Maternal diabetes affects specific extracellular matrix components during placentation

Giachini, Fernanda R.; Carriel, Víctor; Capelo, Luciane Portas; Tostes, Rita C.; Carvalho, Maria Helena Catelli de; Fortes, Zuleica Bruno; Zorn, T. M. T.; Martin, Séverine

doi:10.1111/j.1469-7580.2007.00839.x

Cited by 38 publications

(27 citation statements)

References 37 publications

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“…Contrarily, diabetic rats become anestrous shortly after the induction of diabetes and they are unable to mate and maintain pregnancy without insulin replacement, as achieved by our group and others (Katayama et al. 1984; González 2002; Giachini et al. 2008).…”

Section: Discussionmentioning

confidence: 59%

Effects of long‐term diabetes on the structure and cell proliferation of the myometrium in the early pregnancy of mice

Favaro

Salgado

Raspantini

et al. 2010

Int J Experimental Path

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It is known that the development of diabetic complications in human pregnancy is directly related to the severity and the duration of this pathology. In this study, we developed a model of long-term type 1 diabetes to investigate its effects on the cytoarchitecture, extracellular matrix and cell proliferation during the first adaptation phase of the myometrium for pregnancy. A single dose of alloxan was used to induce diabetes in mice prior to pregnancy. To identify the temporal effects of diabetes the mice were divided into two groups: Group D1 (females that became pregnant 90-100 days after alloxan); Group D2 (females that became pregnant 100-110 days after alloxan). Uterine samples were collected after 168 h of pregnancy and processed for light and electron microscopy. In both groups the histomorphometric evaluation showed that diabetes promoted narrowing of the myometrial muscle layers which was correlated with decreased cell proliferation demonstrated by PCNA immunodetection. In D1, diabetes increased the distance between muscle layers and promoted oedema. Contrarily, in D2 the distance between muscle layers decreased and, instead of oedema, there was a markedly deposition of collagen in the myometrium. Ultrastructural analysis showed that diabetes affects the organization of the smooth muscle cells and their myofilaments. Consistently, the immunoreaction for smooth muscle α-actin revealed clear disorganization of the contractile apparatus in both diabetic groups. In conclusion, the present model demonstrated that long-term diabetes promotes significant alterations in the myometrium in a time-sensitive manner. Together, these alterations indicate that diabetes impairs the first phenotypic adaptation phase of the pregnant myometrium.

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Section: Discussionmentioning

confidence: 59%

Effects of long‐term diabetes on the structure and cell proliferation of the myometrium in the early pregnancy of mice

Favaro

Salgado

Raspantini

et al. 2010

Int J Experimental Path

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“…A rise in fibronectin expression in the parotid gland and placenta of diabetic rats has been described. (Lamers et al 2007;Giachini et al 2008). In the case of the prostate, there was no increase in areas containing this glycoprotein, although greater intensity of DAB deposition was observed around the blood vessels.…”

Section: Discussionmentioning

confidence: 86%

Diabetes induces stromal remodelling and increase in chondroitin sulphate proteoglycans of the rat ventral prostate

Ribeiro

Taboga

Góes

2009

Int J Experimental Path

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Extracellular matrix (ECM) remodelling is an important process involved in prostate cancer progression. Alterations in ECM caused by diabetes in different tissues such as kidney is well described; however, it is poorly investigated in prostate. The aim of this study was to evaluate changes in ECM of rat prostate showing gland atrophy caused by diabetes and their implications in development of malignant lesions. Diabetes was induced in Wistar rats using alloxan (45 mg/kg bw). After 90 days of diabetes onset, animals were killed and ventral prostate was removed and prepared for light microscopy following immunoreaction for fibronectin, chondroitin sulphate and Picrossirius staining for collagen fibres. Proteoglycans (PG) were identified at transmission electron microscopy after fixation with Cuprolinic Blue. Diabetes led to a thickening of 25% in the acinar basement membrane accompanied by increase and disorganization of its proteoglycans (P1). Three additional populations of prostatic stromal PGs were identified: collagen fibril linked (P2) and interstitial (P3) and (P4) PGs. Diabetes increased P3 and mainly P4 which had higher dimension and accumulated around the smooth muscle cells. In addition, an increase in chondrotin sulphate (33%, mainly in sites where P4 were noted) and collagen (44%) was noted in diabetic rats, whereas fibronectin did not change. Atrophic changes observed in rat ventral prostate after diabetes are accompanied by stromal remodelation related to increase in collagen and chondroitin sulphate proteoglycans. Thus, diabetes can promote a stromal microenvironment rich in elements that could favour cell migration, proliferation and pathological process.

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“…In GDM, relation with abnormal placental morphology and accordingly with fetal morbidity was demonstrated (Giachini et al, 2008). E-cadherin is an important molecule in the maintenance of epithelial integrity (Takeichi, 1990).…”

Section: Discussionmentioning

confidence: 99%

Histopathological and Immunohistochemical Changes in the Amniotic Membrane of Gestational Diabetic Mothers

et al. 2017

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TOGRUL, C.; GÖRKEM, Ü.; COSKUN, B.; NERGISLI, C. K.; GÜNGÖR, T. & DEVECI, E.Histopathological and immunohistochemical changes in the amniotic membrane of gestational diabetic mothers. Int. J. Morphol., 35(1):184-188, 2017. SUMMARY:The aim of this study is to examine the changes in the amniotic membrane diagnosed with gestational diabetes mellitus. In this study, as a control group human amnion membrane from normotensive pregnancies was collected from diabetic women at 28-35 weeks of gestation. Gestational diabetes (n= 6) and normal amnion membrane (n= 6) for a total of 12 units were received. Amniotic membrane thickness was measured (p<0.0001) and it was significantly higher in GDM groups compared to control group. The diameter of the amniotic epithelial cell nuclei was measured (p=0.0022). Gestational diabetes results show that there was weakening between amniotic epithelial cell-cell junction. This study showed that structural changes in epithelial cells of amniotic membrane were formed due to diabetes. The membrane thickness has led to structural changes in diameter and in diabetes group cause extracellular matrix to increase, thus leading to MMP-9 expression increase eventually disrupting matrix balance. In addition, with cd44 increase angiogenesis has been induced and thought to influence material pass between fetus and mother.

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Maternal diabetes affects specific extracellular matrix components during placentation

Cited by 38 publications

References 37 publications

Effects of long‐term diabetes on the structure and cell proliferation of the myometrium in the early pregnancy of mice

Effects of long‐term diabetes on the structure and cell proliferation of the myometrium in the early pregnancy of mice

Diabetes induces stromal remodelling and increase in chondroitin sulphate proteoglycans of the rat ventral prostate

Histopathological and Immunohistochemical Changes in the Amniotic Membrane of Gestational Diabetic Mothers

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