The Ritchie Centre, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
Biol Reprod. 2012 Jun 22;86(6):184. doi: 10.1095/biolreprod.112.099309. Print 2012 Jun.
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.
人类子宫内膜具有惊人的动态性，在女性生殖生命期间经历每月的生长和退化周期。在月经停止时进行子宫内膜修复对于重建接受胚胎植入的功能性子宫内膜至关重要；然而，对于这个快速且高效的过程背后的机制知之甚少。本研究利用子宫内膜崩解和修复的功能性小鼠模型来评估伴随这些动态过程的子宫内膜血管变化。鉴于在人类和小鼠子宫内膜中鉴定的成年子宫内膜干细胞/祖细胞可能是子宫内膜惊人再生能力的贡献者，我们还评估了标记保留细胞（LRC）作为候选基质干细胞/祖细胞，并检查了它们与子宫内膜血管的关系。新生小鼠幼仔用溴脱氧尿苷（BrdU）脉冲标记，然后追踪 5 周，然后通过激素处理诱导蜕膜化、子宫内膜崩解和修复。在崩解和修复过程中，平均血管密度没有明显变化；然而，在蜕膜组织中观察到内皮细胞增殖显著增加。在崩解和修复过程中都鉴定出基质 LRC，在子宫内膜修复期间观察到的 LRC 明显少于蜕膜化之前。在修复期间与血管相关的 LRC 比例明显高于蜕膜化之前，并且有一部分正在增殖，表明其功能能力。这项研究首次在子宫内膜崩解和修复的功能性小鼠模型中检查了子宫内膜血管和候选基质干细胞/祖细胞，并提供了功能证据表明，在与该过程相关的广泛重塑期间，血管周围的 LRC 可能有助于子宫内膜基质的扩张。
