scholarly journals N6-Methyladenosine Induced miR-34a-5p Promotes TNF-α-Induced Nucleus Pulposus Cell Senescence by Targeting SIRT1

2021 ◽  
Vol 9 ◽  
Author(s):  
Hao Zhu ◽  
Bao Sun ◽  
Liang Zhu ◽  
Guoyou Zou ◽  
Qiang Shen
Keyword(s):  
Cell Cycle ◽  
Low Back Pain ◽  
Cell Cycle Arrest ◽  
Nucleus Pulposus ◽  
Intervertebral Disc Degeneration ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence ◽  
Low Back ◽  
Cycle Arrest ◽  
Tnf Α

Low back pain is tightly associated with intervertebral disc degeneration (IVDD) and aberrant nucleus pulposus (NP) is a critical cause. miRNAs N6-methyladenosine (m6A) modification accounts for the TNF-α-induced senescence of NP cells. The aim of this study was to investigate whether m6A modification regulates TNF-α-mediated cell viability, cell cycle arrest, and cell senescence and how it works. The results showed that METTL14 expression positively correlated with m6A and TNF-α expression in HNPCs. The knockdown of METTL14 led to the inhibition of the TNF-α-induced cell senescence. METTL14 overexpression promoted cell senescence. METTL14 regulated the m6A modification of miR-34a-5p and interacted with DGCR8 to process miR-34a-5p. The miR-34a-5p inhibitor inhibited the cell cycle senescence of HNPCs. miR-34a-5p was predicted to interact with the SIRT1 mRNA. SIRT1 overexpression counteracted the miR-34a-5p-promoted cell senescence. METTL14 participates in the TNF-α-induced m6A modification of miR-34a-5p to promote cell senescence in HNPCs and NP cells of IVDD patients. Downregulation of either METTL14 expression or miR-34a-5p leads to the inhibition of cell cycle arrest and senescence. SIRT1 mRNA is an effective binding target of miR-34a-5p, and SIRT1 overexpression mitigates the cell cycle arrest and senescence caused by miR-34a-5p.

scholarly journals Delivery of a TNF‐α–derived peptide by nanoparticles enhances its antitumor activity by inducing cell‐cycle arrest and caspase‐dependent apoptosis

2018 ◽  
Vol 32 (12) ◽  
pp. 6948-6964 ◽  
Author(s):  
Qiuxia Yan ◽  
Xueming Chen ◽  
Huizhen Gong ◽  
Pei Qiu ◽  
Xing Xiao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Antitumor Activity ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Tnf Α

scholarly journals Melatonin Protects Intervertebral Disc from Degeneration by Improving Cell Survival and Function via Activation of the ERK1/2 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jun Ge ◽  
Quan Zhou ◽  
Junjie Niu ◽  
Yingjie Wang ◽  
Qi Yan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Intervertebral Disc ◽  
Signaling Pathway ◽  
Nucleus Pulposus ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Nucleus Pulposus Cell ◽  
Cell Physiology ◽  
Cell Degeneration

Melatonin, a neuroendocrine hormone secreted by the pineal body, has a positive effect on intervertebral disc degeneration. The present study is aimed at investigating the biological role of melatonin in intervertebral disc degeneration and its underlying mechanism. A human nucleus pulposus cell (NPC) line was exposed to melatonin at different concentrations. Cell proliferation was measured by CCK-8 assay. Cell cycle and apoptosis were analyzed by flow cytometry. Western blot was performed to measure the protein expression of indicated genes. A rabbit model of intervertebral disc degeneration was established to detect the role and mechanism of melatonin on intervertebral disc degeneration. Our study showed that melatonin promoted NPC viability and inhibited cell arrest. Furthermore, melatonin treatment led to the upregulation of collagen II and aggrecan and downregulation of collagen X. Moreover, melatonin significantly elevated the activity of the ERK signaling pathway. Inhibition of the ERK1/2 signals reversed the role of melatonin in the regulation of NPCs both in vitro and in vivo. Melatonin increased NPC viability through inhibition of cell cycle arrest and apoptosis. Moreover, melatonin promoted the secretion of functional factors influencing the nucleus pulposus cell physiology and retarded cell degeneration. Our results suggest that melatonin activated the ERK1/2 signaling pathway, thereby affecting the biological properties of the intervertebral disc degeneration.

HL-60 Cell Death Induced by Lycorine Is Due to p21-Mediated Cell Cycle Arrest and TNF-α Signaling Stimulation.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4158-4158
Author(s):  
Jing Liu ◽  
Ji-liang Hu ◽  
Yang He ◽  
Bi-Wei Shi ◽  
Wei-Xin Hu
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Conflicts Of Interest ◽  
Rt Pcr ◽  
Cycle Arrest ◽  
Tnf Α ◽  
Induced Apoptosis ◽  
Related Proteins ◽  
Human Acute Promyelocytic Leukemia ◽  
Differential Genes

Abstract Abstract 4158 Lycorine displays various biological functions including remarkable anti-tumor effect. We previously reported that lycorine induced anti-leukemia effect via arresting cell cycle and inducing apoptosis on human acute promyelocytic leukemia (APL) cell line HL-60. To explore the molecular mechanism how lycorine induced HL-60 cell apoptosis, cDNA microarray was used to investigate the expression profile of 494 apoptosis-associated genes. Real-time RT-PCR, Western blotting and immunocytochemistry were used to analyze the expression of related genes, as well as the modification and distribution of related proteins in the presence of lycorine. The results showed that 89 differential genes were expressed significantly (Cy3:Cy5 > 2 or < 0.5) among all the 494 apoptosis-related genes. 78 genes were up-regulated and 11 genes were down-regulated. We are particularly interested in the expression increase of p21 (9.271 folds) and TNF-α (8.242 folds). Furthermore, we found that lycorine could down-regulate p21-related gene expression including Cdc2, Cyclin B, Cdk2 and Cyclin E, promote the truncation of Bid protein and the release of cytochrome c from mitochondria, decrease the phosphorylation of IκB, block the nuclear import of NF-κB and down-regulate expression of survivin. This study revealed that lycorine decreased HL-60 cells survival through p21-mediated cell cycle arrest and stimulation of TNF-α signaling pathway which induced apoptosis. Disclosures: No relevant conflicts of interest to declare.

18 MICROPARTICLES INDUCE ENDOTHELIAL CELL SENESCENCE AND CELL CYCLE ARREST THROUGH REDOX-SENSITIVE PROCESSES

2012 ◽  
Vol 30 ◽  
pp. e6
Author(s):  
Dylan Burger ◽  
Dylan Kwart ◽  
Augusto C Montezano ◽  
Charlie S Thompson ◽  
Rhian M Touyz
Keyword(s):  
Cell Cycle ◽  
Endothelial Cell ◽  
Cell Cycle Arrest ◽  
Cell Senescence ◽  
Cycle Arrest

Cell cycle arrest and apoptosis of OVCAR-3 and MCF-7 cells induced by co-immobilized TNF-α plus IFN-γ on polystyrene and the role of p53 activation

Biomaterials ◽  
2012 ◽  
Vol 33 (26) ◽  
pp. 6162-6171 ◽  
Author(s):  
Yan-Qing Guan ◽  
Zhibin Li ◽  
Aini Yang ◽  
Zheng Huang ◽  
Zhe Zheng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Tnf Α ◽  
P53 Activation ◽  
Ifn Γ ◽  
Mcf 7

scholarly journals Blocking Smad2 signalling with loganin attenuates SW10 cell cycle arrest induced by TNF-α

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0176965 ◽  
Author(s):  
Gao Chao ◽  
Xiaoning Tian ◽  
Wentao Zhang ◽  
Xuehai Ou ◽  
Fei Cong ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Tnf Α

scholarly journals Upregulated lnc‑HRK‑2:1 prompts nucleus pulposus cell senescence in intervertebral disc degeneration

2020 ◽  
Vol 22 (6) ◽  
pp. 5251-5261
Author(s):  
Dongbo Liang ◽  
Dinggang Hong ◽  
Fuyu Tang ◽  
Yuan Wang ◽  
Jianfeng Li ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence

scholarly journals Intervertebral Disc Degeneration and Low Back Pain: Molecular Mechanisms and Stem Cell Therapy

2018 ◽  
Vol 10 (1) ◽  
pp. 1 ◽  
Author(s):  
Anna Meiliana ◽  
Nurrani Mustika Dewi ◽  
Andi Wijaya
Keyword(s):  
Stem Cells ◽  
Extracellular Matrix ◽  
Stem Cell ◽  
Low Back Pain ◽  
Back Pain ◽  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Low Back

BACKGROUND: Low back pain (LBP) mostly caused by disc degeneration, reflects to a tremendous of health care system and economy. More knowledge about these underlying pathologies will improve the opportunities that may represent critical therapeutic targets.CONTENT: Basic research is advancing the understanding of the pathogenesis and management of LBP at the molecular and genetic levels. Cytokines such as matrix metalloproteinases, phospholipase A2, nitric oxide, and tumor necrosis factor-α are thought to contribute to the development of LBP. Mesenchymal stem cells (MSCs) transplant to cartilage-like cells and secrete extracellular matrix and encourage nucleus pulposus (NP) cell activity inhibiting NP cell apoptosis, together with some chemical mediators such as cytokines and growth factors become a safe and effective new strategy for intervertebral disc degeneration (IDD) treatment and regeneration.SUMMARY: IDD occurs where there is a loss of homeostatic balance with a predominantly catabolic metabolic profile. A basic understanding of the molecular changes occurring in the degenerating disc is important for practicing clinicians to help them to inform patients to alter lifestyle choices, identify beneficial or harmful supplements, or offer new biologic, genetic, or stem cell therapies.KEYWORDS: low back pain (LBP), intervertebral disc (IVD), degeneration, nucleus pulposus (NP), annulus fibrosus (AF), extracellular matrix (ECM), genetic, stem cells

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