Quantitative Investigations of Placental Terminal Villi in Maternal Diabetes Mellitus by Scanning and Transmission Electron Microscopy.

Honda, Masashi; Toyoda, Chisato; Nakabayashi, Masao; Omori, Yasue

doi:10.1620/tjem.167.247

Cited by 29 publications

(17 citation statements)

References 15 publications

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“…The placentae of diabetic rats displayed significant cell hyperplasia and thickening of the basal membrane of syncytial cells, while these could not be observed in the placentae of rats in the control group. Cytotrophoblastic cell prolifera- tion is accepted as an indicator of uteroplacental ischemia, as reported in other studies (10). In this study, we observed an increase in embryonic loss, a decrease in the number of living fetuses, and a lower rate of implantation in diabetic rats.…”

Section: Discussionsupporting

confidence: 86%

“…This basal membrane thickening could be the result of mucopolysaccharide storage (19), which results in maternal uteroplacental vascular insufficiency and intrauterine growth retardation (1). In addition, we also observed thickening of the capillary basal membrane of diabetic rat placentae, which leads to an increased diffusion distance between maternal and fetal blood (10).…”

Section: Discussionmentioning

confidence: 58%

“…Some forms of intrauterine fetal growth retardations have been correlated with insufficient placental blood flow and transfer of nutrients from mother to fetus in humans as well as in animals (10).…”

Section: Discussionmentioning

confidence: 99%

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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: 86%

Section: Discussionmentioning

confidence: 58%

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Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Gül¹,

Bayat²,

Çetin³

et al. 2015

Balkan Med J

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“…Oxidative stress is enhanced in pregnancies complicated by insulindependent diabetes (8, 9), toxemia (5, 6, 10-13) and cigarette smoking (39). In many of these cases a structurally abnormal, small or poorly functioning placenta is found (40)(41)(42)(43)(44)(45). In some diabetic placentas, obliterative endarteritis of fetal stem cells and villous fibrinoid necrosis are observed (42).…”

Section: Discussionmentioning

confidence: 99%

LDL Oxidation and Human Placental Trophoblast and Macrophage Cytotoxicity

Bonet

Hauge-Gillenwater

Zhu

et al. 1998

Experimental Biology and Medicine

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We have previously shown that LDL is oxidized by placental cells in primary tissue culture and that this process causes cytotoxicity proportional to LDL oxidation in the presence of sex steroid hormones. Here we describe further experiments linking LDL oxidation to placental cell cytotoxicity. Trophoblast and macrophages were isolated from healthy elective caesarean section placentas by enzymatic digestion and separated by centrifugation on a 40% Percoll gradient and maintained in primary culture for up to 5 days. LDL was oxidized by exposure to 5 microM CuCl2, cells were incubated in the absence of albumen to favor oxidation, and cytotoxicity was measured by 51Cr release from prelabelled cells and cell protein content. Native LDL was oxidized by both cell types with a 10%-50% increase in lipid peroxides and an approximately 4-fold increase in TBARS formation. Increasing concentrations of native LDL and oxidized-LDL increased 51Cr release and diminished protein content in cells incubated in HAM's F-10 medium. Addition of 5 microM Cu2+ augmented cytotoxicity of LDL in macrophage and trophoblast culture, but more in macrophages than trophoblast. Cytotoxicity was diminished by adding 0.001-0.1 mM EDTA to the system, diminishing 51Cr release from 91 +/- 0.5 to 40.8 +/- 1.0% in macrophages and 54.2 +/- 1.2 to 33.1 +/- 1.3% in trophoblast (P < 0.001 in both instances). Similarly, the absence of transition metal ion in culture (MEM medium) blocked an increase in 51Cr release compared to its presence (HAM's F-10 medium). An antioxidant, butylated hydroxytoluene, diminished 51Cr release and LDL electrophoretic mobility in HAM's F-10 medium in placental macrophage culture. LDL oxidation injures placental macrophages and trophoblast, the former more than the latter. The process is LDL- and transition metal ion-dependent and is inhibited by antioxidant. This model of LDL oxidation and placental cell damage in vitro provides a basis for studying mechanisms of placental dysfunction and senescence in human pregnancy.

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“…occurrence of shorter villi in the centre and longer villi in periphery, is disrupted, and villi (and villous vessels, as deduced by authors) are more branched in diabetic placentas (Bjork & Persson, 1984). The analysis performed by scanning electron microscopy revealed hypo-and hyperramified villi in diabetic placentas as compared with normal ones (Honda et al, 1992).…”

Section: Light Microscopymentioning

confidence: 89%

The Morphology of Villous Capillary Bed in Normal and Diabetic Placenta

Jirkovská¹

2012

Recent Advances in Research on the Human Placenta

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Quantitative Investigations of Placental Terminal Villi in Maternal Diabetes Mellitus by Scanning and Transmission Electron Microscopy.

Cited by 29 publications

References 15 publications

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

Histopathological, Ultrastructural and Apoptotic Changes in Diabetic Rat Placenta

LDL Oxidation and Human Placental Trophoblast and Macrophage Cytotoxicity

The Morphology of Villous Capillary Bed in Normal and Diabetic Placenta

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