| First Author | Spooner-Harris M | Year | 2023 |
| Journal | Cell Tissue Res | Volume | 391 |
| Issue | 2 | Pages | 393-408 |
| PubMed ID | 36401092 | Mgi Jnum | J:361472 |
| Mgi Id | MGI:7857030 | Doi | 10.1007/s00441-022-03711-z |
| Citation | Spooner-Harris M, et al. (2023) A re-appraisal of mesenchymal-epithelial transition (MET) in endometrial epithelial remodeling. Cell Tissue Res 391(2):393-408 |
| abstractText | Mesenchymal-epithelial transition (MET) is a mechanism of endometrial epithelial regeneration. It is also implicated in adenocarcinoma and endometriosis. Little is known about this process in normal uterine physiology. Previously, using pregnancy and menses-like mouse models, MET occurred only as an epithelial damage/repair mechanism. Here, we hypothesized that MET also occurs in other physiological endometrial remodeling events, outside of damage/repair, such as during the estrous cycle and adenogenesis (gland development). To investigate this, Amhr2-Cre-YFP/GFP mesenchyme-specific reporter mice were used to track the fate of mesenchymal-derived (MD) cells. Using EpCAM (epithelial marker), EpCAM(+)YFP(+) MD-epithelial cells were identified in all stages of the estrous cycle except diestrus, in both postpartum and virgin mice. EpCAM(+)YFP(+) MD-epithelial cells comprised up to 80% of the epithelia during estrogen-dominant proestrus and significantly declined to indistinguishable from control uteri in diestrus, suggesting MET is hormonally regulated. MD-epithelial cells were also identified during postnatal epithelial remodeling. MET occurred immediately after birth at postnatal day (P) 0.5 with EpCAM(+)GFP(+) cells ranging from negligible (0.21%) to 82% of the epithelia. EpCAM(+)GFP(+) MD-epithelial cells declined during initiation of adenogenesis (P8, avg. 1.75%) and then increased during gland morphogenesis (P14, avg. 10%). MD-epithelial cells expressed markers in common with non-MD-epithelial cells (e.g., EpCAM, FOXA2, ESR1, PGR). However, MD-epithelial cells were differentially regulated postnatally and in adults, suggesting a functional distinction in the two populations. We conclude that MET occurs not only as an epithelial damage/repair mechanism but also during other epithelial remodeling events, which to our knowledge has not been demonstrated in other tissues. |
