Tension induces intervertebral disc degeneration via endoplasmic reticulum stress-mediated autophagy

Chen, Jiangwei; Lin, Zongming; Deng, Kui; Shao, Bin; Yang, Dong

doi:10.1042/bsr20190578

Cited by 27 publications

(29 citation statements)

References 36 publications

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“…IDD is a general degenerative illness, which often leads to neck and shoulder pain and severely influences the quality of life of the patients [20]. miRNAs were manifested to be linked with IDD.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

Gao

Zhou

et al. 2020

Cell Cycle

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Literatures indicate that microRNA-129-5p (miR-129-5p) or Fas-associated death domain (FADD) is related to intervertebral disc degeneration (IDD), but the effect of miR-129-5p/FADD axis on IDD is not studied. The study aimed to investigate whether miR-129-5p influenced immune privilege and nucleus pulposus (NP) cell apoptosis in rats with IDD via regulating FADD.A rat model with caudal IDD was established, and injected with miR-129-5p agomir or miR-129-5p antagomir to figure out the character of miR-129-5p in the cell apoptosis and inflammation in the nucleus pulposus (NP) tissues of IDD rats. NP cells were grouped as the same ways for determining proliferation, apoptosis, and senescence in NP cells of IDD rats. Annexin V-FITC/PI double staining detected the apoptosis of macrophages and CD8 + cells co-cultured via transfected NP cells. Expression of miR-129-5p, FADD, collagen I, collagen II, aggrecan and Sox-9 in NP tissues and cells were determined.Up-regulated miR-129-5p decreased FADD, collagen I and elevated collagen Ⅱ, aggrecan, and Sox-9 in NP tissues and repressed inflammation in serum and NP tissues in IDD rats. Up-regulated miR-129-5p facilitated proliferation, inhibited senescence, apoptosis, and decreased FADD, collagen I and increased collagen Ⅱ, aggrecan, and Sox-9 in NP cells of IDD rats. Elevated miR-129-5p promoted the apoptosis of macrophages and CD8 + cells.We pronounced that up-regulated miR-129-5p inhibited the apoptosis and facilitated the proliferation of NP cells, as well as the apoptosis of macrophages and CD8 + cells via decreased FADD in IDD, suggesting that miR-129-5p had a protective effect on IDD.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

Gao

Zhou

et al. 2020

Cell Cycle

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show abstract

“…The staining procedure was carried out based on standard methods. 41 WB was carried out to detect the expression of caspase-3, caspase-7, caspase-9, MMP-3, MMP-13, ADAMTS4, ADAMTS 5, collagen II, aggrecan, and SIRT1 in NP tissues.…”

Section: Methodsmentioning

confidence: 99%

“…The NP tissues were collected for H&E staining and TUNEL assays, and the stained slides were viewed under a fluorescence microscope. The staining procedure was carried out based on standard methods 41 . WB was carried out to detect the expression of caspase-3, caspase-7, caspase-9, MMP-3, MMP-13, ADAMTS4, ADAMTS 5, collagen II, aggrecan, and SIRT1 in NP tissues.…”

Section: Methodsmentioning

confidence: 99%

Exosome-Transported circRNA_0000253 Competitively Adsorbs MicroRNA-141-5p and Increases IDD

Song

Chen

Zheng

et al. 2020

Molecular Therapy - Nucleic Acids

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The pathogenesis of intervertebral disc degeneration (IDD) is complex, and a better understanding of IDD pathogenesis may provide a better method for the treatment of IDD. Exosomes are 40–100 nm nanosized vesicles that are released from many cell types into the extracellular space. We speculated that exosome-transported circular RNAs (circRNAs) could regulate IDD. Exosomes from different degenerative grades were isolated and added to nucleus pulposus cells (NPCs), and indicators of proliferation and apoptosis were detected. Based on the previous circRNA microarray results, the top 10 circRNAs were selected. PCR was performed to determine the circRNA with the maximum upregulation. Competing endogenous RNA (ceRNA) analysis was carried out, and the sponged microRNA (miRNA) was identified. Further functional verification of the selected circRNA was carried out in vivo and in vitro . NPCs of different degenerative grades secreted exosomes, which could regulate IDD. circRNA_0000253 was selected as having the maximum upregulation in degenerative NPC exosomes. ceRNA analysis showed that circRNA_0000253 could adsorb miRNA-141-5p to downregulate SIRT1. circRNA_0000253 was confirmed to increase IDD by adsorbing miRNA-141-5p and downregulating SIRT1 in vivo and in vitro . Exosomal circRNA_0000253 owns the maximum upregulation in degenerative NPC exosomes and could promote IDD by adsorbing miRNA-141-5p and downregulating SIRT1.

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“…IDD-associated apoptosis pathways include the exogenous death receptor pathway, endogenous mitochondrial pathway, and ERS pathway. These pathways induce IDD by mediating IVD cell death, which is the leading cause of IDD induced by apoptotic factors 16 , 17 .…”

Section: Apoptosismentioning

confidence: 99%

“…The death receptor pathway involves various external factors that promote and mediate apoptosis through different death receptor signaling pathways. The death receptor pathway is a type of exogenous apoptosis 18 , a critical way to regulate apoptosis and is crucial for cell proliferation and apoptosis balance 17 , 18 . There are three death receptor pathways: Fas, tumor necrosis factor receptor 1 (TNFR1), and TNF-related apoptosis-inducing ligand (TRAIL) 19 (Fig.…”

Section: Apoptosismentioning

confidence: 99%

Targeted therapy for intervertebral disc degeneration: inhibiting apoptosis is a promising treatment strategy

Zhang¹,

Hu²,

Peng³

et al. 2021

Int. J. Med. Sci.

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Intervertebral disc (IVD) degeneration (IDD) is a multifactorial pathological process associated with low back pain (LBP). The pathogenesis is complicated, and the main pathological changes are IVD cell apoptosis and extracellular matrix (ECM) degradation. Apoptotic cell loss leads to ECM degradation, which plays an essential role in IDD pathogenesis. Apoptosis regulation may be a potential attractive therapeutic strategy for IDD. Previous studies have shown that IVD cell apoptosis is mainly induced by the death receptor pathway, mitochondrial pathway, and endoplasmic reticulum stress (ERS) pathway. This article mainly summarizes the factors that induce IDD and apoptosis, the relationship between the three apoptotic pathways and IDD, and potential therapeutic strategies. Preliminary animal and cell experiments show that targeting apoptotic pathway genes or drug inhibition can effectively inhibit IVD cell apoptosis and slow IDD progression. Targeted apoptotic pathway inhibition may be an effective strategy to alleviate IDD at the gene level. This manuscript provides new insights and ideas for IDD therapy.

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Tension induces intervertebral disc degeneration via endoplasmic reticulum stress-mediated autophagy

Cited by 27 publications

References 36 publications

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

Exosome-Transported circRNA_0000253 Competitively Adsorbs MicroRNA-141-5p and Increases IDD

Targeted therapy for intervertebral disc degeneration: inhibiting apoptosis is a promising treatment strategy

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