Ischemia/Reperfusion Injury Promotes and Granulocyte-Colony Stimulating Factor Inhibits Migration of Bone Marrow-Derived Stem Cells to Endometrium
Ischemia/Reperfusion Injury Promotes and Granulocyte-Colony Stimulating Factor Inhibits Migration of Bone Marrow-Derived Stem Cells to Endometrium
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DOI：
10.1089/scd.2011.0193
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发表时间：
2012-12-01
影响因子：
4
通讯作者：
Taylor, Hugh S.
中科院分区：
文献类型：
--
作者：
Du, Hongling;Naqvi, Hanyia;Taylor, Hugh S.
子宫内膜是一种动态组织，在每个生殖周期(发情期或月经周期)经历反复的再生。我们之前已经证明，骨髓来源的干细胞在啮齿类动物和人类体内植入子宫内膜；然而，目前尚不清楚这些细胞是在生理上促进子宫周期再生，还是主要参与子宫损伤后的修复。在这里，我们进行了男性到女性的骨髓移植，并测试了在存在和不存在性类固醇的情况下，子宫损伤将骨髓来源的细胞招募到子宫内膜的能力。子宫缺血/再灌注损伤导致BM来源的干细胞募集到子宫内膜的数量增加了近2倍。这种影响与性激素或发情周期的存在无关。骨髓间充质干细胞(MSCs)参与子宫损伤后的修复，但不参与动情/月经周期内膜的周期再生。粒细胞集落刺激因子(G-CSF)被用来增加移植时骨髓的动员，并被认为是一种将干细胞动员到子宫的方法。在这里，G-CSF治疗导致损伤后子宫骨髓植入减少，这可能是由于有利于造血干细胞的动员而不是MSCs。G-CSF不太可能对修复人类子宫损伤有好处。综上所述，我们证明，缺血损伤推动骨髓间充质干细胞植入子宫，不受发情周期、性激素或G-CSF的影响。
The endometrium is a dynamic tissue that undergoes repeated rounds of regeneration in each reproductive (estrous or menstrual) cycle. We have previously shown that bone marrow (BM)-derived stem cells engraft the endometrium in rodents and humans; however, it is not known if these cells contribute physiologically to uterine cyclic regeneration or alternatively are primarily involved in uterine repair in response to injury. Here we performed male-to-female BM transplant and tested the ability of uterine injury to recruit BM-derived cells to endometrium in the presence and absence of sex steroids. Uterine ischemia/reperfusion injury resulted in an similar to 2-fold increase in BM-derived stem cell recruitment to the endometrium. The effect was independent of sex steroids or the existence of an estrous cycle. BM-derived mesenchymal stem cells (MSCs) are involved in uterine repair after injury, but not the cyclic regeneration of the endometrium in the estrous/menstrual cycle. Granulocyte-colony stimulating factor (G-CSF) is used to increase BM mobilization for transplant and has been proposed as a means of mobilizing stem cells to the uterus. Here G-CSF treatment led to decreased BM engraftment of the uterus after injury, likely by favoring mobilization of hematopoietic stem cells over the MSCs. G-CSF is unlikely to be of benefit in repair of uterine injury in humans. Taken together, we demonstrate that ischemic injury drives BM MSC engraftment of the uterus, independent of estrous cycle, sex steroids, or G-CSF.