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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
DOI
发表期刊
ISSN
1942-0900
EISSN
1942-0994
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
学校署名
第一
资助项目
Shenzhen Science and Technology Innovative Project[JCYJ20180302144621755] ; Project of Yantian District in Shenzhen City, Guangdong Province, China[20190106]
WOS研究方向
Cell Biology
WOS类目
Cell Biology
WOS记录号
WOS:000860025600006
出版者
Scopus记录号
2-s2.0-85137900352
来源库
Scopus
引用统计
被引频次[WOS]:6
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.
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.
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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