Oral Presentation 6th Annual Meeting for Australasian Society for Stem Cell Research 2013

Telomerase reverse transcriptase expression marks endometrial progenitors with epithelial differentiation potential. (#29)

James A Deane 1 , David T Breault 2 , Caroline E Gargett 1
  1. Monash Institute of Medical Research, Monash University, Clayton, VIC, Australia
  2. Division of Endocrinology, Children's Hospital , Harvard Medical School, Boston, MA, USA
The endometrium is the highly regenerative lining of the uterus and contains small populations of epithelial and stromal cells with stem/progenitor properties. However the lack of a traceable marker for endometrial stem/progenitor cells in mouse models has meant their role in endometrial regeneration is unclear. Telomerase activity preserves stem/progenitor cell viability by maintaining telomere length during repeated cycles of cell division. We have used the expression of mouse telomerase reverse transcriptase (mTert), the rate limiting catalytic component of the telomerase complex, as a marker to identify progenitor cells in the mouse endometrium. GFP expression driven by the mTert promoter marks an infrequent population of intrinsic (CD45negative) endometrial stromal cells during development and adulthood, and rare focal regions of epithelium in the adult endometrium. These mTert expressing cells are distinct from the stromal and epithelial label-retaining cells previously described in the mouse endometrium.  mTert endometrial cells do not express estrogen receptor-alpha or undergo proliferation in response to estrogen. However a close spatial relationship between mTert positive epithelial cells and proliferating epithelial cells suggests that mTert cells may give rise to proliferative epithelial transit amplifying cells. We used inducible Cre recombinase expression driven by the mTert promoter to permanently label the endometrial mTert lineage with LacZ expression in postnatal mice. The mTert lineage is confined to the stroma of prepubertal endometrium, but contributes to glandular and luminal epithlelium in adult endometrium cycling under the influence of ovarian hormones. Depriving the adult endometrium of hormones through ovariectomy causes endometrial atrophy and prevents the epithelial expansion of the mTert lineage. These results suggest that epithelial structures of the adult cycling endometrium originate from an mTert positive stromal progenitor that undergoes mesenchymal-to-epithelial transition during endometrial regeneration. This is the first report of a traceable marker for endometrial progenitors with epithelial differentiation potential.