Publication: Molecular and morphological characterization of neural
tube defects in embryos of diabetic Swiss Albino mice
Authors
Loh, Wan Ting ; Dheen, S. Thameem ; Jiang, Boran ; Kumar, S. Dinesh ; Tay, Samuel S.W.
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Publisher
Editores F. Hernández y Juan F. Madrid. Murcia, Universidad de Murcia, Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Background and Results: Embryos from
diabetic mice exhibit several forms of neural tube
defects, including non-closure of the neural tube. In the
present study, embryos collected at embryonic day 11.5
from diabetic pregnancies displayed open neural tube
with architectural disruption of the surrounding tissues.
The percentage of proliferating cells was found to be
increased in the dorsal and ventral domains of the spinal
neural tube of embryos from diabetic mice, indicating a
defect in the proliferation index. We have analyzed the
development of various cell types, including
motoneurons, interneurons, oligodendrocytes and
migrating neurons, as well as radial glial cells in the
open neural tube using specific molecular markers.
Immunofluorescence results revealed a significantly
reduced number of Pax2+ interneurons and increased
number of Isl-1+ motoneurons, as well as Olig2+
oligodendrocytes in the neural tube of embryos from
diabetic mice as compared to controls. In addition, these
embryos exhibited a decreased number of doublecortin
positive migrating neurons and Glast/Blbp positive
radial glial cells with shortened processes in the neural
tube. Expression levels of several developmental control
genes involved in the generation of different neuronal
cell types (such as Shh, Ngn, Ngn2, Ascl1) were also
found to be altered in the neural tube of embryos from
diabetic mice.
Conclusions: Overall, the open neural tube in embryos
of diabetic mice exhibits defects in the specification of
different cell types, including motoneurons and
interneurons, as well as glial cells along the dorsoventral
axis of the developing spinal cord. Although these
defects are associated with altered expression of several
development control genes, the exact mechanisms by
which maternal diabetes contributes to these changes
remain to be investigated.
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