题名 | Leukemia Inhibitory Factor Facilitates Self-Renewal and Differentiation and Attenuates Oxidative Stress of BMSCs by Activating PI3K/AKT Signaling |
作者 | |
发表日期 | 2022
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DOI | |
发表期刊 | |
ISSN | 1942-0900
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EISSN | 1942-0994
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卷号 | 2022 |
摘要 | Objective: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) remains a hopeful therapeutic approach for bone defect reconstruction. Herein, we investigated the effects and mechanisms of leukemia inhibitory factor (LIF) in the function and viability of hypoxic BMSCs as well as bone defect repair. Methods: The effects of LIF on apoptosis (flow cytometry, TUNEL staining), mitochondrial activity (JC-1 staining), proliferation (colony formation, EdU staining), and differentiation (CD105, CD90, and CD29 via flow sorting) were examined in hypoxic BMSCs. LIF, LIFR, gp130, Keap1, Nrf2, antioxidant enzymes (SOD1, catalase, GPx-3), bone-specific matrix proteins (ALP, BSP, OCN), PI3K, and Akt were detected via immunoblotting or immunofluorescent staining. BMSCs combined with biphasic calcium phosphate scaffolds were implanted into calvarial bone defect mice, and the therapeutic effect of LIF on bone defect was investigated. Results: Hypoxic BMSCs had increased apoptosis and oxidative stress and reduced mitochondrial activity. Additionally, LIF, LIFR, and gp130 were upregulated and PI3K/Akt activity was depressed in hypoxic BMSCs. Upregulated LIF alleviated apoptosis and oxidative stress and heightened mitochondrial activity and PI3K/Akt signaling in hypoxic BMSCs. Additionally, LIF overexpression promoted self-renewal and osteogenic differentiation of BMSCs with hypoxic condition. Mechanically, LIF facilitated self-renewal and differentiation as well as attenuated oxidative stress of BMSCs through enhancing PI3K/AKT signaling activity. Implantation of LIF-overexpressed BMSC-loaded BCP scaffolds promoted osteogenesis as well as alleviated oxidative stress and apoptosis through PI3K/Akt signaling. Conclusion: Our findings demonstrate that LIF facilitates self-renewal and differentiation and attenuates oxidative stress of BMSCs by PI3K/AKT signaling. |
相关链接 | [Scopus记录] |
收录类别 | |
语种 | 英语
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学校署名 | 第一
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资助项目 | Shenzhen Science and Technology Innovative Project[JCYJ20180302144621755]
; Project of Yantian District in Shenzhen City, Guangdong Province, China[20190106]
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WOS研究方向 | Cell Biology
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WOS类目 | Cell Biology
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WOS记录号 | WOS:000860025600006
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出版者 | |
Scopus记录号 | 2-s2.0-85137900352
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来源库 | Scopus
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引用统计 |
被引频次[WOS]:6
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成果类型 | 期刊论文 |
条目标识符 | http://sustech.caswiz.com/handle/2SGJ60CL/402404 |
专题 | 南方科技大学盐田医院 南方科技大学第二附属医院 |
作者单位 | 1.Department of Stomatology,Southern University of Science and Technology Yantian Hospital,Shenzhen,China 2.Department of Neurology,Changhai Hospital,Naval Medical University,China |
第一作者单位 | 南方科技大学盐田医院 |
第一作者的第一单位 | 南方科技大学盐田医院 |
推荐引用方式 GB/T 7714 |
Liang,Youde,Zhou,Ruiping,Liu,Xin,et al. Leukemia Inhibitory Factor Facilitates Self-Renewal and Differentiation and Attenuates Oxidative Stress of BMSCs by Activating PI3K/AKT Signaling[J]. Oxidative Medicine and Cellular Longevity,2022,2022.
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APA |
Liang,Youde.,Zhou,Ruiping.,Liu,Xin.,You,Lin.,Chen,Chang.,...&Zhao,Xiangxiang.(2022).Leukemia Inhibitory Factor Facilitates Self-Renewal and Differentiation and Attenuates Oxidative Stress of BMSCs by Activating PI3K/AKT Signaling.Oxidative Medicine and Cellular Longevity,2022.
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MLA |
Liang,Youde,et al."Leukemia Inhibitory Factor Facilitates Self-Renewal and Differentiation and Attenuates Oxidative Stress of BMSCs by Activating PI3K/AKT Signaling".Oxidative Medicine and Cellular Longevity 2022(2022).
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