Conditional deletion of Sox17 reveals complex effects on uterine adenogenesis and function.
Dev Biol
; 414(2): 219-27, 2016 06 15.
Article
em En
| MEDLINE
| ID: mdl-27102016
ABSTRACT
The importance of canonical Wnt signaling to murine uterine development is well established. Mouse models in which uterine-specific Wnt ligands, ß-catenin, or Lef1 are disrupted result in failure of postnatal endometrial gland development. Sox17 is a transcription factor characterized in numerous tissues as an antagonist of Wnt signaling. Thus, we hypothesized that conditional ablation of Sox17 would lead to hyperproliferation of endometrial glands in mice. Contrary to our prediction, disruption of Sox17 in epithelial and stromal compartments led to inhibition of endometrial adenogenesis and a loss of reproductive capacity. Epithelium-specific Sox17 disruption resulted in normal adenogenesis although reproductive capacity remained impaired. These findings suggest that non-epithelial, Sox17-positive cells are necessary for adenogenesis and that glands require Sox17 to properly function. To our knowledge, these findings are the first to implicate Sox17 in endometrial gland formation and reproductive success. The data presented herein underscore the importance of studying Sox17 in uterine homeostasis and function.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas HMGB
/
Endométrio
/
Células Epiteliais
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Glândulas Exócrinas
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Fatores de Transcrição SOXF
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Pregnancy
Idioma:
En
Revista:
Dev Biol
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
Estados Unidos