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The mechanisms of enhanced acidosis on ischemic neuronal damage

Research Project

Project/Area Number 10670610
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Neurology
Research InstitutionNippon Medical School

Principal Investigator

KATSURA Kenichiro  Nippon Medical School, Lecturer, 医学部, 講師 (50297892)

Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
KeywordsHyperglycemia / Acidosis / Cerebral ischemia / Apoptosis / Protein kinase C / calcium / calmodulin-dependent protein kinase II
Research Abstract

Acidification is reported to be able to activate protein phosphorylation, protein synthesis and immediate-early-gene transcription. Our aim is to study the changes in subcellular redistributions of protein kinases C during complete ischemia, changing intraischemic acidotic levels by either injecting glucose (Hyperglycemic, HG) or adding CO2 (Hypercapnic, HC). The translocation of PKC from the cytosolic fraction to particulate fraction was enhanced under ischemia with severe acidosis. Overactivation (the enhanced traslocation) of the enzyme seems to be harmful to the neuronal survival after ischemia (Katsura et al. Brain Research 1999).
The PKC translocation was significantly increased in the goups with enhanced acidosis. These results raise questions whether the enhanced acidosis affects the lipid metabloism, especially the release of free fatty acids (FFAs) and diacylglycerides (DAGs). The parietal cortex was chosen since the ischemic damage was significantly aggravated by both HG and HC ; besides, we know the change of pH during ischemia. Countrary to our expectations, the FFA and DAG contents were less in the animals with superimposed acidosis. Thus, animals with enhanced acidosis showed significantly decreased levels of DAGs at 10 min when the PKC translocation is significantly enhanced. The reasons are still to be studied, however, the massive influx of calcium upon cellular deporalization and liberation of various FFAs may decrease the necessity and dependence of DAGs for PKC translocation (paper in preparation).

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • Research Products

    (8 results)

All Other

All Publications (8 results)

  • [Publications] 桂研一郎 他: "Acidosis enhances translocation of protein kinase C but not Ca2+/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia"Brain Research. 849. 119-127 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] "高血糖の脳虚血後のエネルギー代謝および細胞内pHに及ぼす影響"Brain Hypoxia. 12. 83-91 (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Katsura and Siesjo: ""Acid-Base Metabolism in Ischemia" PH and Brain Function"Kai Kaila and Bruce R. Ransom.

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Katsura et al.: "Acidosis enhances translocation of protein kinase C but not Ca2+/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia"Brain Research. 849. 119-127 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Katsura et al.: "Effect of Hyperglycemia on Cerebral Energy Metabolism and Intracellular pH after Ischemia"Brain Hypoxia. 12. 83-91 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Katsura and Siesjo: "Acid-Base Metabolism in Ischemia"pH and Brain Function Kai Kaila and Bruce R. Ransom (Eds). 563-582 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] 桂 研一郎: "Acidosis enhances translocation of protein kinase C but not Ca2+/calmodulin-dependent protein kinase II to cell membranes during complete cerebral ischemia"Brain Research. 849. 119-127 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] 桂研一郎: "高血糖の脳虚血後のエネルギー代謝および細胞内pHに及ぼす影響" Brain Hypoxia. 12. 83-91 (1998)

    • Related Report
      1998 Annual Research Report

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Published: 1998-04-01   Modified: 2016-04-21  

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