Bone Marrow Mesenchymal Stem Cells (BMSCs) Promote Neuronal Cell Repair in Spinal Cord Injury by Regulating Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

被引:1
作者
Huang, Wei [1 ]
Cao, Zheng [1 ]
Wu, Ye [1 ]
Li, Zhenzhou [1 ]
Li, Li [1 ]
Zhao, Yantao [1 ,2 ]
机构
[1] Gen Hosp CPLA, Dept Orthoped, Med Ctr 4, Beijing 100048, Peoples R China
[2] Beijing Engn Res Ctr Orthoped Implants, Beijing 100048, Peoples R China
关键词
SCI; BMSCs; TLR4; NF-Kappa B; Repair; MYOCARDIAL-INFARCTION; CONDITIONED MEDIUM; BMP/SMAD PATHWAY; EXPRESSION; TRANSPLANTATION; CARDIOMYOCYTES; INFLAMMATION; ACTIVATION; DAMAGE; MODEL;
D O I
10.1166/jbt.2021.2791
中图分类号
Q813 [细胞工程];
学科分类号
摘要
SCI (SCI) poses a challenge to nerve cell repair strategies. SCI injury can lead to the development of inflammation, which in turn can exacerbate nerve cell damage. The TLR4/NF-kappa B signaling pathway is a common inflammatory signaling pathway. Since BMSCs are involved in injury repair, whether they can promote the repair of SCI neuronal cells have not been reported. Spinal cord nerve cells were cultured in vitro and divided into mechanical injury group and BMSCs group followed by analysis of cell proliferation activity and detection of altered apoptotic activity. Changes in the concentrations of IL-6 and IL-1 beta were measured by ELISA and cellular mitochondrial alterations was assessed by JG-B staining along with analysis of NF-kappa B, TLR4, related neurodevelopmental factor BDNF, and NGF expression by western blot. Mechanical damage to neuronal cells resulted in decreased cell proliferation, increased apoptotic activity, decreased cellular mitochondrial activity, increased TLR4 and NF-kappa B expression, decreased BDNF and NGF expression, as well as increased secertions of IL-6 and IL-1 beta (P < 0.05). In contrast, co-culture with BMSCs resulted in increased proliferation and decreased apoptosis of mechanically injured neuronal cells, increased cellular mitochondrial activity, with observation of the inverse changes in other factors (P < 0.05). In conclusion, BMSCs can suppress inflammation and promote repair of injured neuronal cells by inhibiting TLR4/NF-kappa B signaling.
引用
收藏
页码:2064 / 2069
页数:6
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