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體外實驗表明，適度低氧下MSCs的生長和存活能力更好，產(chǎn)生集落形成單位的能力顯著增高，且干細胞標志性基因表達水平更高[7]。氧濃度可以影響MSCs向成骨、成軟骨、成脂的分化傾向，低氧能提高特異性受體和配體相結(jié)合所介導的遷移。低氧誘導因子1信號通路[8]在MSCs對缺氧反應(yīng)的分子機制中占重要地位。
對缺氧反應(yīng)的分子機制本實驗主要研究了CMS患者骨髓MSC的形態(tài)、表型、傳代能力、生長曲線及擴增能力等特征，其結(jié)果為CMS的研究提供了重要信息。但研究報道例數(shù)尚較少，結(jié)論還需要深入的體內(nèi)實驗及分子生物學研究支持。
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