A re-appraisal of mesenchymal-epithelial transition (MET) in endometrial epithelial remodeling.
A re-appraisal of mesenchymal-epithelial transition (MET) in endometrial epithelial remodeling.
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DOI:
10.1007/s00441-022-03711-z
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发表时间:
2023-03
影响因子:
3.6
通讯作者:
中科院分区:
文献类型:
--
作者:
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. The online version contains supplementary material available at 10.1007/s00441-022-03711-z.
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影响因子:
3.7
作者:
Cousins FL;Murray A;Esnal A;Gibson DA;Critchley HO;Saunders PT
通讯作者:
Saunders PT
影响因子:
2.7
作者:
Guioli, Silvana;Sekido, Ryohei;Lovell-Badge, Robin
通讯作者:
Lovell-Badge, Robin
影响因子:
4.8
作者:
OGASAWARA, Y;OKAMOTO, S;MATSUMOTO, K
通讯作者:
MATSUMOTO, K
DOI:
10.3791/55168
发表时间:
2017-03-02
期刊:
Journal of visualized experiments : JoVE
影响因子:
--
作者:
De Clercq K;Hennes A;Vriens J
通讯作者:
Vriens J
影响因子:
16.6
作者:
Kerns K;Zigo M;Drobnis EZ;Sutovsky M;Sutovsky P
通讯作者:
Sutovsky P