| First Author | Wang Y | Year | 2011 |
| Journal | Mol Cell Endocrinol | Volume | 341 |
| Issue | 1-2 | Pages | 48-54 |
| PubMed ID | 21664244 | Mgi Jnum | J:183739 |
| Mgi Id | MGI:5319156 | Doi | 10.1016/j.mce.2011.05.026 |
| Citation | Wang Y, et al. (2011) Loss of APC function in mesenchymal cells surrounding the Mullerian duct leads to myometrial defects in adult mice. Mol Cell Endocrinol 341(1-2):48-54 |
| abstractText | The WNT signal transduction pathway plays a rate limiting role in early development of many different organs. To study the functional consequences of constitutive activation of the canonical WNT pathway in the developing uterus, we generated a novel mouse model where loss of the tumor suppressor gene Apc was induced. A mouse model was generated and evaluated where Amhr2(Cre/+) driven loss of Apc exon 15 was induced. The Apc recombination was detected mainly in the myometrial layer of the adult uterus. A significant loss of muscle fibers in myometrium was apparent, though with very few muscle cells earmarked by nuclear beta-catenin. The finding was confirmed in the Pgr(Cre/+);Apc(15lox/15lox) mouse model. Loss of APC function in mesenchymal cells surrounding the fetal Mullerian ducts results in severe defects in the myometrial layers of the uterus in adult mice, suggesting that the WNT signaling pathway plays important roles in maintaining myometrial integrity. |
