LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition

Jiang, Xin; Chen, Dong

doi:10.21037/atm-20-7056

Cited by 13 publications

(12 citation statements)

References 46 publications

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“…LncRNA MT1DP was found to mitigate anti-oxidation through miR-365/NRF-2 signal pathway, leading to NP cells apoptosis and IDD ( 70 ). Notably, LncRNA FAM83H-AS1 alleviated inflammatory response and promoted NP cells proliferation through miR-22-3p, preventing further deterioration of IDD in rat models caused by advanced glycation end products ( 71 ).…”

Section: The Roles Of Lncrnas In the Development Of Iddmentioning

confidence: 99%

The potential mechanisms and application prospects of non-coding RNAs in intervertebral disc degeneration

et al. 2022

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Low back pain (LBP) is one of the most common musculoskeletal symptoms and severely affects patient quality of life. The majority of people may suffer from LBP during their life-span, which leading to huge economic burdens to family and society. According to the series of the previous studies, intervertebral disc degeneration (IDD) is considered as the major contributor resulting in LBP. Furthermore, non-coding RNAs (ncRNAs), mainly including microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), can regulate diverse cellular processes, which have been found to play pivotal roles in the development of IDD. However, the potential mechanisms of action for ncRNAs in the processes of IDD are still completely unrevealed. Therefore, it is challenging to consider ncRNAs to be used as the potential therapeutic targets for IDD. In this paper, we reviewed the current research progress and findings on ncRNAs in IDD: i). ncRNAs mainly participate in the process of IDD through regulating apoptosis of nucleus pulposus (NP) cells, metabolism of extracellular matrix (ECM) and inflammatory response; ii). the roles of miRNAs/lncRNAs/circRNAs are cross-talk in IDD development, which is similar to the network and can modulate each other; iii). ncRNAs have been attempted to combat the degenerative processes and may be promising as an efficient bio-therapeutic strategy in the future. Hence, this review systematically summarizes the principal pathomechanisms of IDD and shed light on the therapeutic potentials of ncRNAs in IDD.

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Section: The Roles Of Lncrnas In the Development Of Iddmentioning

confidence: 99%

The potential mechanisms and application prospects of non-coding RNAs in intervertebral disc degeneration

et al. 2022

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“…Increasing evidence suggests that lncRNA interacts with miRNA, inducing cell autophagy and death through a lncRNA–miRNA–mRNA competitive endogenous RNA (ceRNA) network [ 167 , 291 ]. The lncRNA-FAM83H-AS1 pathway preserves IVD tissue homeostasis and reduces inflammation-related discomfort by inhibiting miR-22-3p, which promotes NP cell proliferation [ 292 ]. lncRNA-H19 increases autophagy and death in NP cells, exacerbating IVDD via the miR-139/CXCR4/NF-B axis [ 293 ].…”

Section: Autophagy As a Potential Therapeutic Target For Ivddmentioning

confidence: 99%

Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration

et al. 2022

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Intervertebral disc degeneration (IVDD) is a prevalent cause of low back pain. IVDD is characterized by abnormal expression of extracellular matrix components such as collagen and aggrecan. In addition, it results in dysfunctional growth, senescence, and death of intervertebral cells. The biological pathways involved in the development and progression of IVDD are not fully understood. Therefore, a better understanding of the molecular mechanisms underlying IVDD could aid in the development of strategies for prevention and treatment. Autophagy is a cellular process that removes damaged proteins and dysfunctional organelles, and its dysfunction is linked to a variety of diseases, including IVDD and osteoarthritis. In this review, we describe recent research findings on the role of autophagy in IVDD pathogenesis and highlight autophagy-targeting molecules which can be exploited to treat IVDD. Many studies exhibit that autophagy protects against and postpones disc degeneration. Further research is needed to determine whether autophagy is required for cell integrity in intervertebral discs and to establish autophagy as a viable therapeutic target for IVDD.

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“…Mechanically, growing studies have proposed that lncRNAs interact with microRNAs (miRNAs), thereby exerting effects on cell autophagy and apoptosis via a lncRNA-miRNA-mRNA competing endogenous RNA (ceRNA) network [ 12 , 13 ]. For example, lncRNA FAM83H-AS1 can promote the growth of NP cells and maintain the tissue homeostasis of IVDs by inhibiting miR-22-3p [ 14 ]. LncRNA H19 can promote autophagy and apoptosis of NP cells, thus aggravating IDD via the miR-139/CXCR4/NF- κ B axis [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Long Noncoding RNA HOTAIR in Nucleus Pulposus Cell Autophagy and Apoptosis in Intervertebral Disc Degeneration

Zhang

Song

Cui

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. Intervertebral disc degeneration (IDD) contributes to cervical and lumbar diseases. Long noncoding RNAs (lncRNAs) are implicated in IDD. This study explored the mechanism of lncRNA HOTAIR in IDD. Methods. Normal and degenerative nucleus pulposus (NP) cells were isolated from NP tissues obtained in intervertebral disc surgery. Cell morphology was observed by immunocytochemistry staining and toluidine blue staining. NP cell markers were detected by RT-qPCR. Proliferation was detected by MTT assay. Autophagy-related proteins were detected by Western blot. Autophagosome was observed by monodansylcadaverine fluorescence staining. Apoptosis was detected by TUNEL staining and flow cytometry. si-HOTAIR and/or miR-148a inhibitor was introduced into degenerative NP cells. Binding relationships among HOTAIR, miR-148a, and PTEN were predicted and verified by dual-luciferase reporter assay and RNA pull-down. Finally, IDD rat models were established. Rat caudal intervertebral discs were assessed by HE staining. Expressions of HOTAIR, miR-148a, and PTEN were determined by RT-qPCR. Results. HOTAIR was highly expressed in degenerative NP cells p < 0.05 . si-HOTAIR inhibited degenerative NP cell apoptosis and autophagy p < 0.05 . HOTAIR upregulated PTEN as a sponge of miR-148a. miR-148a was poorly expressed in degenerative NP cells. miR-148a deficiency partially reversed the inhibition of si-HOTAIR on degenerative NP cell autophagy and apoptosis (all p < 0.05 ). In vivo assay confirmed that si-HOTAIR impeded autophagy and apoptosis in intervertebral disc tissues, thus improving pathological injury in IDD rats (all p < 0.05 ). Conclusion. LncRNA HOTAIR promoted NP cell autophagy and apoptosis via promoting PTEN expression as a ceRNA of miR-148a in IDD.

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LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition

Cited by 13 publications

References 46 publications

The potential mechanisms and application prospects of non-coding RNAs in intervertebral disc degeneration

The potential mechanisms and application prospects of non-coding RNAs in intervertebral disc degeneration

Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration

Mechanism of Long Noncoding RNA HOTAIR in Nucleus Pulposus Cell Autophagy and Apoptosis in Intervertebral Disc Degeneration

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