Increased Rat Placental Fatty Acid, but Decreased Amino Acid and Glucose Transporters Potentially Modify Intrauterine Programming

CD36 胎盘 葡萄糖转运蛋白 内科学 生物 内分泌学 宫内生长受限 胎儿 免疫印迹 男科 生物化学 怀孕 医学 基因 胰岛素 遗传学
作者
Eva Nüsken,Alexandra Gellhaus,Elisabeth Kühnel,Isabelle Swoboda,Maria Wohlfarth,Christina Vohlen,Holm Schneider,Jörg Dötsch,Kai‐Dietrich Nüsken
出处
期刊:Journal of Cellular Biochemistry [Wiley]
卷期号:117 (7): 1594-1603 被引量:19
标识
DOI:10.1002/jcb.25450
摘要

ABSTRACT Regulation of placental nutrient transport significantly affects fetal development and may modify intrauterine growth restriction (IUGR) and fetal programming. We hypothesized that placental nutrient transporters are differentially affected both by utero‐placental insufficiency and prenatal surgical stress. Pregnant rats underwent bilateral uterine artery and vein ligation (LIG), sham operation (SOP) or no operation (controls, C) on gestational day E19. Placentas were obtained by caesarean section 4 h (LIG, n=20 placentas; SOP, n=24; C, n=12), 24 h (LIG, n=28; SOP, n=20; C, n=12) and 72 h (LIG, n=20; SOP, n=20; C, n=24) after surgery. Gene and protein expression of placental nutrient transporters for fatty acids (h‐FABP, CD36), amino acids (SNAT1, SNAT2) and glucose (GLUT‐1, Connexin 26) were examined by qRT‐PCR, western blot and immunohistochemistry. Interestingly, the mean protein expression of h‐FABP was doubled in placentas of LIG and SOP animals 4, 24 (SOP significant) and 72 h (SOP significant) after surgery. CD36 protein was significantly increased in LIG after 72 h. SNAT1 and SNAT2 protein and gene expressions were significantly reduced in LIG and SOP after 24 h. Further significantly reduced proteins were GLUT‐1 in LIG (4 h, 72 h) and SOP (24 h), and Connexin 26 in LIG (72 h). In conclusion, placental nutrient transporters are differentially affected both by reduced blood flow and stress, probably modifying the already disturbed intrauterine milieu and contributing to IUGR and fetal programming. Increased fatty acid transport capacity may affect energy metabolism and could be a compensatory reaction with positive effects on brain development. J. Cell. Biochem. 117: 1594–1603, 2016. © 2015 Wiley Periodicals, Inc.
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