Publication: Maternal diabetes affects cell proliferation in developing rat placenta
Authors
Zorn, T.M.T. ; Zúñiga, M. ; Madrid, E. ; Tostes, R. ; Fortes, Z. ; Giachini, F. ; San Martín, S.
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Publisher
Editores F. Hernandez y Juan F. Madrid. Murcia, Universidad de Murcia, Departamento de Biologia Celular e Histologia
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DOI
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info:eu-repo/semantics/article
Description
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.
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