| 低氧激活自噬促进人间充质干细胞成骨分化的研究 |
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| 引用本文： | 刘宇佳,楼斯悦,章燕棋,曹戟,楼剑书,应美丹,何俏军.低氧激活自噬促进人间充质干细胞成骨分化的研究[J].中国现代应用药学,2016,33(3):284-289. |
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| 作者姓名： | 刘宇佳 楼斯悦 章燕棋 曹戟 楼剑书 应美丹 何俏军 |
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| 作者单位： | 浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058,浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058,浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058；杭州市中医院药剂科，杭州 310007,浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058,浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058,浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058,浙江大学药学院药理毒理研究所，浙江省抗肿瘤药物临床前研究重点实验室，杭州 310058 |
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| 基金项目： | 浙江省自然科学基金项目(LY13H310002)；浙江省教育厅项目(Y201430401) |
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| 摘 要： | 目的 探讨低氧对人间充质干细胞(human mesenchymal stem cells，hMSCs)成骨分化的效应及分子机制。方法 在正常氧压(20% O2)和低氧(5% O2)条件下培养hMSCs；采用成骨分化诱导液(BDM)诱导hMSCs成骨分化；利用茜素红染色法考察细胞钙沉积情况；通过Western blotting检测细胞自噬相关蛋白的表达水平以及MAPK、PI3K-AKT-mTOR信号通路的激活情况。结果 低氧条件下，hMSCs钙沉积较常氧条件增强；BDM诱导hMSCs成骨分化过程伴随着LC3表达增加，抑制细胞自噬可以明显减弱低氧促进的细胞钙沉积；低氧促进的细胞发生钙沉积伴随着MAPK以及PI3K-AKT-mTOR信号通路的失活；抑制MAPK以及PI3K-AKT-mTOR信号通路有利于细胞自噬发生，进而促进hMSCs钙沉积。结论 低氧下可以通过激活细胞自噬来促进hMSCs成骨分化，抑制MAPK以及PI3K-AKT-mTOR信号通路可以进一步促进细胞自噬的发生，从而协同促进hMSCs成骨分化。
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| 关 键 词： | 人间充质干细胞 低氧 自噬 钙沉积 成骨分化 |
| 收稿时间： | 2015/10/8 0:00:00 |
| 修稿时间： | 3/4/2016 12:00:00 AM |
Study of Hypoxia Induced Autophagy on Human Mesenchymal Stem Cells Differentiation |
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| LIU Yuji,LOU Siyue,ZHANG Yanqi,CAO Ji,LOU Jianshu,YING Meidan and HE Qiaojun.Study of Hypoxia Induced Autophagy on Human Mesenchymal Stem Cells Differentiation[J].The Chinese Journal of Modern Applied Pharmacy,2016,33(3):284-289. |
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| Authors: | LIU Yuji LOU Siyue ZHANG Yanqi CAO Ji LOU Jianshu YING Meidan and HE Qiaojun |
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| Institution: | Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China,Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China,Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China; Department of Pharmacy, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou 310007, China,Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China,Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China,Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China and Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Zhejiang Province Key Laboratory of Anti-cancer Drug Research, Hangzhou 310058, China |
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| Abstract: | OBJECTIVE To explore the effects and molecular mechanisms of hypoxia on hMSCs differentiation. METHODS hMSCs were cultured under normoxic or hypoxic conditions; hMSCs differentiation were obtained by treated with BDM(bone differentiation medium); Calcium deposit was assessed by Alizard Red S dye; The protein levels were analyzed by western blotting. RESULTS Hypoxia can significantly promoted calcium deposit in hMSCs; The expression of LC3 was increased in hMSCs, hypoxia induced calcium deposit was inhibited by autophagy inhibitor 3MA; Hypoxia induced hMSCs calcium deposit was accompanied by inactivation of MAPK and PI3K-AKT-mTOR pathway, inhibition of these pathway could mediate hMSCs calcium deposit by promoted autophagy. CONCLUSION Hypoxia can significantly triger hMSCs differentiation by induced autophagy, inhibition of MAPK and PI3K-AKT-mTOR pathway could contribute to autophagy which could mediate hMSCs differentiation. |
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| Keywords: | human mesenchymal stem cells hypoxia autophagy calcium deposit osteoblastic differentiation |
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