Biol Reprod Keystone Symposia Conference on Frontiers in Reproductive Biology & Regulation of Fertility.
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BOR - Papers in Press, published online ahead of print October 17, 2002.
Biol Reprod 2002, 10.1095/biolreprod.102.004820
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BIOLOGY OF REPRODUCTION 68, 530–535 (2003)
DOI: 10.1095/biolreprod.102.004820
© 2003 by the Society for the Study of Reproduction, Inc.

Ovary

Changes in the Expression of Tumor Necrosis Factor (TNF) {alpha}, TNF{alpha} Receptor (TNFR) 2, and TNFR-Associated Factor 2 in Granulosa Cells During Atresia in Pig Ovaries1

Mizuho Nakayamaa, Noboru Manabe2,a, Naoko Inouea, Toshikatsu Matsuia, and Hajime Miyamotoa

a Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University, Kyoto 606-8502, Japan

Tumor necrosis factor (TNF) {alpha} can induce both cell death and cell proliferation and exerts its effects by binding to either TNF receptor (TNFR) 1 or 2. When TNF{alpha}-bound TNFR2 interacts with TNFR-associated factor 2 (TRAF2), expression of survival/antiapoptotic genes is up-regulated. In the present study we determined the changes in localization of TNF{alpha} and TRAF2 and their mRNAs and the expression of TNFR2 in granulosa cells during follicular atresia in pig ovaries. In healthy follicles, intense signals for TNF{alpha} and TRAF2 and their mRNAs were demonstrated in the outer zone of the granulosa layer, where many proliferating cells and no apoptotic cells were observed. In atretic follicles, decreased or trace staining for TRAF2 and its mRNA and decreased expression of TNFR2 were observed in the granulosa layer, where many apoptotic cells were seen. These findings suggested that TNF{alpha} acts as a survival factor in granulosa cells during follicular atresia in pig ovaries.

1 This work was supported by Grant-in-Aid 13GS0008 for Creative Scientific Research to N.M. from the Japan Society for the Promotion of Science.

2 Correspondence: FAX: 81 75 753 6345; manabe{at}kais.kyoto-u.ac.jp






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Copyright © 2003 by the Society for the Study of Reproduction.