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dc.contributor.authorYumura, W.es_ES
dc.contributor.authorImasawa, T.es_ES
dc.contributor.authorSuganuma, S.-
dc.contributor.authorIshigami, A.-
dc.contributor.authorHanda, S.-
dc.contributor.authorKubo, S.-
dc.contributor.authorJoh, K.-
dc.contributor.authorMaruyama, N.-
dc.description.abstractAn 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.es_ES
dc.publisherMurcia : F. Hernándezes_ES
dc.relation.ispartofHistology and histopathologyes_ES
dc.subjectRenal senescencees_ES
dc.subjectTubular cellses_ES
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes_ES
dc.titleAccelerated tubular cell senescence in SMP30 knockout micees_ES
Aparece en las colecciones:Vol.21, nº11 (2006)

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