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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Maternal diabetes affects cell proliferation in developing rat placenta

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Author(s):
Zorn, T. M. T. [1] ; Zuniga, M. ; Madrid, E. ; Tostes, R. [1] ; Fortes, Z. [1] ; Giachini, F. [1] ; San Martin, S. [2, 3]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, BR-05508 Sao Paulo - Brazil
[2] Univ Valparaiso, Fac Med, Sch Med, Biomed Res Ctr, Valparaiso - Chile
[3] Reg Ctr Study Healthy Foods, CREAS, Valparaiso - Chile
Total Affiliations: 3
Document type: Journal article
Source: HISTOLOGY AND HISTOPATHOLOGY; v. 26, n. 8, p. 1049-1056, AUG 2011.
Web of Science Citations: 16
Abstract

Placentation starts with the formation of a spheroidal trophoblastic shell surrounding the embryo, thus facilitating both implantation into the uterine stroma and contact with maternal blood. Although it is known that diabetes increases the placental size and weight, the mechanisms responsible for this alteration are still poorly understood. In mammals, cellular proliferation occurs in parallel to placental development and it is possible that diabetes induces abnormal uncontrolled cell proliferation in the placenta similar to that seen in other organs (e.g. retina). To test this hypothesis, the objective of this work was to determine cell proliferation in different regions of the placenta during its development in a diabetic rat model. Accordingly, diabetes was induced on day 2 of pregnancy in Wistar rats by a single injection of alloxan (40 mg/kg i.v.). Placentas were collected on days 14, 17, and 20 postcoitum. Immunoperoxidase was used to identify Ki67 nuclear antigen in placental sections. The number of proliferating cells was determined in the total placental area as well as in the labyrinth, spongiotrophoblast and giant trophoblast cell regions. During the course of pregnancy, the number of Ki67 positive cells decreased in both control and diabetic rat placentas. However, starting from day 17 of pregnancy, the number of Ki67 positive cells in the labyrinth and spongiotrophoblast regions was higher in diabetic rat placentas as compared to control. The present results demonstrate that placentas from the diabetic rat model have a significantly higher number of proliferating cells in specific regions of the placenta and at defined developmental stages. It is possible that this increased cell proliferation promotes thickness of the placental barrier consequently affecting the normal maternal-fetal exchanges. (AU)