RhTSG-6 inhibits IL-1β-induced extracellular matrix degradation and apoptosis by suppressing the p38, and JNK pathways in nucleus pulposus cells

Pei, Shishen; Ying, Jinwei; Zhang, Yan; Su, Linhao; Cheng, Shi; Ruan, Dike

doi:10.5603/fhc.a2020.0019

Cited by 9 publications

(4 citation statements)

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“…Similarly, in TNF-α and IL-1β-treated NPCs, p38 MAPK promotes the activation of caveolin-1/β-catenin signaling, thereby promoting apoptosis [93]. However, recombinant human tumor necrosis factor-α induced protein 6 (RHTSG-6) inhibits the JNK and p38 MAPK signaling pathways and inhibits apoptosis and ECM degradation in HNPCs induced by IL-1β [22]. In addition, mechanical overload induces NPC apoptosis and activates p38 MAPK.…”

Section: Jnk and P38 Mapk Signaling Pathways Promote Apoptosismentioning

confidence: 99%

“…As IDD progresses, various stress stimuli can enhance the activity of JNK and p38 MAPK, as well as increase the number of senescent cells [20,21]. In degenerate IVD cells, JNK and p38 MAPK promote apoptosis and initiate the programmed death process [22,23]. JNK and p38 MAPK can also increase the content of intracellular reactive oxygen species (ROS), leading to oxidative stress damage, and affect the excessive accumulation of iron in cells, leading to the occurrence of ferroptosis [24,25].…”

Section: Introductionmentioning

confidence: 99%

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Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK

Li,

Zhang,

Yang

et al. 2024

Biomolecules

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Intervertebral disc degeneration (IDD) is a major cause of lower back pain. The pathophysiological development of IDD is closely related to the stimulation of various stressors, including proinflammatory cytokines, abnormal mechanical stress, oxidative stress, metabolic abnormalities, and DNA damage, among others. These factors prevent normal intervertebral disc (IVD) development, reduce the number of IVD cells, and induce senescence and apoptosis. Stress-activated protein kinases (SAPKs), particularly, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), control cell signaling in response to cellular stress. Previous studies have shown that these proteins are highly expressed in degenerated IVD tissues and are involved in complex biological signal-regulated processes. Therefore, we summarize the research reports on IDD related to JNK and p38 MAPK. Their structure, function, and signal regulation mechanisms are comprehensively and systematically described and potential therapeutic targets are proposed. This work could provide a reference for future research and help improve molecular therapeutic strategies for IDD.

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Section: Jnk and P38 Mapk Signaling Pathways Promote Apoptosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK

Li,

Zhang,

Yang

et al. 2024

Biomolecules

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“…When the estrogen function is activated or inhibited, the activity of the p38 MAPK pathway also increases or decreases, and the synthesis trend of the NP cell matrix is also consistent with the estrogen function. Pei et al (2020) found that Recombinant human TNF-α induced protein 6 (RhTSG-6) suppresses IL-1β-induced ECM degradation and apoptosis by blocking p38 and JNK pathways in NPCs. When NPCs were treated with HBO, the phosphorylation of p38 MAPK, ERK, and JNK was decreased, and the secretion of MMP3, MMP9, and MMP13 was significantly reduced, which reduced the breakdown of matrix by MMPs (Niu et al, 2019).…”

Section: Regulate Ecm Metabolic Imbalancementioning

confidence: 99%

“…found that quercetin (QUE) partially inhibited the p38 MAPK signaling pathway and inhibited p38 MAPK through SB203580-activated autophagy, indicating that QUE protected NPCs from apoptosis and prevented ECM degradation through the p38 MAPK autophagy pathway. Besides, RhTSG-6 (Pei et al, 2020), miR-15a (Cai et al, 2017), and DHJSD (Duhuo jisheng decoction) (Liu et al, 2020) have all demonstrated that they could attenuate NP cell apoptosis by inhibiting or blocking the p38 MAPK pathway. Hence, these data imply that the p38 MAPK pathway is also implicated in the promotion of apoptosis.…”

Section: Mediate Cell Apoptosismentioning

confidence: 99%

Unraveling the mechanisms of intervertebral disc degeneration: an exploration of the p38 MAPK signaling pathway

Zhang,

Zou

et al. 2024

Front. Cell Dev. Biol.

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Intervertebral disc (IVD) degeneration (IDD) is a worldwide spinal degenerative disease. Low back pain (LBP) is frequently caused by a variety of conditions brought on by IDD, including IVD herniation and spinal stenosis, etc. These conditions bring substantial physical and psychological pressure and economic burden to patients. IDD is closely tied with the structural or functional changes of the IVD tissue and can be caused by various complex factors like senescence, genetics, and trauma. The IVD dysfunction and structural changes can result from extracellular matrix (ECM) degradation, differentiation, inflammation, oxidative stress, mechanical stress, and senescence of IVD cells. At present, the treatment of IDD is basically to alleviate the symptoms, but not from the pathophysiological changes of IVD. Interestingly, the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway is involved in many processes of IDD, including inflammation, ECM degradation, apoptosis, senescence, proliferation, oxidative stress, and autophagy. These activities in degenerated IVD tissue are closely relevant to the development trend of IDD. Hence, the p38 MAPK signaling pathway may be a fitting curative target for IDD. In order to better understand the pathophysiological alterations of the intervertebral disc tissue during IDD and offer potential paths for targeted treatments for intervertebral disc degeneration, this article reviews the purpose of the p38 MAPK signaling pathway in IDD.

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A20 ameliorates disc degeneration by suppressing mTOR/BNIP3 axis-mediated mitophagy

et al. 2022

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RhTSG-6 inhibits IL-1β-induced extracellular matrix degradation and apoptosis by suppressing the p38, and JNK pathways in nucleus pulposus cells

Cited by 9 publications

References 0 publications

Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK

Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK

Unraveling the mechanisms of intervertebral disc degeneration: an exploration of the p38 MAPK signaling pathway

A20 ameliorates disc degeneration by suppressing mTOR/BNIP3 axis-mediated mitophagy

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