Orcy Rafael Bueno, Schroeder Sabrina, Martins-Costa Sérgio Hofmeister, Ramos José Geraldo Lopes, Schechinger Wolfgang, Klein Harald, Brum Ilma Simoni, von Eye Corleta Helena, Capp Edison
Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Laboratório de Ginecologia e Obstetrícia Molecular, Centro de Pesquisas, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil.
Gynecol Obstet Invest. 2008;66(4):231-6. doi: 10.1159/000147169. Epub 2008 Jul 22.
Preeclampsia (PE) is a significant cause of fetal and maternal mortality around the world and there is evidence that insulin resistance has been implicated in the pathophysiology of PE. The Akt/PKB pathway is stimulated by insulin and performs several vital functions relative to growth, survival and cellular metabolism.
To investigate the basal expression of Akt/PKB, HSP90 expression, proteins that regulate Akt/PKB activity and substrate in the placenta, skeletal muscle and adipocytes of normal and PE parturient.
Samples were collected from 17 normal patients and 17 PE patients, and analyzed by Western blot to quantify the protein expression involved in signaling cascade of Akt/PKB.
Total Akt/PKB expression for normal placentas was 1.85 (1.07-3.12) and 1.53 (1.27-3.08) in PE (p = 1.00); in the adipose tissue of normal placentas it was 1.10 (0.53-1.73) and 1.66 (0.83-2.00) in PE (p = 0.37).
There was no difference in the Akt/PKB pathway, in basal state, in placentas and skeletal muscle of normal and PE patients. However, defects in this signaling pathway as pathophysiology of PE cannot be excluded because it is necessary to analyze this pathway during stimulation.
子痫前期(PE)是全球范围内导致胎儿和产妇死亡的重要原因,有证据表明胰岛素抵抗与子痫前期的病理生理过程有关。Akt/PKB信号通路受胰岛素刺激,在细胞生长、存活及细胞代谢方面发挥着多种重要功能。
研究正常产妇和子痫前期产妇胎盘、骨骼肌及脂肪细胞中Akt/PKB的基础表达、HSP90表达、调节Akt/PKB活性的蛋白及底物。
收集17例正常产妇和17例子痫前期产妇的样本,采用蛋白质印迹法分析参与Akt/PKB信号级联反应的蛋白表达量。
正常胎盘的总Akt/PKB表达量为1.85(1.07 - 3.12),子痫前期胎盘为1.53(1.27 - 3.08)(p = 1.00);正常胎盘脂肪组织中该表达量为1.10(0.53 - 1.73),子痫前期为1.66(0.83 - 2.00)(p = 0.37)。
正常产妇和子痫前期产妇胎盘及骨骼肌中,基础状态下Akt/PKB信号通路无差异。然而,由于需要在刺激过程中分析该信号通路,因此不能排除该信号通路缺陷作为子痫前期病理生理机制的可能性。