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首页> 外文期刊>Journal of Pediatric Surgery: Official Journal of the Surgical Section of the American Academy of Pediatric, the British Association of Paediatric Surgeons, the American Pediatric Surgical Association, and the Canadian Association of Paediatric Surgeons >Stromal progenitor cells promote leukocyte migration through production of stromal-derived growth factor 1alpha: a potential mechanism for stromal progenitor cell-mediated enhancement of cellular recruitment to wounds.
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Stromal progenitor cells promote leukocyte migration through production of stromal-derived growth factor 1alpha: a potential mechanism for stromal progenitor cell-mediated enhancement of cellular recruitment to wounds.

机译:基质干祖细胞通过产生基质衍生生长因子1alpha促进白细胞迁移:基质祖细胞介导增强细胞向伤口募集的潜在机制。

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BACKGROUND/PURPOSE: Stromal progenitor cells (SPC) enhance tissue repair in a variety of injury models. However, the mechanisms by which SPCs facilitate tissue repair remain poorly understood. We hypothesized that SPC-enhanced tissue repair is, in part, because of SPC-mediated recruitment of circulating cells to areas of tissue injury. To test this, we examined the migration of leukocytes in response to SPC in vitro. METHODS: Leukocyte migration was assessed in response to SPC, SPC + transforming growth factor (TGF)-beta1, or SPC + AMD3100 using a Transwell assay system (Corning, distributed by Fisher Scientific, Pittsburgh, PA). Supernatants were collected from lower chambers and analyzed for leukocyte content, leukocyte viability, and stromal-derived growth factor (SDF)-1alpha concentration. RESULTS: Stromal progenitor cells increased leukocyte migration compared to media alone (450 +/- 70 vs 112 +/- 17 cells/microL; P .05). SPC treatment with TGF-beta1 resulted in a 36% increase in leukocyte migration and correlated with an increase in SDF-1alpha production. Treatment with AMD3100 resulted in inhibition of leukocyte migration. CONCLUSIONS: Stromal progenitor cells promote leukocyte migration, and this appears to be mediated through SDF-1alpha production. The SPC production of SDF-1alpha may be modulated by other cytokines present in the microenvironment during wound healing. Together, these observations provide a potential mechanism by which SPC may augment healing through enhanced recruitment of inflammatory cells and tissue progenitor cells to areas of tissue injury.
机译:背景/目的:基质祖细胞(SPC)在多种损伤模型中增强组织修复。但是,SPC促进组织修复的机制仍然知之甚少。我们假设SPC增强的组织修复部分是由于SPC介导的循环细胞募集到组织损伤区域。为了测试这一点,我们在体外检查了响应SPC的白细胞迁移。方法:使用Transwell测定系统(康宁公司,宾夕法尼亚州匹兹堡的Fisher Scientific公司发行),对SPC,SPC +转化生长因子(TGF)-β1或SPC + AMD3100的反应评估白细胞迁移。从下室收集上清液,并分析白细胞含量,白细胞活力和基质衍生生长因子(SDF)-1alpha浓度。结果:与单独的培养基相比,基质干祖细胞增加了白细胞迁移(450 +/- 70 vs 112 +/- 17细胞/微升; P <.05)。用TGF-beta1进行SPC处理可导致白细胞迁移增加36%,并与SDF-1alpha产量增加相关。用AMD3100处理可抑制白细胞迁移。结论:基质祖细胞促进白细胞迁移,这似乎是通过SDF-1alpha产生介导的。在伤口愈合过程中,微环境中存在的其他细胞因子可能会调节SDF-1alpha的SPC产生。总之,这些观察结果提供了一种潜在的机制,通过该机制,SPC可以通过增强炎症细胞和组织祖细胞募集到组织损伤区域来增强愈合。

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