Publication: Accelerated tubular cell senescence in SMP30 knockout mice
Authors
Yumura, W. ; Imasawa, T. ; Suganuma, S. ; Ishigami, A. ; Handa, S. ; Kubo, S. ; Joh, K. ; Maruyama, N.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
An experimental model with accelerated but
not drastic renal senescence seemed useful to recognize
the mechanisms of how kidney function deteriorates
with age. Senescence marker protein-30 (SMP30),
whose expression decreased with age and was sexindependent,
is mainly expressed in hepatocytes and
proximal tubular cells. Therefore, we established a
SMP30 deficient strain of mice with a C57BL/6
background by gene targeting to investigate whether this
molecule is involved in renal tubular cell senescence.
Male SMP30 knockout (SMP30Y/-) mice and male
wild-type (SMPY/+) mice (n=5) aged 12 months were
examined histologically. Their tubular epithelia showed
the deposition of lipofuscin and the presence of
senescence-associated ß-galactosidase (SA-ß-GAL).
However, no tubular cells were atrophic. In electron
microscopy, SMP30-KO mice showed markedly
enlarged lysosomes containing an electron dense
substance. These are convincing hallmarks of
senescence. We recognized the early manifestation of
senescence hallmarks in SMP30-KO mice at 12 months
old. Thus, this model represents the first report of a
mouse strain that manifests accelerated ordinal
senescence in a kidney after gene manipulation.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.