(Journal Article): Aberrant patterns of cellular communication in diabetes-induced embryopathy in rats: II, apoptotic pathways.
 
Reece EA, Ma XD, Zhao Z, Wu YK, Dhanasekaran D (Department of Obstetrics and Gynecology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205-7199, USA., reeceealbert@uams.edu )
 
IN: Am J Obstet Gynecol 2005; 192(3):967-972
Impact Factor(s) of Am J Obstet Gynecol: 2.437 (2004), 2.518 (2003), 2.556 (2002), 2.871 (2001)

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ABSTRACT: OBJECTIVE: The objective was to test the hypothesis that hyperglycemia-induced injury of yolk sac cell membranes is associated with disruption of cellular apoptotic signaling pathways. STUDY DESIGN: Pregnant rats were induced to become diabetic by injection of streptozotocin. Fourteen normal control and 24 diabetic rats were killed on day 12 of gestation. Yolk sac membranes in 3 conceptus groups (nondiabetic, diabetic with normal, or diabetic with malformed conceptus) were collected for study. DNA was extracted from yolk sac cells and assayed for fragmentation by using gel electrophoresis, which indicates apoptosis. Protein expression was evaluated by Western blot assays. Statistical analyses were performed with the Student t-test. RESULTS: The level of phosphorylated Akt was significantly decreased, whereas that of the proapoptotic protein Bax was increased. These changes were correlated with the presence of DNA fragmentation in yolk sac cells of the diabetic malformed conceptuses. CONCLUSION: Hyperglycemia-induced embryopathy involves apoptosis, during which the expression of proapoptotic protein Bax is upregulated and the activity of the cell-survival factor, Akt kinase, is decreased in yolk sac cells. These observations suggest that hyperglycemia of maternal diabetes triggers apoptotic signaling pathways and inhibits cell survival pathways, leading to embryonic malformations.

TYPE OF PUBLICATION: Original article

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• Mammon K, Keshet R, Savion S, Pekar O, Zaslavsky Z, Fein A, Toder V, Torchinsky A. Diabetes-Induced Fetal Growth Retardation is Associated with Suppression of NF-κB Activity in Embryos. Rev Diabetic Stud 2005. 2: 27-34.
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