Publication: The vertebrae of prematurely aging mice as a skeletal model of involutional osteoporosis
Authors
Portal Núñez, Sergio ; Cruces, Julia ; Lozano, Daniel ; Ardura, Juan Antonio ; Villanueva-Peñacarrillo, María L. ; Fuente, Mónica de la ; Esbrit, Pedro
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Publisher
F. Hernández y Juan F. Madrid. 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
Oxidative stress in bone increases with age,
which leads to bone frailty and a high fracture risk.
Animal models show that early changes in trabecular
structure occur in age-related osteopenia. These models
might be valuable to assess the contribution of oxidative
stress in age-related bone loss. Premature aging mice
(PAM) have previously been characterized as a model of
premature immunological and neurological senescence.
PAM long bones (mainly consisting of cortical bone)
display features of aging bone. Thus, we aimed to
evaluate the vertebrae, representing a unique poorly
loaded type of trabecular bone in mice, in PAM and no
PAM (NPAM) controls. PAM showed an anxious
behaviour, based on physical activity evaluation. These
mice had decreased bone mineral density (0.078 mg/cm2
in NPAM vs 0.070 g/cm2 in PAM; p<0.05); a decreased
number of osteocytes per bone field (404±36 in NPAM
vs 320±27 in PAM; p<0.01); and downregulation of
various osteoblastic genes and low eroded surface/bone
surface, 4.2±0.5 in NPAM vs 1.9±0.2 in PAM; p<0.01).
This was associated with increased expression of
oxidative stress markers, Foxo1 and GADD45, in PAM
vertebrae. Mesenchymal progenitors in the bone marrow
of PAM have a poor mineralization capacity (assessed
by the number of mineralized nodules and suface), and
showed a lower response to an osteogenic input -
represented by parathormone-related protein-, compared
to NPAM. Collectively, these results indicate that PAM
vertebrae show osteopenia related to diminished bone
formation and remodeling. Our findings further support
the validity of PAM as a suitable model for involutional
osteoporosis and its treatment.
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Citation
Histology and Histopathology, vol. 28, nº 11 (2013)
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