Senescence Marker Protein-30 Knockout Mouse as an Aging Model

: 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...

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Published inAnnals of the New York Academy of Sciences Vol. 1019; no. 1; pp. 383 - 387
Main Authors MARUYAMA, NAOKI, ISHIGAMI, AKIHITO, KURAMOTO, MASASHI, HANDA, SETSUKO, KUBO, SACHIHO, IMASAWA, TOSHIYUKI, SEYAMA, KUNIAKI, SHIMOSAWA, TATSUO, KASAHARA, YASUSHI
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.06.2004
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Summary:: 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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ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1297.068