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ID 115732
Author
Masaki, Kaito Shinshu University
Sakai, Mizuki Shinshu University
Jo, Jun-Ichiro Kyoto University
Hoshina, Kazuo Nagano Animal Industry Experiment Station
Fujimori, Yuki Nagano Animal Industry Experiment Station
Oka, Kenji Shinshu University
Amano, Toshiyasu Nagano Red Cross Hospital
Yamanaka, Takahiro Shinshu University
Tabata, Yasuhiko Kyoto University
Shiozawa, Tanri Shinshu University
Ishizuka, Osamu Shinshu University
Hochi, Shinichi Shinshu University
Takashima, Seiji Shinshu University
Content Type
Journal Article
Description
Both glial cell line-derived neurotrophic factor (GDNF) and fibroblast growth factor 2 (FGF2) are bona fide self-renewal factors for spermatogonial stem cells, whereas retinoic acid (RA) induces spermatogonial differentiation. In this study, we investigated the functional differences between FGF2 and GDNF in the germline niche by providing these factors using a drug delivery system in vivo. Although both factors expanded the GFRA1+ subset of undifferentiated spermatogonia, the FGF2-expanded subset expressed RARG, which is indispensable for proper differentiation, 1.9-fold more frequently than the GDNF-expanded subset, demonstrating that FGF2 expands a differentiation-prone subset in the testis. Moreover, FGF2 acted on the germline niche to suppress RA metabolism and GDNF production, suggesting that FGF2 modifies germline niche functions to be more appropriate for spermatogonial differentiation. These results suggest that FGF2 contributes to induction of differentiation rather than maintenance of undifferentiated spermatogonia, indicating reconsideration of the role of FGF2 in the germline niche.
Journal Title
Stem Cell Reports
ISSN
22136711
Publisher
International Society for Stem Cell Research|Cell Press
Volume
10
Issue
6
Start Page
1782
End Page
1792
Published Date
2018-04-19
Rights
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Institute of Advanced Medical Sciences