Lnc<scp>RNA</scp>‐<scp>RMRP</scp> promotes nucleus pulposus cell proliferation through regulating miR‐206 expression

Wang, Xuesong; Peng, Lei; Gong, Xiaojin; Zhang, Xiugong; Sun, Ruifu; Du, Jinlong

doi:10.1111/jcmm.13817

Cited by 23 publications

(17 citation statements)

References 42 publications

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“… 36 RMRP has also been indicated to promote cell proliferation of nucleus pulposus by regulating miR-206 expression. 37 Likewise, in our study, we also found that RMRP can directly bind with miR-206. Subsequently, we innovatively identified that DDX5 is a direct target of miR-206 and that its expression is inhibited by miR-206.…”

Section: Discussionsupporting

confidence: 80%

Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury

et al. 2021

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Purpose This study aimed to explore the role of the long non-coding RNA (lncRNA) RNA component of mitochondrial RNAase P (RMRP) in sepsis-induced acute kidney injury (AKI). Materials and Methods Venous blood was collected from septic patients and healthy people. C57BL/6 mice who underwent cecal ligation and puncture (CLP) were used as in vivo models of septic AKI. Lipopolysaccharide (LPS)-induced HK-2 cells were employed as in vitro models of AKI. Flow cytometry analysis was conducted to detect cell apoptosis. Enzyme-linked immunosorbent assay and Western blot assays were used to detect levels of pro-inflammatory cytokines. Results RMRP was upregulated in sera from patients with AKI and in LPS-induced cells. Knockdown of RMRP inhibited cell apoptosis and reduced production of inflammatory factors in LPS-induced cells, as well as alleviated AKI in CLP mice. RMRP facilitated inflammation by activating NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome. We found that microRNA 206 (miR-206) binds with and is negatively regulated by RMRP: miR-206 directly targets the 3′ untranslated region of DEAD-box helicase 5 (DDX5) and negatively regulates DDX5 expression. By binding with miR-206, RMRP upregulated DDX5 expression. Rescue assays revealed that overexpression of DDX5 counteracted the effect of RMRP inhibition on cell apoptosis and inflammatory response in LPS-induced cells. Conclusion The lncRNA RMRP contributes to sepsis-induced AKI through upregulation of DDX5 in a miR-206 dependent manner and through activation of NLRP3 inflammasome. This novel discovery may provide a potential strategy for treating AKI.

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Section: Discussionsupporting

confidence: 80%

Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury

et al. 2021

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“…SNHG1 promotes NP cell proliferation via sponging miR-326, and downregulated miR-326 disinhibits NP cell proliferation by inactivating PCNA and cyclin D1 expression. Similarly, RP11-296A18.3/miR-138/HIF1A, RMRP/miR-206/PCNA, H19/miR-22/LEF1/Wnt/β-catenin signaling, and HCG18/miR-146a-5p/TRAF6/NF-κB axis can also increase or decrease the level of proliferation, respectively [ 10 , 25 , 106 – 108 ]. Targeting extracellular signal-regulated kinase (Erk) and miR-146a-5p/TRAF6/NF-κB axis, respectively, lncRNA FAF1 and HCG18 modulate the ratio of synthesis-phase cells among all the cells in NP tissue [ 109 ].…”

Section: The Regulatory Mechanism Of Lncrnas In Iddmentioning

confidence: 99%

“…Owing to that, we established the coding-noncoding SuperSeries Datasets as GSE67567 in human IDD, including lncRNAs, mRNAs, and circRNAs, and miRNAs datasets as GSE19943, GSE63492, GSE56081, and GSE67566, as well as studies from other investigators (Table 1 ). Given the scarcity of studies summarizing the research progress of ncRNAs in IDD, we designed and conducted a review across the published papers [ 13 , 17 , 18 , 20 – 25 ]. In the current work, the state-of-art research advance and therapeutic potentials concerning the regulatory roles of miRNAs/circRNAs/lncRNAs in degenerated discs of human or animal models were summarized and discussed (Fig.…”

Section: Introductionmentioning

confidence: 99%

Emerging evidence on noncoding-RNA regulatory machinery in intervertebral disc degeneration: a narrative review

Guo

Wan

et al. 2020

Arthritis Res Ther

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Intervertebral disc degeneration (IDD) is the most common cause of low-back pain. Accumulating evidence indicates that the expression profiling of noncoding RNAs (ncRNAs), including microRNAs (miRNAs), circular RNAs (circRNAs), and long noncoding RNAs (lncRNAs), are different between intervertebral disc tissues obtained from healthy individuals and patients with IDD. However, the roles of ncRNAs in IDD are still unclear until now. In this review, we summarize the studies concerning ncRNA interactions and regulatory functions in IDD. Apoptosis, aberrant proliferation, extracellular matrix degradation, and inflammatory abnormality are tetrad fundamental pathologic phenotypes in IDD. We demonstrated that ncRNAs are playing vital roles in apoptosis, proliferation, ECM degeneration, and inflammation process of IDD. The ncRNAs participate in underlying mechanisms of IDD in different ways. MiRNAs downregulate target genes’ expression by directly binding to the 3′-untranslated region of mRNAs. CircRNAs and lncRNAs act as sponges or competing endogenous RNAs by competitively binding to miRNAs and regulating the expression of mRNAs. The lncRNAs, circRNAs, miRNAs, and mRNAs widely crosstalk and form complex regulatory networks in the degenerative processes. The current review presents novel insights into the pathogenesis of IDD and potentially sheds light on the therapeutics in the future.

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“…Previous studies have investigated the role of RMRP in numerous cancer types, including lung cancer (8), gastric cancer (9) and glioma (10). Furthermore, Wang et al (11) demonstrated that higher RMRP expression in nucleus pulposus tissues was associated with disc degeneration grade. Another study has indicated that RMRP overexpression increased nucleus pulposus cell growth and regulated ECM expression by targeting miR-206 (11).…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, Wang et al (11) demonstrated that higher RMRP expression in nucleus pulposus tissues was associated with disc degeneration grade. Another study has indicated that RMRP overexpression increased nucleus pulposus cell growth and regulated ECM expression by targeting miR-206 (11). Recently, Greco et al (12) profiled the expression of 83 lncRNAs, which are known to be associated with numerous human diseases, in the left ventricle biopsies of patients with heart failure and demonstrated that RMRP was significantly upregulated in these patients.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of lncRNA RMRP promotes the activation of cardiac fibroblasts by regulating miR‑613

et al. 2019

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Long non-coding RNAs (lncRNAs) have been reported to serve a key role in a variety of cardiovascular diseases, including in cardiac fibrosis. The present study aimed to investigate the biological role and underlying mechanisms of the induction of cardiac fibroblasts by the lncRNA, RNA component of mitochondrial RNA processing endoribonuclease (RMRP). The results demonstrated that RMRP expression was upregulated in the presence of cardiac fibrosis in an abdominal aortic banding-treated rat model. Treatment with angiotensin II increased RMRP expression in cardiac fibroblasts, while the knockdown of RMRP by small-interfering RNA inhibited cardiac fibroblast proliferation, differentiation and collagen accumulation. To further investigate the underlying mechanisms of this interaction, microRNA (miR)-613 was predicted to be a target miR of RMRP and sequence alignment, luciferase activity and MS2 RNA immunoprecipitation were performed to detect the interaction between RMRP and miR-613. The results suggested that RMRP negatively regulated miR-613 in cardiac fibroblasts. Furthermore, miR-613 was indicated to mediate the promoting effect of RMRP on cardiac fibroblast activation. The current study suggested that RMRP promoted cardiac fibroblast activation by acting as a competing endogenous RNA for miR-613. Therefore, RMRP may be a novel target for the prevention or treatment of cardiac fibrosis.

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LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression

Cited by 23 publications

References 42 publications

Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury

Long Non-Coding RNA RMRP Contributes to Sepsis-Induced Acute Kidney Injury

Emerging evidence on noncoding-RNA regulatory machinery in intervertebral disc degeneration: a narrative review

Upregulation of lncRNA RMRP promotes the activation of cardiac fibroblasts by regulating miR‑613

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