LncRNA MALAT1 is Neuroprotective in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury Through miR-204 Regulation

Qiao, Yong; Peng, Changliang; Li, Ji; Wu, Dongjin; Wang, Xiuwen

doi:10.2174/1567202615666180712153150

Cited by 50 publications

(34 citation statements)

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“…For instance, the lncRNA CCAT2 promotes angiogenesis in glioma through the activation of VEGFA signaling by sponging miR-424 (Sun et al, 2020). The lncRNA MALAT-1 has been shown to have neuroprotective effects on spinal cord ischemic/reperfusion injury by regulating miR-204 (Qiao et al, 2018). LncRNAs have also been reported to participate in the regulation of stem cell self-renewal and differentiation in stroke-induced neurogenesis (Fan et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Cheng

et al. 2020

Front. Cell Dev. Biol.

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Endogenous repair after chronic compressive spinal cord injury (CCSCI) is of great clinical interest. Ischemia-hypoxia-induced angiogenesis has been proposed to play an important role during this repair process. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the pathophysiological processes of various diseases. Here, we identified a lncRNA (Xist; X-inactive specific transcript) with upregulated expression in cervical spine lesions during endogenous neurological repair in CCSCI rats. Therapeutically, the introduction of Xist to rats increased neurological function in vivo as assayed using the Basso, Beattie, and Bresnahan (BBB) score and inclined plane test (IPT). We found that the introduction of Xist enhanced endogenous neurological repair by promoting angiogenesis and microvessel density after CCSCI, while depletion of Xist inhibited angiogenesis and cell sprouting and migration. Mechanistically, Xist promoted angiogenesis by sponging miR-32-5p and modulating Notch-1 expression both in vitro and in vivo. These findings suggest a role of the Xist/miR-32-5p/Notch-1 axis in endogenous repair and provide a potential molecular target for the treatment of ischemia-related central nervous system (CNS) diseases.

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Section: Introductionmentioning

confidence: 99%

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Cheng

et al. 2020

Front. Cell Dev. Biol.

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“…Several studies have reported that lncRNAs suppress miRNA expression by functioning as ceRNAs [47]. For example, the lncRNA MALAT1 protected the spinal cord from IR-induced damage by targeting miR-204 [48]. Similarly, ablation of CasC7 promoted apoptosis in the ischemic spinal cord [49] via upregulation of miR-30c.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Long Noncoding RNA TUG1 Attenuate MTDH /NF-κB/IL-1β mediated inflammatory damage via Targeting miR-29b-1-5p After Spinal cord ischemia reperfusion in rats

Jia

Fang

et al. 2020

Preprint

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Background: Spinal cord ischemia reperfusion (IR) is associated with an inflammatory response. The long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) and microRNA-29b (miR-29b) family are frequently dysregulated in neuro-ischemic diseases. However, their potential roles in spinal cord IR injury (IR) are unknown. Methods: A spinal cord IR model was established in rats by14-minute occlusion of aortic arch. The aberrant miRNAs were identified by microarray analysis, and qRT-PCR was used to validate the lncRNA and microRNA levels. The motor function of the differentially-treated animals was assessed by Tarlov scores, and the leakage of Blood-spinal cord barrier (BSCB) was measured in terms of the extravasation of Evans blue (EB) dye. The expression levels of different proteins were analyzed by Western blotting and immunofluorescence. The interaction between TUG1 and miR-29b-1-5p, TRIL and miR-29b-1-5p, and MTDH and miR-29b-1-5p were determined using bioinformatics programs and the dual-luciferase reporter assay. Results: MiR-29b-1-5p was significantly downregulated and TUG1 was upregulated in the spinal cord of rats after IR. In addition, TRIL and MTDH protein levels were also significantly increased after IR. MTDH was predicted as a target of miR-29b-1-5p and its knockdown downregulated NF-κB and IL-1β levels. In addition, a direct interaction was observed between TUG1 and miR-29b-1-5p, and knocking down TUG1 upregulated the miRNA. Furthermore, overexpression of miR-29b-1-5p or TUG1 knockdown alleviated BSCB leakage and improved hind-limb motor function, and downregulated MTDH and its downstream pro-inflammatory cytokines. Suppression of miR-29b-1-5p reversed the neuroprotective effect of TUG1 knockdown, restored the levels of MTDH/ NF-κB/IL-1β and activated astrocytes. Conclusion: Downregulation of TUG1 alleviated MTDH/NF-κB/IL-1β pathway-mediated inflammatory damage after IR by targeting miR-29b-1-5p. Keywords: Spinal cord ischemia reperfusion injury, Neuroinflammation, Blood-spinal cord barrier, Astrocytes, TUG1, miR-29b-1-5p, MTDH

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“…In recent years, studies on the function of lncRNA in SCII have also gradually increased. Liu et al proved that hydrogen sulfide up-regulated lncRNA CasC7 and reduced neuronal cell apoptosis in SCII , Wang et al revealed that lncRNA MALAT1 played a neuroprotective role in a rat SCII via regulating miR-204 (Qiao et al, 2018), and a resesrch group indentified expression profile of lncRNAs in the spinal cord at the early stage of reperfusion (2 h post-cardiac I/R) by high-throughput RNA sequencing (Wang et al, 2019). However, lncRNA expression pattern and its roles in SCII at the late stage of reperfusion have not been reported yet.…”

Section: Introductionmentioning

confidence: 99%

Changes in long non-coding RNA transcriptomic profiles after ischemia-reperfusion injury in rat spinal cord

Zhou¹,

Han²,

Jin

et al. 2020

PeerJ

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With the aim of exploring expression profiles and biological functions of long non-coding RNA (lncRNA) and mRNAs after spinal cord ischemia-reperfusion injury (SCII), differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) in rat spinal cords were identified following SCII through high-throughput RNA sequencing. In total, 1,455 lncRNAs and 6,707 mRNAs were observed to be differentially expressed (—Fold Change— ≥ 2 and P < 0.05) after SCII, including 761 up-regulated and 694 down-regulated lncRNAs, 3,772 up-regulated and 2,935 down-regulated mRNAs. Gene ontology and KEGG pathway analysis showed that the DElncRNAs and DEmRNAs were implicated in many different biological processes and pathways. Further, lncRNA-mRNA co-expression networks were built to explore the potential roles of these DElncRNAs. Our results demonstrate genome-wide lncRNA and mRNA expression patterns in spinal cords after SCII, which may play vital roles in post-SCII pathophysiological processes. These findings are important for future functional research on the lncRNAs involved in SCII and might be critical for providing new insight into identification of potential targets for SCII therapy.

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LncRNA MALAT1 is Neuroprotective in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury Through miR-204 Regulation

Abstract: Our data suggested that MALAT1 exerted neuroprotective effect in a rat model of SCIRI by regulating miR-204.

Cited by 50 publications

References 0 publications

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Downregulation of Long Noncoding RNA TUG1 Attenuate MTDH /NF-κB/IL-1β mediated inflammatory damage via Targeting miR-29b-1-5p After Spinal cord ischemia reperfusion in rats

Changes in long non-coding RNA transcriptomic profiles after ischemia-reperfusion injury in rat spinal cord

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