| Project/Area Number |
04836018
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
老化(加齢)
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
KAMAZAKI Tsutomu Hiroshima University Research Institute for Nuclear Medicine and Biology, Department of Biochemistru and Biophysics, Research Associate, 原爆放射能医学研究所, 助手 (20161698)
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| Co-Investigator(Kenkyū-buntansha) |
MITSUI Youji National Institute of Bioscience and Human Technology, Chief senior scientist, 生命工学工業技術研究所, 首席研究官
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Cellular senescence / Vascular endothelial Cell / Gene cloning / Fibronectin / Endothelin |
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| Research Abstract |
The approx. 300 clones isolated last year as senescent specific claones by the differential screening method from the cDNA library of senescent endothelial cells from human umbilical vein were further screened to confirm senescent specificity and to purify the clones. Several 10 clones of these were determined their sequences. The obtained sequences were then compared with all the known sequences reported and 2 clones were found to be unknown. We sill continue to analyze these clones more detail and uncover the roles of these genes on cellular senescence.
On the other hand, we have shown that the secretion of encothelin increases during senescence of vascular encothelial cells. In this year, we showed that, using vascular endothelial cells aged in vitro and in vivo, the increased production of endothelin is mainly achieved by the increase of mRNA.We have shown that the expression of fibronectin gene increases during cellular aging in both vascular endothelial cells and fibroblasts. We also observed the increased blood comcentration of endothelin in the elderly. These observations suggest that aging of vascular endothelial cells proceed in vivo with aging of individual.
As shown by this research, the increased expression of fibronectin during cellular senescence is observed not only in fibroblasts but also in vascular encothelial cells. This suggests that the increase is not a stecific phenomenon on a specific cell type but rather a common phenomenon in cellular senescence of many cell types. We, here, showed that the expression of encothelin increased during senescence of vascular endothelial cells. Thus, it is the next problem to be determined what is the common mechanism of regulation of gene expression.
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