Maternal diabetes increases apoptosis in mice oocytes, not 2-cell embryos
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ORIGINAL ARTICLE
Maternal diabetes increases apoptosis in mice oocytes, not 2-cell embryos Shaoda Lin • Kun Lin • Weiping Li Xiaolin Zhou • Tianhua Huang
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Received: 26 October 2009 / Accepted: 26 March 2010 / Published online: 21 April 2010 Ó Springer Science+Business Media, LLC 2010
Abstract Apoptosis may be closely involved in diabetesinduced embryonic malformations. We aimed to investigate the occurrence of apoptosis at an early stage of development, in oocytes and 2-cell embryos of streptozotocin-induced diabetic mice and nondiabetic mice. Diabetic mouse ovarian sections stained with hematoxylin and eosin showed reduced number of growing follicles and delayed oocyte development. Annexin V-positive oocytes were higher in number in diabetic mice than in nondiabetic mice. Quantitative RT-PCR and immunofluorescence analysis revealed the expression of Bax and caspase-3 significantly higher in diabetic than nondiabetic oocytes. In contrast, 2cell embryos of diabetic and nondiabetic mice showed no annexin V-positive staining. Bax expression was elevated in diabetic 2-cell embryos, but caspase-3 expression did not significantly differ between diabetic and nondiabetic 2-cell embryos. Electron microscopy revealed increased number of swollen mitochondria in diabetic 2-cell embryos. These results suggested that maternal diabetes might increase oocyte apoptosis by a Bax-caspase-3 pathway to play a role in embryonic malformations by delayed oocyte development. Development of 2-cell embryos might be adversely
The sponsors had no involvement in the study design, collection, analysis, and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication. S. Lin (&) K. Lin W. Li Department of Endocrinology, The First Affiliated Hospital of Shantou University Medical College, 515041 Shantou, China e-mail: [email protected] X. Zhou T. Huang Research Center of Reproductive Medicine, Shantou University Medical College, 515041 Shantou, China
affected by maternal diabetes, but not through Bax-regulated caspase-3 apoptotic pathway. Keywords Oocyte 2-cell embryo Diabetic embryopathy Apoptosis Bax Caspase-3
Introduction Maternal diabetes during pregnancy is associated with increased risk of growth disturbance and congenital malformation in offspring [1, 2]. In the clinic, the importance of monitoring and glycemic control for pregnant women with diabetes is undisputed, but the optimal strategy for the care of diabetes during pregnancy has yet to be established [3, 4]. Lowering glucose levels during early pregnancy in such women decreases the incidence of malformation and miscarriage but is still significantly higher than among women without diabetes [5, 6], which suggests that the insult of maternal hyperglycemia occurs before organogenesis, possibly during the pre-implantation period and oocyte maturation. However, most studies of maternal diabetes have focused primarily on the embryo at the stages of blastocyst and the postimplantation embryo. They revealed that diabetes-
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