HISTOLOGY AND HISTOPATHOLOGY

Cellular and Molecular Biology

 

The PI3K/Akt and MAPK-ERK1/2 pathways are altered in STZ induced diabetic rat placentas

Aslı Ozmen1, Gozde Unek1, Dijle Kipmen-Korgun2 and Emin Turkay Korgun1

1Department of Histology and Embryology and 2Department of Biochemistry, Medical Faculty, Akdeniz University, Antalya, Turkey

Offprint requests to: Prof. Dr. Emin Turkay Korgun, Department of Histology and Embryology, Medical Faculty, Akdeniz University, 07070 Antalya, Turkey. e-mail: korgun@akdeniz.edu.tr


Summary. Diabetic pregnancy is associated with complications such as early and late embryonic death, fetal growth disorders, placental abnormalities, and embryonal-placental metabolic disorders. Excessive apoptosis and/or changes of proliferation mechanisms are seen as a major event in the pathogenesis of diabetes-induced embryonic death, placental weight and structural anomalies. Akt and ERK1/2 proteins are important for placental and fetal development associated with cellular proliferation and differentiation mechanisms. The mechanism underlying the placental growth regulatory effects of hyperglycemia have not been elucidated. Moreover, it is still not determined how Akt and ERK1/2 proteins related proliferation and apoptosis mechanisms are influenced by Streptozotocin (STZ) induced diabetic rat placental development. The aim of this study was to investigate the expression levels and spatio-temporal immuno-localizations of Akt, p-Akt, ERK1/2 and p-ERK1/2 proteins in normal and STZ-treated diabetic rat placental development. In order to compose the diabetic group, pregnant females were injected with a single dose of 40mg/kg STZ intraperitonally seven days before their sacrifice at 12th, 14th, 16th, 18th and 20th day of their gestation. We found that maternal diabetic environment led to a decrease in ERK1/2 and Akt phosphorylation during rat placental development. It could be said that MAPK-ERK1/2 and PI3K/Akt cell signaling pathways are affected from hyperglycemic conditions in rat placentas. In conclusion, hyperglycemia-induced placental and embryonal developmental abnormalities could be associated with reduction of Akt and ERK1/2 phosphorylation. Histol Histopathol 29, 743-756 (2014)

Key words: Placental development, Akt, ERK1/2, Diabetes, Rat

DOI: 10.14670/HH-29.743