Publication: Bone biology in postnatal Wistar rats following hypoxia-reoxygenation
Authors
Hameister, Rita ; Lohmann, Christoph H. ; Dheen, Thameem ; Singh, Gurpal ; Kaur, Charanjit
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-143
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info:eu-repo/semantics/article
Description
Abstract
Hypoxia response pathways have a central
role in normal and abnormal bone biology but the effect
of systemic hypoxia-reoxygenation on bone is not clear.
Following hypoxic exposure, aberrant synthesis, folding
and trafficking of proteins has been reported to occur,
which can result in endoplasmic reticulum (ER) stress
and may finally cause cell death. This study aimed to
examine the effect of systemic hypoxia-reoxygenation
injury on bone biology in postnatal rats.
Immunoexpression of HIF-1α and VEGF was
upregulated in femurs of newborn Wistar rats in
response to systemic hypoxia-reoxygenation. Along with
that, increased apoptosis of osteoblast precursors,
osteoblasts, osteocytes and endothelial cells was
observed in comparison to femurs of control animals by
transmission electron microscopy, TUNEL staining and
immunoexpression of cleaved caspase-3. The viability of
osteoclasts was not affected. After hypoxia-
reoxygenation, ER stress was observed in the osteoblasts
and osteocytes as indicated by dilatation of the ER and
enhanced immunoexpression of the ER stress marker
GRP78. Localisation of collagen α1 immunoreaction
was widespread in the bone matrix of control femurs but
was confined to the osteoblasts and osteocytes in
response to hypoxia-reoxygenation. In support of these
findings, in vitro work showed reduced viability of
osteoblast-like SaOs-2 cells and upregulation of GRP78
protein expression in them by western blotting following
exposure to hypoxia. This suggests that systemic
hypoxia-reoxygenation may disturb bone biology in
postnatal Wistar rats by inducing ER stress and
apoptosis in osteoblasts and osteocytes, without
affecting the viability of osteoclasts. More in-depth
research is needed to confirm causality between ER
stress and apoptosis of osteoblasts and osteocytes
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Citation
Histology and Histopathology Vol. 35, nº 1 (2020)
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