| Project/Area Number |
12670220
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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 |
Experimental pathology
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| Research Institution | HYOGO COLLEGE OF MEDICINE |
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Principal Investigator |
TERADA Nobuyuki Hyogo College of Medicine, Professor, 医学部, 教授 (50150339)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Naoko Hyogo College of Medicine, Research Associate, 医学部, 助手 (10319858)
TSUJIMURA Tohru Hyogo College of Medicine, Associate Professor, 医学部, 助教授 (20227408)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | apoptosis / androgen / estrogen / Fas / Fas ligand / VDAC / mouse / cytochrome C / 子宮 / 精嚢 / 前立腺 / 精巣上体 / 凝固腺 |
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| Research Abstract |
1.We examined the effect of castration on apoptosis in the epithelia of the mouse seminal vesicle and epididymis, and found the followings. (1) Castration induces apoptosis in the epithelia of these organs from birth to adulthood. (2) The extent of apoptosis is lower at the slowly growing stage of these organs than at their rapidly growing stage thereafter.
2.By the experiments with mutant mice deficient in Fas or Fas ligand, we have shown that the Fas- Fas ligand system plays little role in castration-induced apoptosis in the mouse seminal vesicle, epididymis, prostate and coagulating gland.
3.We have shown that apoptosis in the mouse uterine epithelium after estrogen deprivation correlates to release of cytochrome C in mitochondria into cytoplasm, activation of caspase-3, the ratio of Bak or Bax/Bcl-2 or Bcl-xL and the amount of voltage dependent anion channel (VDAC) in the mitochondria. These results suggest the followings. (1) Mitochondria play an important role in estrogen deprivation-induced apoptosis in the uterine epithelium. (2) This apoptotic process is regulated by proteins of the Bcl-2 family. (3) The increase in VDAC enhances the sensitivity of cells to apoptosis since VDAC is thought to be a channel, through which cytochrome C moves from mitochondria to cytoplasm.
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