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首页> 外文期刊>Life sciences >Improved survival of mesenchymal stromal cell after hypoxia preconditioning: role of oxidative stress.
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Improved survival of mesenchymal stromal cell after hypoxia preconditioning: role of oxidative stress.

机译：缺氧预处理后改善间充质基质细胞的存活：氧化应激的作用。

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AIMS: To investigate the mechanisms underlying the beneficial effect of hypoxia preconditioning (HPC) on mesenchymal stromal cells (MSCs) and optimize novel non-invasive methods to assess the effect of biological interventions aimed to increased cell survival. MAIN METHODS: MSCs from rat femur, with or without HPC, were exposed to hypoxic conditions in cell culture (1% O(2) for 24h) and cell survival (by the LDH release assay and Annexin-V staining) was measured. Oxidant status (conversion of dichloro-fluorescein-DCF- and dihydro-ethidium-DHE-, protein expression of oxidant enzymes) was characterized, together with the mobility pattern of cells under stress. Furthermore, cell survival was assessed non-invasively using state-of-the-art molecular imaging. KEY FINDINGS: Compared to controls, Hypoxia resulted in increased expression of the oxidative stress enzyme NAD(P)H oxidase (subunit 67(phox): 0.05 +/- 0.01AU and 0.48 +/- 0.02AU, respectively, p<0.05) and in the amount of ROS (DCF: 13 +/-1 and 42 +/- 3 RFU/mug protein, respectively, p<0.05) which led to a decrease in stem cell viability. Hypoxia preconditioning preserved cell biology, as evidenced by preservation of oxidant status (16 +/- 1 RFU/mug protein, p<0.05 vs. hypoxia), and cell viability. Most importantly, the beneficial effect of HPC can be assessed non-invasively using molecular imaging. SIGNIFICANCE: HPC preserves cell viability and function, in part through preservation of oxidant status, and its effects can be assessed using state-of-the-art molecular imaging. Understanding of the mechanisms underlying the fate of stem cells will be critical for the advancement of the field of stem cell therapy.
机译：目的：研究低氧预处理（HPC）对间质基质细胞（MSC）有益作用的潜在机制，并优化新型非侵入性方法，以评估旨在提高细胞存活率的生物干预措施的效果。主要方法：将来自大鼠股骨的MSC（有或没有HPC）暴露于细胞培养中的低氧条件下（1％O（2）持续24h），并测量细胞存活率（通过LDH释放测定和Annexin-V染色）。表征了氧化剂的状态（二氯荧光素-DCF-和二氢-乙二胺-DHE-的转化，氧化剂酶的蛋白表达），以及细胞在压力下的迁移模式。此外，使用最新的分子成像技术无创地评估了细胞存活率。主要发现：与对照组相比，低氧导致氧化应激酶NAD（P）H氧化酶的表达增加（亚基67（phox）：分别为0.05 +/- 0.01AU和0.48 +/- 0.02AU，p <0.05） ROS的量（DCF：13 +/- 1和42 +/- 3 RFU /杯蛋白，p <0.05）导致干细胞活力降低。缺氧预处理可以保持细胞生物学，这可以通过保持氧化剂状态（16 +/- 1 RFU /杯蛋白，相对于缺氧p <0.05）和细胞活力来证明。最重要的是，可以使用分子成像非侵入性地评估HPC的有益效果。意义：HPC可以部分保持氧化剂状态，从而保持细胞活力和功能，并且可以使用最新的分子成像技术来评估其作用。对干细胞命运机制的理解对于干细胞治疗领域的发展至关重要。

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