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LMP-1 的过表达通过抑制 NF-κB 信号通路减少人椎间盘细胞的凋亡。

Overexpression of LMP-1 Decreases Apoptosis in Human Nucleus Pulposus Cells via Suppressing the NF-B Signaling Pathway.

机构信息

Department of Emergency, The First Affiliated Hospital of Zhengzhou University, 1 Jianshe Road, Zhengzhou City, Henan 450052, China.

Department of Orthopedics, The First Affiliated Hospital of Zhengzhou University, 1 Jianshe Road, Zhengzhou City, Henan 450052, China.

出版信息

Oxid Med Cell Longev. 2020 Dec 13;2020:8189706. doi: 10.1155/2020/8189706. eCollection 2020.

DOI:10.1155/2020/8189706
PMID:33414896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7752285/
Abstract

Intervertebral disc degeneration (IDD) is a prevalent disease characterized by low back pain. Increasing extracellular matrix (ECM) synthesis and decreasing nucleus pulposus cell (NPC) apoptosis are promising strategies to recover degenerated NP. LIM mineralization protein- (LMP-) 1 has anti-inflammatory potential and is a promising gene target for the treatment of NP degeneration. In this study, we measured the expression of LMP-1 in the NP of patients. Then, we constructed LMP-1-overexpressing NPCs using lentiviral vectors and investigated the effects of LMP-1 on cell proliferation, apoptosis, and ECM synthesis in NPCs. The results showed that LMP-1 was highly expressed in the NP of patients. LMP-1 overexpression significantly increased proliferation and decreased apoptosis in NPCs. The expression of collagen II and sulfated glycosaminoglycan (sGAG) in NPCs was also upregulated after LMP-1 was overexpressed. Moreover, we demonstrated that LMP-1 decreased apoptosis of NPCs by inhibiting NF-B signaling activation. These findings suggest that LMP-1 plays an essential role in mediating apoptosis in NPCs by regulating NF-B signaling and can be used as a gene target for the treatment of IDD.

摘要

椎间盘退变(IDD)是一种常见疾病,以腰痛为特征。增加细胞外基质(ECM)的合成和减少髓核细胞(NPC)凋亡是恢复退变 NP 的有前途的策略。LIM 矿化蛋白-(LMP-)1 具有抗炎潜力,是治疗 NP 退变的有前途的基因靶点。在这项研究中,我们测量了 NP 中 LMP-1 在患者中的表达。然后,我们使用慢病毒载体构建了 LMP-1 过表达 NPC,并研究了 LMP-1 对 NPC 增殖、凋亡和 ECM 合成的影响。结果表明,LMP-1 在患者的 NP 中高度表达。LMP-1 过表达显着增加了 NPC 的增殖并减少了凋亡。LMP-1 过表达后,NPC 中胶原 II 和硫酸化糖胺聚糖(sGAG)的表达也上调。此外,我们证明 LMP-1 通过抑制 NF-B 信号激活来减少 NPC 的凋亡。这些发现表明,LMP-1 通过调节 NF-B 信号在 NPC 中介导凋亡中起重要作用,并可用作治疗 IDD 的基因靶点。

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