Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway
Intervertebral disc degeneration (IDD) has been generally accepted as the major cause of low back pain (LBP), which imposes massive clinical and socioeconomic burdens. Previous studies have demonstrated that oxidative stress and inflammation-induced senescence and apoptosis of nucleus pulposus cells...
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Frontiers Media S.A.
2021
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oai:doaj.org-article:7e04b2bd64bd4cf8b79e34906b8da1e92021-12-03T14:46:49ZArginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway2296-634X10.3389/fcell.2021.737809https://doaj.org/article/7e04b2bd64bd4cf8b79e34906b8da1e92021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.737809/fullhttps://doaj.org/toc/2296-634XIntervertebral disc degeneration (IDD) has been generally accepted as the major cause of low back pain (LBP), which imposes massive clinical and socioeconomic burdens. Previous studies have demonstrated that oxidative stress and inflammation-induced senescence and apoptosis of nucleus pulposus cells (NPCs) are the main cellular processes that cause IDD. Arginase II (ARG2), an enzyme involved in a variety of pathological processes, including cellular senescence, apoptosis, oxidative stress, and inflammation, has been shown to promote degeneration in several degenerative diseases, including osteoarticular diseases. Based on previous studies, we hypothesized that ARG2 deficiency might be conducive to the treatment of IDD by inhibiting the dyshomeostasis of the extracellular matrix (ECM), and the oxidative stress and inflammatory response-induced senescence and apoptosis via NF-κB. In this study, we found that ARG2 deficiency inhibited senescence and apoptosis of NPCs, and degeneration of the ECM induced by oxidative stress and the inflammatory response. Similar results were found with the selective NF-κB pathway inhibitor JSH-23. In contrast, overexpression of ARG2 had the opposite effect. Taken together, our results suggest that ARG2 deficiency prevents IDD via NF-κB, and may therefore, be a potential therapeutic strategy for IDD.Fudong LiXiaofei SunBing ZhengKaiqiang SunJian ZhuChenglong JiFeng LinLe HuanXi LuoChen YanJiashun XuYun HongYuan WangXiming XuJingchuan SunZheming SongFanqi KongJiangang ShiFrontiers Media S.A.articleARG2intervertebral disc degenerationnucleus pulposusoxidative stressinflammatory responsesenescenceBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021) |
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ARG2 intervertebral disc degeneration nucleus pulposus oxidative stress inflammatory response senescence Biology (General) QH301-705.5 |
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ARG2 intervertebral disc degeneration nucleus pulposus oxidative stress inflammatory response senescence Biology (General) QH301-705.5 Fudong Li Xiaofei Sun Bing Zheng Kaiqiang Sun Jian Zhu Chenglong Ji Feng Lin Le Huan Xi Luo Chen Yan Jiashun Xu Yun Hong Yuan Wang Ximing Xu Jingchuan Sun Zheming Song Fanqi Kong Jiangang Shi Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway |
description |
Intervertebral disc degeneration (IDD) has been generally accepted as the major cause of low back pain (LBP), which imposes massive clinical and socioeconomic burdens. Previous studies have demonstrated that oxidative stress and inflammation-induced senescence and apoptosis of nucleus pulposus cells (NPCs) are the main cellular processes that cause IDD. Arginase II (ARG2), an enzyme involved in a variety of pathological processes, including cellular senescence, apoptosis, oxidative stress, and inflammation, has been shown to promote degeneration in several degenerative diseases, including osteoarticular diseases. Based on previous studies, we hypothesized that ARG2 deficiency might be conducive to the treatment of IDD by inhibiting the dyshomeostasis of the extracellular matrix (ECM), and the oxidative stress and inflammatory response-induced senescence and apoptosis via NF-κB. In this study, we found that ARG2 deficiency inhibited senescence and apoptosis of NPCs, and degeneration of the ECM induced by oxidative stress and the inflammatory response. Similar results were found with the selective NF-κB pathway inhibitor JSH-23. In contrast, overexpression of ARG2 had the opposite effect. Taken together, our results suggest that ARG2 deficiency prevents IDD via NF-κB, and may therefore, be a potential therapeutic strategy for IDD. |
format |
article |
author |
Fudong Li Xiaofei Sun Bing Zheng Kaiqiang Sun Jian Zhu Chenglong Ji Feng Lin Le Huan Xi Luo Chen Yan Jiashun Xu Yun Hong Yuan Wang Ximing Xu Jingchuan Sun Zheming Song Fanqi Kong Jiangang Shi |
author_facet |
Fudong Li Xiaofei Sun Bing Zheng Kaiqiang Sun Jian Zhu Chenglong Ji Feng Lin Le Huan Xi Luo Chen Yan Jiashun Xu Yun Hong Yuan Wang Ximing Xu Jingchuan Sun Zheming Song Fanqi Kong Jiangang Shi |
author_sort |
Fudong Li |
title |
Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway |
title_short |
Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway |
title_full |
Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway |
title_fullStr |
Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway |
title_full_unstemmed |
Arginase II Promotes Intervertebral Disc Degeneration Through Exacerbating Senescence and Apoptosis Caused by Oxidative Stress and Inflammation via the NF-κB Pathway |
title_sort |
arginase ii promotes intervertebral disc degeneration through exacerbating senescence and apoptosis caused by oxidative stress and inflammation via the nf-κb pathway |
publisher |
Frontiers Media S.A. |
publishDate |
2021 |
url |
https://doaj.org/article/7e04b2bd64bd4cf8b79e34906b8da1e9 |
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