| Project/Area Number |
06671598
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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 |
Urology
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| Research Institution | Nagasaki University |
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Principal Investigator |
NOMATA Koichiro NAGASAKI UNIV., SCHOOL OF MED., Hospital, INSTRUCTOR, 医学部附属病院, 講師 (80189430)
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| Co-Investigator(Kenkyū-buntansha) |
KANETAKE Hiroshi NAGASAKI UNIV., SCHOOL OF MED., ASSISTANT PROFESSOR, 医学部, 助教授 (50100839)
SAITO Yutaka NAGASAKI UNIV., SCHOOL OF MED., PROFESSOR, 医学部, 教授 (70039832)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Renal tubular cell / Growth factor / Renal carcinogen / Cell cell communication / Renal cell carcinoma / ギャップ結合 |
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| Research Abstract |
Gap junctional intercellular communications (GJIC) are known as the channels for the direct transfer of cytoplasmic molecules between neighboring cells and are lost during transformation of normal cells. To study the function, and the molecular mechanism for the loss of GJIC,the effects of dimethylnitrosamine, KBrO_3, FeSO_4・7H_2O,which are known as chemical tumor promoters of the kidney on the GJIC function and the expression of connexin 43 of Madin-Darby Canine Kidney (MDCK) cells were examined. These tumor promoters inhibited the GJIC in MDCK cells. The expression of connexin 43 mRNA and connexin 43 protein were not altered by these treatment, whereas immunohistochemical study revealed that the distribution of connexin 43 protein was changed from the cell surface to the cytoplasma. These data suggest that blockage of GJIC in MDCK cells treated with renal carcinogens support the hypothesis that loss of GJIC might be important in renal carcinogenesis.
Freeze-fracture replicas were prepared from the operative specimens of 14 patients with renal cell carcinoma. Gap junctions in the renal cell carcinoma (RCC) tissues were significantly fewer than in the surrounding normal tissue, as for the frequency of gap junctions there was no obvious relation in tumor grade and pathological stage. However, there is no clearly difference in freqency of tight junctions between RCC tissues and surroungins normal tissues. These data suggest that the loss of intercellular communication via gap junction may be associated with renal cell carcinoma formation.
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