1998 Fiscal Year Final Research Report Summary
THE ROLE OF STRESS PROTEINS IN ENDOTOXIN-INDUCED HEPATIC INJURY
| Project/Area Number |
09670303
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | AICHI MEDICAL UNIVERSITY |
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Principal Investigator |
YOKOCHI Takashi AICHI MEDICAL UNIVERSITY,DEPARTMENT OF MICROBIOLOGY AND IMMUNOLOGY,PROFESSOR, 医学部, 教授 (20126915)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIYAMA Tsuyoshi AICHI MEDICAL UNIVERSITY,DEPARTMENT OF MICROBIOLOGY AND IMMUNOLOGY,RESEARCH ASSO, 医学部, 助手 (70268001)
KATO Yutaka AICHI MEDICAL UNIVERSITY,DEPARTMENT OF MICROBIOLOGY AND IMMUNOLOGY,ASSISTANT PRO, 医学部, 講師 (40267985)
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| Project Period (FY) |
1997 – 1998
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| Keywords | lipopolysaccharide / endotoxin / HSP / apoptosis / stress response / TNF / hepatocyte / endotoxic shock |
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| Research Abstract |
The expression of heat shock proteins (HSPs) as stress-induced proteins was studied in mice injected with D-galactosamine (D-GalN) and lipopolysaccharide (LPS) as an experimental endotoxic shock model. The expression of constitutive type heat shock protein 70 (HSC70) was significantly reduced in livers of mice injected with D-GalN and LPS, while its expression was unaffected in livers of mice injected with D-GalN or LPS alone, The expression of other constitutive type HSPs, namely HSP 60, 32 and 25 was also reduced in mice injected with D-GalN and LPS.On the other hand, inducible type HSP70 was detected in livers from mice injected with D-GalN and LPS, but not in livers from mice injected with D-GalN or LPS alone.
Simultaneous injection of anti-tumor necrosis factor (TNF)-alpha antibody prevented the liver from reduced expression of constitutive type HSC70, and lead to marked expression of inducible type HSP70 in the liver. Reduced expression of constitutive type HSC70 was also found when D-GalN and recombinant TNF-alpha was injected. Therefore, TNF-alpha was suggested to play an critical role on altered expression of constitutive HSC70 and inducible type HSP70 in response of D-GalN-sensitized mice to LPS.
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