Aberrant patterns of cellular communication in diabetes-induced embryopathy in rats: II, Apoptotic pathways

Reece, E. Albert; Dong, Xiang; Zhao, Zhiyong; Wu, Ying; Dhanasekaran, Danny N.

doi:10.1016/j.ajog.2004.10.592

Cited by 41 publications

(35 citation statements)

References 26 publications

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“…Among caspases, caspase-3 is considered one of the predominant targets involved in reactive oxygen species-mediated high glucose-induced apoptosis (27). Supporting this data, we observed an increase in caspase-3 immunoreactivity as an indicator of apoptosis in maternal and fetal areas of diabetic placentae.…”

Section: Discussionsupporting

confidence: 75%

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Gül¹,

Bayat²,

Çetin³

et al. 2015

Balkan Med J

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Background:The exchange of substances between mother and fetus via the placenta plays a vital role during development. A number of developmental disorders in the fetus and placenta are observed during diabetic pregnancies. Diabetes, together with placental apoptosis, can lead to developmental and functional disorders. Aims: Histological, ultrastructural and apoptotic changes were investigated in the placenta of streptozotocin (STZ) induced diabetic rats. Study Design: Animal experimentation. Methods: In this study, a total of 12 female Wistar Albino rats (control (n=6) and diabetic (n=6)) were used. Rats in the diabetic group, following the administration of a single dose of STZ, showed blood glucose levels higher than 200 mg/dL after 72 hours. When pregnancy was detected after the rats were bred, two pieces of placenta and the fetuses were collected on the 20 th day of pregnancy by cesarean incision under ketamine/ xylazine anesthesia from in four rats from the control and diabetic groups. Placenta tissues were processed for light microscopy and transmission electron microscopy (TEM). Hematoxylin-eosin (HE) and periodic acid Schiff-diastase (PAS-D) staining for light microscopic and caspase-3 staining for immunohistochemical investigations were performed for each placenta. Electron microscopy was performed on thin sections contrasted with uranyl acetate and lead nitrate. Results: Weight gain in the placenta and fetuses of diabetic rats and thinning of the decidual layer, thickening of the hemal membrane, apoptotic bodies, congestion in intervillous spaces, increased PAS-D staining in decidual cells and caspase-3 immunoreactivity were observed in the diabetic group. After the ultrastructural examination, the apoptotic appearance of the nuclei of trophoblastic cells, edema and intracytoplasmic vacuolization, glycogen accumulation, dilation of the endoplasmic reticulum and myelin figures were observed. In addition, capillary basement membrane thickening, capillary endothelial cells chromatin condensation in the nucleus and corrugation of the nucleus were found. Conclusion: Diabetes causes histomorphometric, ultrastructural and apoptotic changes in rat placenta.

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Section: Discussionsupporting

confidence: 75%

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Gül¹,

Bayat²,

Çetin³

et al. 2015

Balkan Med J

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“…Both increased oxidative stress and nitrosative stress are crucial features in diabetes-induced embryopathy and have been characterized in chemical-induced and genetic models of diabetes and even in mild diabetic experimental models (Eriksson et al 2003;Jawerbaum and González 2006;Ornoy 2007). Impairment of the oxidative and nitrosative stress balance can deregulate multiple signaling pathways and cause massive cell damage, apoptotic events, and defective embryonic and fetal development (Sivan et al 1997;Reece et al 2005;Morgan et al 2008;Sugimura et al 2009). In addition, the malformation rate is clearly correlated with increased glucose concentrations (Jawerbaum and White 2010).…”

Section: Discussionmentioning

confidence: 99%

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

Saito

Damasceno

Dallaqua

et al. 2013

Cell Stress and Chaperones

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We evaluated associations between the concentrations of heat shock proteins (hsp60 and hsp70) and their respective antibodies, alterations in maternal reproductive performance, and fetal malformations in pregnant rats with hyperglycemia. Mild diabetes (MD) or severe diabetes (SD) was induced in Sprague-Dawley rats prior to mating; nontreated non-diabetic rats (ND) served as controls. On day 21 of pregnancy, maternal blood was analyzed for hsp60 and hsp70 and their antibodies; and fetuses were weighed and analyzed for congenital malformations. Hsp and anti-hsp levels were correlated with blood glucose levels during gestation. There was a positive correlation between hsp60 and hsp70 levels and the total number of malformations (R0 0.5908, P00.0024; R00.4877, P00.0134, respectively) and the number of malformations per fetus (R 00.6103, P0 0.0015; R 00.4875, P 00.0134, respectively). The antihsp60 IgG concentration was correlated with the number of malformations per fetus (R00.3887, P00.0451) and the anti-hsp70 IgG level correlated with the total number of malformations (R00.3999, P00.0387). Moreover, both hsp and anti-hsp antibodies showed negative correlations with fetal weight. The results suggest that there is a relationship between hsp60 and hsp70 levels and their respective antibodies and alterations in maternal reproductive performance and impaired fetal development and growth in pregnancies associated with diabetes.

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“…increased apoptosis [3,4], perturbation of prostaglandin synthesis and metabolism [5][6][7], deficiency in membrane lipids [8][9][10][11], and generally altered metabolism in the embryo [12]. Several studies have associated oxidative stress with the maternal diabetic condition, and the administration of anti-oxidants reduced the incidence of developmental defects in experimental models of intrauterine exposure to diabetes [5,[13][14][15][16][17][18][19].…”

mentioning

confidence: 99%

What Makes us Human? A Biased View from the Perspective of Comparative Embryology and Mouse Genetics

2011

Current Research in Embryology

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Background: Maternal diabetes is a well-known risk factor for birth defects, such as heart defects and neural tube defects. The causative molecular mechanisms in the developing embryo are currently unknown, and the pathogenesis of developmental abnormalities during diabetic pregnancy is not well understood. We hypothesized that the developmental defects are due to alterations in critical developmental pathways, possibly as a result of altered gene expression. We here report results from gene expression profiling of exposed embryos from a mouse diabetes model.

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Aberrant patterns of cellular communication in diabetes-induced embryopathy in rats: II, Apoptotic pathways

Cited by 41 publications

References 26 publications

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

What Makes us Human? A Biased View from the Perspective of Comparative Embryology and Mouse Genetics

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