Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling.

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Standard

Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling. / Kaucher, Amy V.

I: Biology of Reproduction, 26.05.2010.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Kaucher, AV 2010, 'Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling.', Biology of Reproduction. https://doi.org/10.1095/biolreprod.109.083352

APA

Kaucher, A. V. (2010). Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling. Biology of Reproduction. https://doi.org/10.1095/biolreprod.109.083352

Vancouver

Kaucher AV. Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling. Biology of Reproduction. 2010 maj 26. https://doi.org/10.1095/biolreprod.109.083352

Author

Kaucher, Amy V. / Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling. I: Biology of Reproduction. 2010.

Bibtex

@article{ab3766a5d141439bb403a680e54cd063,
title = "Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling.",
abstract = "Homeostasis of many tissues is maintained by self-renewal and differentiation of stem cells. Spermatogenesis is one such system relying on the activity of spermatogonial stem cells (SSCs). Several key regulators of SSC self-renewal have been identified, yet knowledge of molecules that control SSC differentiation is undefined. In this study, we found that transient impairment of STAT3 signaling enhances SSC self-renewal in vitro without affecting general spermatogonial proliferation, indicating an alteration in the balance of SSC fate decisions that inhibited differentiation. Confirming this observation, short hairpin RNA-mediated stable reduction of STAT3 expression in cultured SSCs abolished their ability to differentiate beyond the undifferentiated spermatogonial stage following transplantation into recipient testes. Collectively, these results demonstrate that STAT3 promotes the differentiation of SSCs. In contrast, STAT3 plays a central role in maintaining self-renewal of mouse embryonic stem cells, and STAT signaling is essential for self-renewal of male germline stem cells in Drosophila.",
author = "Kaucher, {Amy V}",
year = "2010",
month = may,
day = "26",
doi = "10.1095/biolreprod.109.083352",
language = "English",
journal = "Biology of Reproduction",
issn = "0006-3363",
publisher = "Society for the Study of Reproduction",

}

RIS

TY - JOUR

T1 - Regulation of mouse spermatogonial stem cell differentiation by STAT3 signaling.

AU - Kaucher, Amy V

PY - 2010/5/26

Y1 - 2010/5/26

N2 - Homeostasis of many tissues is maintained by self-renewal and differentiation of stem cells. Spermatogenesis is one such system relying on the activity of spermatogonial stem cells (SSCs). Several key regulators of SSC self-renewal have been identified, yet knowledge of molecules that control SSC differentiation is undefined. In this study, we found that transient impairment of STAT3 signaling enhances SSC self-renewal in vitro without affecting general spermatogonial proliferation, indicating an alteration in the balance of SSC fate decisions that inhibited differentiation. Confirming this observation, short hairpin RNA-mediated stable reduction of STAT3 expression in cultured SSCs abolished their ability to differentiate beyond the undifferentiated spermatogonial stage following transplantation into recipient testes. Collectively, these results demonstrate that STAT3 promotes the differentiation of SSCs. In contrast, STAT3 plays a central role in maintaining self-renewal of mouse embryonic stem cells, and STAT signaling is essential for self-renewal of male germline stem cells in Drosophila.

AB - Homeostasis of many tissues is maintained by self-renewal and differentiation of stem cells. Spermatogenesis is one such system relying on the activity of spermatogonial stem cells (SSCs). Several key regulators of SSC self-renewal have been identified, yet knowledge of molecules that control SSC differentiation is undefined. In this study, we found that transient impairment of STAT3 signaling enhances SSC self-renewal in vitro without affecting general spermatogonial proliferation, indicating an alteration in the balance of SSC fate decisions that inhibited differentiation. Confirming this observation, short hairpin RNA-mediated stable reduction of STAT3 expression in cultured SSCs abolished their ability to differentiate beyond the undifferentiated spermatogonial stage following transplantation into recipient testes. Collectively, these results demonstrate that STAT3 promotes the differentiation of SSCs. In contrast, STAT3 plays a central role in maintaining self-renewal of mouse embryonic stem cells, and STAT signaling is essential for self-renewal of male germline stem cells in Drosophila.

UR - http://europepmc.org/articles/PMC2924805

U2 - 10.1095/biolreprod.109.083352

DO - 10.1095/biolreprod.109.083352

M3 - Journal article

C2 - 20505165

JO - Biology of Reproduction

JF - Biology of Reproduction

SN - 0006-3363

ER -

ID: 301735532