MicroRNA-137 inhibits the inflammatory response and extracellular matrix degradation in lipopolysaccharide-stimulated human nucleus pulposus cells by targeting activin a receptor type I

Yu, Bin; Zhu, Zhaojin; Shen, Beiduo; Lu, Jiawei; Guo, Kai; Zhao, Weidong; Wu, Desheng

doi:10.1080/21655979.2022.2042987

Cited by 7 publications

(7 citation statements)

References 48 publications

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“…Zhou et al (2022) showed that miR-206 ameliorated IDD through targeting GJA1. Yu et al (2022) 2021) demonstrated that miR-502 inhibited TNF-α-induced NP cell apoptosis through targeting TARF2. These results suggested that miRNAs play important roles in the development of IDD.…”

Section: Discussionmentioning

confidence: 99%

The new ceRNA crosstalk between mRNAs and miRNAs in intervertebral disc degeneration

Wang

et al. 2022

Front. Cell Dev. Biol.

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Degeneration of the intervertebral disc has been linked to lower back pain. To date, pathophysiological mechanisms of intervertebral disc degeneration (IDD) remain unclear; it is meaningful to find effective diagnostic biomarkers and new therapeutic strategies for IDD. This study aimed to reveal the molecular mechanism of IDD pathogenesis from the multidimensional transcriptomics perspective. Here, we acquired IDD bulk omics datasets (GSE67567 and GSE167199) including mRNA, microRNA expression profiles, and single-cell RNA sequencing (GSE199866) from the public Gene Expression Omnibus (GEO) database. Through principal component analysis and Venn analysis, we found different expression patterns in the IDD transcription level and identified 156 common DEGs in both bulk datasets. GO and KEGG functional analyses showed these dysregulators were mostly enriched in the collagen-containing extracellular matrix, cartilage development, chondrocyte differentiation, and immune response pathways. We also constructed a potentially dysregulated competing endogenous RNA (ceRNA) network between mRNAs and miRNAs related to IDD based on microRNA target information and co-expression analysis of RNA profiles and identified 36 ceRNA axes including ZFP36/miR-155-5p/FOS, BTG2/hsa-miR-185-5p/SOCS3, and COL9A2/hsa-miR-664a-5p/IBA57. Finally, in integrating bulk and single-cell transcriptome data analyses, a total of three marker genes, COL2A1, PAX1, and ZFP36L2, were identified. In conclusion, the key genes and the new ceRNA crosstalk we identified in intervertebral disc degeneration may provide new targets for the treatment of IDD.

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Section: Discussionmentioning

confidence: 99%

The new ceRNA crosstalk between mRNAs and miRNAs in intervertebral disc degeneration

Wang

et al. 2022

Front. Cell Dev. Biol.

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“…Myostatin plays an inhibitory role in cartilage formation and chondrocyte proliferation, and its serum levels exhibit a positive correlation with the severity of conditions such as osteoarthritis and rheumatoid arthritis ( 121 , 138 ). Additionally, ACVR1 silencing reversed lipopolysaccharide-induced inflammation and matrix degradation in NP cells, implying the potential unfavorable impacts of ACVR1 activation by myostatin upon discs ( 120 ). However, earlier studies indicated the fundamental role of myostatin in disc homeostasis.…”

Section: Myokines and Cardiokinesmentioning

confidence: 99%

Roles of organokines in intervertebral disc homeostasis and degeneration

He,

Liu,

Lin

et al. 2024

Front. Endocrinol.

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The intervertebral disc is not isolated from other tissues. Recently, abundant research has linked intervertebral disc homeostasis and degeneration to various systemic diseases, including obesity, metabolic syndrome, and diabetes. Organokines are a group of diverse factors named for the tissue of origin, including adipokines, osteokines, myokines, cardiokines, gastrointestinal hormones, and hepatokines. Through endocrine, paracrine, and autocrine mechanisms, organokines modulate energy homeostasis, oxidative stress, and metabolic balance in various tissues to mediate cross-organ communication. These molecules are involved in the regulation of cellular behavior, inflammation, and matrix metabolism under physiological and pathological conditions. In this review, we aimed to summarize the impact of organokines on disc homeostasis and degeneration and the underlying signaling mechanism. We focused on the regulatory mechanisms of organokines to provide a basis for the development of early diagnostic and therapeutic strategies for disc degeneration.

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“… 25 Lipopolysaccharide (LPS) can induce apoptosis, inflammation and ECM degradation of NP cells, so the NP cells treated with LPS have been widely used in the study of IDD in vitro. 26 …”

Section: Introductionmentioning

confidence: 99%

“…In addition, inflammation, especially the abnormal excretion of inflammatory cytokines (TNF‐α, IL‐1β, and IL‐6) contributes to the occurrence and progress of IDD 25 . Lipopolysaccharide (LPS) can induce apoptosis, inflammation and ECM degradation of NP cells, so the NP cells treated with LPS have been widely used in the study of IDD in vitro 26 …”

Section: Introductionmentioning

confidence: 99%

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Role of lncRNA MAGI2‐AS3 in lipopolysaccharide‐induced nucleus pulposus cells injury by regulating miR‐374b‐5p/interleukin‐10 axis

2023

Immunity Inflam & Disease

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Background: Intervertebral disc degeneration (IDD) is a pathological process that occurs during the natural aging of intervertebral discs. Accumulating evidence suggests that noncoding RNAs (ncRNAs), including microRNAs and long ncRNAs (lncRNAs), participate in the pathogenesis and development of IDD. Herein, we examined the role of lncRNA MAGI2-AS3 in the pathogenic mechanism of IDD.Material and Methods: To develop an IDD in vitro model, we treated human nucleus pulposus (NP) cells with lipopolysaccharide (LPS). Aberrant levels of lncRNA MAGI2-AS3, miR-374b-5p, interleukin (IL)-10 and extracellular matrix (ECM)-related proteins in NP cells were examined using reverse transcriptionquantitative PCR and western blot analysis. LPS-induced NP cell injury and inflammatory response were confirmed using the MTT assay, flow cytometry, Caspase3 activity, and enzyme-linked immunosorbent assay. Dual-luciferase reporter assay and rescue experiments were performed to confirm targets between lncRNA MAGI2-AS3 and miR-374b-5p or miR-374b-5p and IL-10. Results: LPS-induced NP cells exhibited low levels of lncRNA MAGI2-AS3 and IL-10 expression, along with high miR-374b-5p expression. miR-374b-5p was a target of lncRNA MAGI2-AS3 and IL-10. LncRNA MAGI2-AS3 ameliorated injury, inflammatory response, and ECM degradation in LPS-treated NP cells by downregulating miR-374b-5p to upregulate IL-10 expression. Conclusions: LncRNA MAGI2-AS3 increased IL-10 expression levels by sponging miR-374b-5p, which, in turn, alleviated LPS-triggered decreased NP cell proliferation and increased apoptosis, inflammatory response, and ECM degradation. Therefore, lncRNA MAGI2-AS3 may be a potential therapeutic target for IDD.

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MicroRNA-137 inhibits the inflammatory response and extracellular matrix degradation in lipopolysaccharide-stimulated human nucleus pulposus cells by targeting activin a receptor type I

Cited by 7 publications

References 48 publications

The new ceRNA crosstalk between mRNAs and miRNAs in intervertebral disc degeneration

The new ceRNA crosstalk between mRNAs and miRNAs in intervertebral disc degeneration

Roles of organokines in intervertebral disc homeostasis and degeneration

Role of lncRNA MAGI2‐AS3 in lipopolysaccharide‐induced nucleus pulposus cells injury by regulating miR‐374b‐5p/interleukin‐10 axis

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