The human endometrium undergoes approximately 450 cycles of proliferation, differentiation, shedding and regeneration over a woman’s reproductive lifetime. The regenerative capacity of the endometrium is attributed to stem/progenitor cells residing in the basalis layer of the tissue. Mesenchymal stem cells have been extensively studied in the endometrium, whereas endometrial epithelial stem/progenitor cells have remained more elusive. This review details the discovery of human and mouse endometrial epithelial stem/progenitor cells. It highlights recent significant developments identifying putative markers of these epithelial stem/progenitor cells that reveal their in vivo identity, location in both human and mouse endometrium, raising common but also different viewpoints. The review also outlines the techniques used to identify epithelial stem/progenitor cells, specifically in vitro functional assays and in vivo lineage tracing. We will also discuss their known interactions and hierarchy and known roles in endometrial dynamics across the menstrual or estrous cycle including re-epithelialization at menses and regeneration of the tissue during the proliferative phase. We also detail their potential role in endometrial proliferative disorders such as endometriosis.
During oocyte differentiation in mouse fetal ovaries, sister germ cells are connected by intercellular bridges, forming germline cysts. Within the cyst, primary oocytes form via gaining cytoplasm and organelles from sister germ cells through germ cell connectivity. To uncover the role of intercellular bridges in oocyte differentiation, we analyzed mutant female mice lacking testis-expressed 14 (TEX14), a protein involved in intercellular bridge formation and stabilization. In Tex14 homozygous mutant fetal ovaries, germ cells divide to form a reduced number of cysts in which germ cells remained connected via syncytia or fragmented cell membranes, rather than normal intercellular bridges. Compared with wild-type cysts, homozygous mutant cysts fragmented at a higher frequency and produced a greatly reduced number of primary oocytes with precocious cytoplasmic enrichment and enlarged volume. By contrast, Tex14 heterozygous mutant germline cysts were less fragmented and generate primary oocytes at a reduced size. Moreover, enlarged primary oocytes in homozygous mutants were used more efficiently to sustain folliculogenesis than undersized heterozygous mutant primary oocytes. Our observations directly link the nature of fetal germline cysts to oocyte differentiation and development.
The ubiquitin processing protease, UbpA (a homolog of yeast Ubp14 and human IsoT/USP5), is required for the growth‐to‐development transition of Dictyostelium. To understand the role of UbpA in regulating this transition, ubpA− cells were used to elucidate UbpA‐dependent pathways. ubpA− cells were hypersensitive to oxidative and nitrosative stresses, and miss‐regulated genes at the growth‐to‐development transition, including lmcB. ubpA is required for growth‐stage expression of lmcB which is involved in sensing nutrient levels and signaling cells to develop upon starvation. Exogenous expression of ubpA in ubpA− cells restored lmcB transcript levels, while exogenous expression of lmcB partially restored the developmental defect in ubpA− cells. Interestingly, lmcB is downregulated in wild‐type cells once the growth‐to‐development transition has occurred. Pull down experiments utilizing His‐tagged LmcB and TAP‐tagged LmcB expressed in Dictyostelium identified putative interacting proteins that included LmcA, PsmC5, CdaA, and a cAMP‐inducible protein. Direct binding experiments confirmed the interaction between LmcB and LmcA, and between LmcB and CdaA, a cytidine deaminase. To investigate cytidine deaminase (CDA) activity levels at the growth‐to‐development transition, a CDA assay was adapted for Dictyostelium. Wild‐type cells showed relatively low levels of CDA activity when growing and substantially increased levels upon starvation. Both growing and starving ubpA− cells have high CDA levels similar to the starving wild type cells. It is possible that LmcB binds CdaA to repress CDA activity during growth; then, upon starvation, LmcB is downregulated releasing CdaA. These results will lead to a better understanding of the mechanisms cells use to sense starvation stress and respond by making the transition from growth to development.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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