TRADD is Involved in Apoptosis Induction in Granulosa Cells during Atresia in Pig Ovaries.
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- WADA Satoko
- Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
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- MANABE Noboru
- Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
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- INOUE Naoko
- Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
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- NAKAYAMA Mizuho
- Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
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- MATSUI Toshikatsu
- Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
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- MIYAMOTO Hajime
- Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
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Abstract
Previously, we histochemically demonstrated the expression of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and its receptors, death receptor-4 (DR4), death receptor-5 (DR5) and decoy receptor-1 (DcR1) in granulosa cells of porcine follicles. However, TRAIL can induce both cell death and cell proliferation. In the present study, reverse transcription polymerase chain reaction and in situ hybridization analyses revealed increased mRNA expression of TNF receptor-associated death domain protein (TRADD), which transmits the death signal from DR4 and/or DR5 to intracellular apoptosis-signal transduction components, in granulosa cells was demonstrated only in atretic follicles but not in healthy follicles. These findings indicate that TRADD is involved in induction of apoptosis in granulosa cells, and that the TRAIL-receptor system induces apoptosis in granulosa cells during atresia in porcine ovaries.
Journal
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- Journal of Reproduction and Development
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Journal of Reproduction and Development 48 (2), 175-181, 2002
The Society for Reproduction and Development
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Keywords
Details 詳細情報について
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- CRID
- 1390001206337852288
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- NII Article ID
- 130000054979
- 10026616184
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- NII Book ID
- AA10936678
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- COI
- 1:CAS:528:DC%2BD38XkvVantr0%3D
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- ISSN
- 13484400
- 09168818
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- NDL BIB ID
- 6145465
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed