Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis

Liu, Min; Li, Weixin; Song, Fuxing; Zhang, Ling; Sun, Xianjun

doi:10.18632/aging.202284

Cited by 20 publications

(12 citation statements)

References 48 publications

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“…In cancer-related studies, miR-147a has been identified as a tumor suppressor to regulate cancer progression, such as non-small-cell lung cancer [ 24 ] and cervical cancer [ 25 ]. MiR-147a might inhibit cellular inflammation to mitigate pneumonia process [ 26 ]. Ji et al .…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

Wang

Huangfu

et al. 2022

Diabetol Metab Syndr

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Background Long non-coding RNAs (lncRNAs) have been shown to be involved in the regulation of many disease progression. However, the role of lncRNA HOX transcript antisense RNA (HOTAIR) in diabetic nephropathy (DN) remains unclear. Methods High glucose (HG)-induced human mesangial cells (HMC) was used to construct DN cell models in vitro. HMC proliferation was evaluated by CCK8 assay and EDU staining. Protein levels of proliferation markers, fibrosis markers, and wingless-type family member 2B (WNT2B) were measured using western blot analysis. HMC oxidative stress was assessed by determining the levels of oxygen species and malondialdehyde, as well as superoxide dismutase activity. Relative expression levels of lncRNA HOTAIR, microRNA (miR)-147a, and WNT2B were examined using quantitative real-time PCR. The interaction between miR-147a and lncRNA HOTAIR or WNT2B was confirmed by dual-luciferase reporter assay and RIP assay. Results Our data showed that lncRNA HOTAIR knockdown could inhibit the proliferation, fibrosis, and oxidative stress in HG-induced HMC. LncRNA HOTAIR could serve as a sponge of miR-147a. The inhibition effect of lncRNA HOTAIR silencing on the biological functions of HG-induced HMC could be reversed by miR-147a inhibitor. WNT2B was targeted by miR-147a, and its overexpression also overturned the suppressive effect of miR-147a on the proliferation, fibrosis, and oxidative stress of HG-induced HMC. Conclusion In total, our research pointed out that lncRNA HOTAIR could mediate miR-147a/WNT2B axis to promote DN progression.

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Section: Discussionmentioning

confidence: 99%

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

Wang

Huangfu

et al. 2022

Diabetol Metab Syndr

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“…The interaction between miRNAs and lncRNAs is indispensable in the development of diseases ( 32 , 35 , 36 ). Tang et al ( 26 ) reported that as the ceRNA for miR-20b-5p, HOTAIR knockdown attenuates autophagy in hepatic I/R injury by improving the inhibitory effect of miR-20b-5p on ATG7.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA NEAT1 participates in ventilator-induced lung injury by regulating miR-20b expression

Liu

Tang

2022

Mol Med Rep

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Long non-coding (lnc)RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to serve an important role in cancer, but its effects on ventilator-induced lung injury (VILI) remain unclear. The present study aimed to investigate the role of lncRNA NEAT1 in alveolar macrophages (AMs) on ventilator-induced lung injury (VILI). Mouse and cell models were established to detect NEAT1 expression, pathological changes in lung tissues, apoptosis of AMs, expression of the M1 phenotype marker, CD86 and M2 phenotype marker, CD206, and the expression levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α and inducible nitric oxide synthase (iNOS). The associations between NEAT1, microRNA (miRNA/miR)-20b and STAT3 were predicted using StarBase and TargetScan, and verified via the dual-luciferase reporter and RIP assays. NEAT1 short hairpin RNA and miR-20b inhibitor were co-transfected into AMs to assess the effect of NEAT1 and miR-20b in VILI. The results demonstrated that NEAT1 was highly expressed in lung tissues of VILI mice and cell stretch (CS) treated AMs. Furthermore, NEAT1 knockdown inhibited lung injury and cell apoptosis induced by VILI. Compared with VILI mice or CS-treated AMs, NEAT1 knockdown accelerated the phenotypic transformation from M1 to M2, and decreased the expression levels of IL-1β, IL-6, TNF-α and iNOS. Notably, miR-20b was identified as the target of NEAT1, and STAT3 was the target of miR-20b. NEAT1 knockdown decreased STAT3 protein expression, the effects of which were reversed following transfection with miR-20b inhibitor. Furthermore, the protective effect of NEAT1 knockdown on VILI was reversed following transfection with miR-20b inhibitor. Taken together, the results of the present study suggest that NEAT1 knockdown promotes phenotypic transformation of AMs from M1 to M2 and alleviates lung injury and apoptosis of VILI by regulating miR-20b expression.

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“…Emerging pieces of evidence on the pathophysiology of non-coding RNAs in infectious diseases have been published recently [ 31 ]. For instance, elimination of MIAT suppressed cell apoptosis, and ultimately protect the balance of lung function via miR-147a/NKAP crosstalk [ 32 ]. Besides, SNHG16 partially restores the damage of LPS in A549 cells on the aspects of cell viability, inflammation, and apoptosis [ 33 ] Interference of circ-0059930 can notably improve proliferation and inhibit apoptosis of LPS-induced MRC-5 cells [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism

Guo

Zhang

et al. 2021

Bioengineered

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Severe pneumonia is a high-mortality disorder in children. The expression and underlying effects of lncRNA maternally expressed 3 (MEG3) were detected. The relationships between MEG3 and other parameters were reported by Pearson correlation. The prognostic importance of MEG3 was assessed by Kaplan-Meier (K-M) curve and COX analysis and its diagnostic potential was uncovered by the receiver operating characteristic (ROC) curve. Luciferase activity assay was performed to demonstrate the target gene of MEG3. Elevated expression of MEG3 and reduced microRNA-29 c (miR-29 c) were evaluated in severe pneumonia children, and a negative relationship between MEG3 and miR-29 c was propounded. MEG3 might function as an independent prognostic indicator. The diagnostic efficiency of MEG3 was also indicated for severe pneumonia children. In MRC-5 cell models and MH-S cell models, lipopolysaccharide (LPS) contributed to the increased expression of MEG3. Interference of MEG3 restricted the upregulation of MEG3 triggered by LPS. Silenced MEG3 protected MRC-5 and MH-S cells against damages managed by LPS on cell apoptosis, viability, and inflammation. MiR-29 c was a ceRNA of MEG3 and the absence of MEG3 abrogated the decreased expression of miR-29 c caused by LPS. Overall, the increased expression of MEG3 and the reduced levels of miR-29 c were identified in severe pneumonia. Prognostic and diagnostic significances of MEG3 provided a novel perspective for severe pneumonia. Disruption of MEG3 alleviated cell injury and inflammation as characterized by high LPS by binding miR-29 c.

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Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis

Cited by 20 publications

References 48 publications

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

LncRNA HOTAIR facilitates high glucose-induced mesangial cell proliferation, fibrosis and oxidative stress in diabetic nephropathy via regulating miR-147a/WNT2B axis

Long non-coding RNA NEAT1 participates in ventilator-induced lung injury by regulating miR-20b expression

Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism

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