LncRNA H19 targets miR-22 to modulate H2 O2 -induced deregulation in nucleus pulposus cell senescence, proliferation, and ECM synthesis through Wnt signaling

2018 ◽  
Vol 119 (6) ◽  
pp. 4990-5002 ◽  
Author(s):  
Xiaobin Wang ◽  
Mingxiang Zou ◽  
Jing Li ◽  
Bing Wang ◽  
Qianshi Zhang ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Nucleus Pulposus ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence

scholarly journals The response of nucleus pulposus cell senescence to static and dynamic compressions in a disc organ culture

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Jianmin Shi ◽  
Lianglong Pang ◽  
Shouguo Jiao
Keyword(s):  
Organ Culture ◽  
Nucleus Pulposus ◽  
Dynamic Compression ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence ◽  
Degenerative Changes ◽  
Mechanical Stimuli ◽  
Static Compression

Mechanical stimuli obviously affect disc nucleus pulposus (NP) biology. Previous studies have indicated that static compression exhibits detrimental effects on disc biology compared with dynamic compression. To study disc NP cell senescence under static compression and dynamic compression in a disc organ culture, porcine discs were cultured and subjected to compression (static compression: 0.4 MPa for 4 h once per day; dynamic compression: 0.4 MPa at a frequency of 1.0 Hz for 4 h once per day) for 7 days using a self-developed mechanically active bioreactor. The non-compressed discs were used as controls. Compared with the dynamic compression, static compression significantly promoted disc NP cell senescence, reflected by the increased senescence-associated β-galactosidase (SA-β-Gal) activity, senescence-associated heterochromatic foci (SAHF) formation and senescence markers expression, and the decreased telomerase (TE) activity and NP matrix biosynthesis. Static compression accelerates disc NP cell senescence compared with the dynamic compression in a disc organ culture. The present study provides that acceleration of NP cell senescence may be involved in previously reported static compression-mediated disc NP degenerative changes.

scholarly journals N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression

2017 ◽  
Author(s):  
Ming Niu ◽  
Fei Ma ◽  
Jun Qian ◽  
Junwei Li ◽  
Tong Wang ◽  
...  
Keyword(s):  
Nucleus Pulposus ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence ◽  
High Magnitude

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 Nucleus pulposus cell senescence is alleviated by resveratrol through regulating the ROS/NF-κB pathway under high-magnitude compression

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Yanhai Jiang ◽  
Guozhang Dong ◽  
Yeliang Song
Keyword(s):  
Nucleus Pulposus ◽  
Bone Matrix ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence ◽  
Ros Generation ◽  
Dependent Manner ◽  
Protective Effects ◽  
Concentration Dependent Manner ◽  
High Magnitude

Mechanical overloading is a risk factor of disc degeneration. Studies have demonstrated that resveratrol helps to maintain the disc cell’s healthy biology. The present study aims to investigate whether resveratrol can suppress mechanical overloading-induced nucleus pulposus (NP) cell senescence in vitro and the potential mechanism. The isolated rat NP cells were seeded in the decalcified bone matrix (DBM) and cultured under non-compression (control) and compression (20% deformation, 1.0 Hz, 6 h/day) for 5 days using the mechanically active bioreactor. The resveratrol (30 and 60 μM) was added into the culture medium of the compression group to investigate its protective effects against the NP cell senescence. NP cell senescence was evaluated by cell proliferation, cell cycle, senescence-associated β-galactosidase (SA-β-Gal) activity, telomerase (TE) activity, and gene expression of the senescence markers (p16 and p53). Additionally, the reactive oxygen species (ROS) content and activity of the NF-κB pathway were also analyzed. Compared with the non-compression group, the high-magnitude compression significantly promoted NP cell senescence, increased ROS generation and activity of the NF-κB pathway. However, resveratrol partly attenuated NP cell senescence, decreased ROS generation and activity of the NF-κB pathway in a concentration-dependent manner under mechanical compression. Resveratrol can alleviate mechanical overloading-induced NP cell senescence through regulating the ROS/NF-κB pathway. The present study provides that resveratrol may be a potential drug for retarding mechanical overloading-induced NP cell senescence.

In vitro and in vivo effects of hyperglycemia and diabetes mellitus on nucleus pulposus cell senescence

2022 ◽  
Author(s):  
Zengxin Jiang ◽  
Chang Jiang ◽  
Lixia Jin ◽  
Zixian Chen ◽  
Zhenzhou Feng ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Nucleus Pulposus ◽  
Nucleus Pulposus Cell ◽  
Cell Senescence ◽  
In Vivo Effects

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.

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