2002 Fiscal Year Final Research Report Summary
Moluecular analysis of the lesion induced by SMP30
| Project/Area Number |
12670224
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Experimental pathology
|
|---|
| Research Institution | Tokyo Metropolitan Institute of Gerontology |
|---|
Principal Investigator |
MARUYAMA Naoki Tokyo Metropolitan Inst. Gerontol., Dept. Mol Path., Head, 東京老人総合研究所・加齢臓器障害研究グループ・グループリーダー(研究部長) (00115940)
|
|---|
| Project Period (FY) |
2000 – 2002
|
| Keywords | aging / SMP30 / lysosome / lipofuscin / carolie-restriction / renal glomeruli / 老化 |
|---|
| Research Abstract |
To elucidate of the roles in ageassociated diseases the enzyme activities were investigated. SMP30 works as organphosphatese in liver. DFPase activity of SMP30 requires divalent ions like as Mg, Mn, or Co but not Ca. The authentic enzyme activity is seemetd to be acid phosphatase. This function might be related with the function of lysosome. The morphological features of aged kidney showed marked formation of lipofuscin in renal tubular epithelia. This finding indicates that SMP30 is suitable for senescence marker. In diabetic nephropathy the distribution of SMP30 in tubular cells is characteristic. SMP30 will be useful for pathological diagnosis. Carolie restriction enhances the life span of experimental animals. Along with the elongated life-span the amounts of SMP30 in organs was significantly enhanced.
|
-
-
-
-
-
-
-
-
-
[Publications] Ishigami A, Fujita T, Handa S, Shirasawa T, Koseki H, Kitamura T, Enomoto N, Sato N, Shimosawa T, Sato N, Maruyama N: "Senescence marker protein-30 knockout mouse liver is highly susceptible to TNF-α- and Fas-mediated apoptosis"Amr J Pathol. 161. 1273-1281 (2002)
Description
「研究成果報告書概要(欧文)」より
-
-
-
