| First Author | Tyberghein K | Year | 2012 |
| Journal | Placenta | Volume | 33 |
| Issue | 7 | Pages | 554-60 |
| PubMed ID | 22534068 | Mgi Jnum | J:187209 |
| Mgi Id | MGI:5435670 | Doi | 10.1016/j.placenta.2012.04.002 |
| Citation | Tyberghein K, et al. (2012) Tissue-wide overexpression of alpha-T-catenin results in aberrant trophoblast invasion but does not cause embryonic mortality in mice. Placenta 33(7):554-60 |
| abstractText | Transcriptional activation of CTNNA3, encoding alphaT-catenin, by the Y153H mutated form of the human STOX1 transcription factor was proposed to be responsible for altered fetal trophoblast invasion into the maternal endometrium during placentation in pre-eclampsia. Here we have generated a mouse model to investigate the in vivo effects of ectopic alphaT-catenin expression on trophoblast invasion. Histological analysis was used to determine the invasive capacities of trophoblasts from transgenic embryos, as well as proliferation rates of spongiotrophoblasts in the junctional zone. Augmented expression of alphaT-catenin reduced the number of invading trophoblasts but did not cause embryonic mortality. The, alphaT-catenin positive cells could still invade into the decidual layer and migrated as deeply as wild-type trophoblasts. Furthermore, the junctional zone is enlarged in placentas of mice overexpressing alphaT-catenin due to hyperproliferation of the residing spongiotrophoblasts, suggesting a pivotal role of alphaT-catenin levels in the control of the proliferative versus invasive state of trophoblasts during placentation. Our study provides, for the first time, in vivo data on the effects of increased levels of alphaT-catenin in the placenta. |
