Senescence marker protein-30 knockout mouse as an aging model.
Ann N Y Acad Sci
; 1019: 383-7, 2004 Jun.
Article
em En
| MEDLINE
| ID: mdl-15247050
ABSTRACT
A mouse strain lacking SMP30 can be regarded as a strain showing ultimate decrease of the SMP30 molecule. After three months of age, SMP30-KO mice had an increased mortality rate, compared with the SMP30-WT mice, all of which remained alive. Electron microscopic observation of the hepatocytes from 12-month-old SMP30-KO mice revealed many empty vacuoles, presumably lipid droplets, abnormally enlarged mitochondria with indistinct cristae, and exceptionally large lysosomes filled with electron-dense bodies. The total hepatic triglyceride concentration of SMP30-KO mice was approximately 3.6-fold higher than that of the age-matched wild type. Similarly, the total hepatic cholesterol of SMP30-KO mice reached an approximate 3.3-fold greater value than that of the comparative group. Total hepatic phospholipids of SMP30-KO mice achieved an approximately 3.7-fold higher level compared with that of the wild-type mice. The cells from SMP30-KO mice were sensitive to apoptotic reagents. Those results supported the idea that SMP30 has an antiapoptotic function with wide spectrum. These findings indicate that SMP30-KO mice are highly susceptible to various harmful reagents. This strain might be a useful tool for aging and biological monitoring.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas de Ligação ao Cálcio
/
Envelhecimento
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Ann N Y Acad Sci
Ano de publicação:
2004
Tipo de documento:
Article
País de afiliação:
Japão