarında Aqp8 ve Aqp9 Dağılımlarının İncelenmesi

Abstract

During pregnancy, fetal water requirements increase markedly due to the exponential growth of fetus. Physiological data indicate that both a transcellular and a paracellular pathway are available for water transport across the human placenta. Transcellular water flux may be facililated by aquaporins (AQPs), a family of small integral membrane proteins. Aquaporins transport either water alone or water and small solutes such as gliserol. In mammals, there are at least 13 AQPs, which show a wide range distribution in organs that are actively involved in water transport. AQP9 is a member of aquaglyseroporin subfamily of AQPs and share the highest amino acid sequence homology with AQP3, AQP7 and AQP10. In addition to water, AQP9 transports small uncharged molecules like glycerol, urea, purines and pyrimidines. It is generally accepted that in addition to stimulating glucose transport, binding of insulin to cell surface receptors alters the expression of numerous genes in a variety of tissues. In placental trophoblastic cells, insulin has no stimulatory effect on glucose uptake or glycogen synthesis, but it is involved in the synthesis of human placental lactogen (hPL) and hCG and the regulation of 3ß-hydroxysteroid dehidrogenase. In literature, the relationship of AQP9 and insulin has been investigated. It has been reported that insulin decreased the molecular expression of AQP9 exclusively in explant from normal placentas in a concentration-dependent manner. TNF-alfa is an antiinflamatory cytokine. It is one of the reason of insulin resistance in the pregnancy. Treatment with TNF-alfa previous to insulin addition in normal placental explants, prevent the changes in AQP9 expression. Gestational diabetes mellitus (GDM) is a pregnancy releated metabolic disorder and it is characterized by impaired glucose tolerance. GDM is the most common metabolic disorder in the pregnancy. Pathology in the GDM can occurs because of different etiological reasons which cause the deficiency or peripheric resistance of insulin. The objective of this study is to evaluate the expression of AQP8 and AQP9 in placentas with GDM. Samples from normal and gestational diabetic placentas which is regulated with diet or insulin were studied by immunohistochemical staining. Specific anti- AQP8 and anti-AQP9 antibody was used for cellular localization of the molecules. In comparison to the other groups, AQP8 expression of mesenchymal cells in villi and Hofbauer cells were significantly decreased in the insulin regulated GDM group. In diet regulated GDM group, fetal capillary endothelial cells; there was a significant descrease in the AQP8 expression compared with the other groups. AQP9 expression of mesenchymal cells in villi in control group was lower in comparison to the other groups. In syncytiotrophoblast cell layer, AQP8 and AQP9 immunoreactivitiy shows similar expression patterns when we compared the groups with each other. Our results support the data that ‘insulin descreased the molecular expression of AQP9 in placental explants’ .