title: Identification of label-retaining perivascular cells in a mouse model of endometrial decidualization, breakdown, and repair.
abstract: The human endometrium is incredibly dynamic, undergoing monthly cycles of growth and regression during a woman's reproductive life. Endometrial repair at the cessation of menstruation is critical for reestablishment of a functional endometrium receptive for embryo implantation; however, little is understood about the mechanisms behind this rapid and highly efficient process. This study utilized a functional mouse model of endometrial breakdown and repair to assess changes in endometrial vasculature that accompany these dynamic processes. Given that adult endometrial stem/progenitor cells identified in human and mouse endometrium are likely contributors to the remarkable regenerative capacity of endometrium, we also assessed label-retaining cells (LRC) as candidate stromal stem/progenitor cells and examined their relationship with endometrial vasculature. Newborn mouse pups were pulse-labeled with bromodeoxyuridine (BrdU) and chased for 5 wk before decidualization, endometrial breakdown, and repair were induced by hormonal manipulation. Mean vessel density did not change significantly throughout breakdown and repair; however, significantly elevated endothelial cell proliferation was observed in decidual tissue. Stromal LRC were identified throughout breakdown and repair, with significantly fewer observed during endometrial repair than before decidualization. A significantly higher percentage of LRC were associated with vasculature during repair than before decidualization, and a proportion were undergoing proliferation, indicative of their functional capacity. This study is the first to examine the endometrial vasculature and candidate stromal stem/progenitor cells in a functional mouse model of endometrial breakdown and repair and provides functional evidence suggesting that perivascular LRC may contribute to endometrial stromal expansion during the extensive remodeling associated with this process.
authors.affiliation: The Ritchie Centre, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
authors.forename: Tu'uhevaha J
authors.initials: TJ
authors.lastname: Kaitu'u-Lino
authors.forename: Louie
authors.initials: L
authors.lastname: Ye
authors.forename: Lois A
authors.initials: LA
authors.lastname: Salamonsen
authors.forename: Jane E
authors.initials: JE
authors.lastname: Girling
authors.forename: Caroline E
authors.initials: CE
authors.lastname: Gargett
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D049109:Cell Proliferation; D004717:Endometrium / Q000098:blood supply / Q000166:cytology / Q000502:physiology*; D042783:Endothelial Cells / Q000502:physiology; D004967:Estrogens; D030762:Estrous Cycle; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D055806:Microvessels / Q000033:anatomy & histology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D011374:Progesterone; D013234:Stem Cells / Q000166:cytology* / Q000378:metabolism
chemical_list: C558396:Acta2 protein, mouse; D000199:Actins; D004967:Estrogens; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011374:Progesterone