Knockdown of lncRNA NORAD inhibits the proliferation, inflammation and fibrosis of human mesangial cells under high‑glucose conditions by regulating the miR‑485/NRF1 axis

Wang, Linna; Yuan, Xiao-Ying; Lifeng, Lian; Guo, Huali; Zhang, Hongxia; Zhang, Minghui

doi:10.3892/etm.2021.10306

Cited by 16 publications

(18 citation statements)

References 31 publications

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“…Qin et al reported that lncRNA PVT1 regulated HG-induced viability, oxidative stress, fibrosis, and inflammation in DN through the miR-325-3p/Snail1 axis [ 5 ]. It has been found that knockdown of lncRNA NORAD inhibits the proliferation, inflammation, and fibrosis of human mesangial cells under HG conditions by regulating the miR-485/NRF1 axis [ 6 ]. lncRNA HCP5 knockdown has been found to inhibit HG-induced excessive proliferation, fibrosis, and inflammation of human glomerular mesangial cells by regulating the miR-93-5p/HMGA2 axis [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis

Zhao

Cui

Dong³

et al. 2022

Journal of Healthcare Engineering

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Background. Diabetic nephropathy (DN) is the most common microvascular complication of diabetes and has become the second leading cause of end-stage renal disease in the world. This study aims to clarify the regulatory mechanism of the lncRNA MSC-AS1/miR-325/cyclin G1 (CCNG1) axis in DN. Methods. The regulatory mechanism of lncRNA MSC-AS1/miR-325/CCNG1 was evaluated by RT-qPCR, CCK-8 assay, flow cytometry assay, RNA pull-down assay, ELISA, and western blot assay. Results. Upregulation of lncRNA MSC-AS1 was detected in DN patients and HRMC cells treated with high glucose (HG). Knockdown of lncRNA MSC-AS1 reduced the proliferation, fibrosis, and inflammation of HRMC cells induced by HG. In addition, lncRNA MSC-AS1 acts as a miR-325 sponge in the DN. CCNG1 is the direct target of miR-325, which can be positively regulated by lncRNA MSC-AS1 in DN. More importantly, downregulation of miR-325 and upregulation of CCNG1 can attenuate the protective effect of lncRNA MSC-AS1 knockdown on DN. Conclusion. lncRNA MSC-AS1 aggravates DN by downregulating miR-325 and upregulating CCNG1.

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Section: Introductionmentioning

confidence: 99%

lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis

Zhao

Cui

Dong³

et al. 2022

Journal of Healthcare Engineering

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“…In the model of LPS-induced lung injury, lncRNA SNHG16 is highly expressed, effectively binds to miR-146a-5p and restores CCL 5 expression, thereby promoting the inflammatory response and apoptosis (64). Wang et al observed that lncRNA NORAD inhibits the proliferation, inflammation and fibrosis of human mesangial cells under high-glucose conditions by acting as a molecular sponge of miR-485 to modulate NRF1 expression (65). And Chu et al found that lncRNA MARL functions as a ceRNA for miR-122 to control protein abundance of MAVS, thereby inhibiting the SCRV replication and promoting antiviral responses (66).…”

Section: Discussionmentioning

confidence: 99%

“…Wang et al. observed that lncRNA NORAD inhibits the proliferation, inflammation and fibrosis of human mesangial cells under high-glucose conditions by acting as a molecular sponge of miR-485 to modulate NRF1 expression ( 65 ). And Chu et al.…”

Section: Discussionmentioning

confidence: 99%

Lnc90386 Sponges miR-33-5p to Mediate Mycoplasma gallisepticum-Induced Inflammation and Apoptosis in Chickens via the JNK Pathway

et al. 2022

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Mycoplasma gallisepticum (MG) is one of the most important pathogens, that causes chronic respiratory disease (CRD) in chickens. Long non-coding RNAs (lncRNAs) are emerging as new regulators for many diseases and some lncRNAs can function as competing endogenous RNAs (ceRNAs) to regulate mRNAs by competitively binding to miRNAs. Here, we found that miR-33-5p was significantly up-regulated both in MG-infected chicken embryonic lungs and chicken embryo fibroblast cells (DF-1), and Lnc90386 negatively correlated with miR-33-5p. miR-33-5p, as a new regulator for MG infection, repressed apoptosis, inflammatory factors in DF-1 cells by targeting JNK1. Further analyses showed that Lnc90386 sponged miR-33-5p to weaken its inhibitory effect on JNK1, forming the ceRNA regulatory network. Furthermore, knockdown of Lnc90386 significantly inhibited apoptosis and inflammatory factors, and promoted DF-1 cells proliferation. However, co-treatment with miR-33-5p inhibitor and Lnc90386 siRNA showed that knockdown of Lnc90386 could partially eliminate the inhibiting effect of miR-33-5p inhibitor on inflammation, cell apoptosis and proliferation. In conclusion, Lnc90386 sponges miR-33-5p to defend against MG infection by inhibiting the JNK signaling pathway.

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“…In a cell model engendered by high glucose, suppressed NORAD expression inhibits the secretion of pro-inflammatory cytokines, including IL-6. 26 In neuroblastoma cells, NORAD plays a role in the inflammatory condition by sponging miR-204-5p. 27 All these pieces of evidence manifest NORAD expression might participate in NS by mediating inflammatory actions.…”

Section: Dovepressmentioning

confidence: 99%

Clinical Significance of the Serum lncRNA NORAD Expression in Patients with Neonatal Sepsis and Its Association with miR-410-3p

Zhang

2021

JIR

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Purpose Neonatal sepsis (NS) is one of the most crucial causes of death in newborns. This investigation aimed to validate the expression level of NORAD and the probable mechanism underlying the function of NORAD in NS. Patients and Methods The expression of NORAD and miR-410-3p was identified by qRT-PCR. The diagnostic sensitivity and specificity of NORAD were examined by the ROC curve. The NS cell models were established by the treatment of lipopolysaccharide (LPS) in the macrophage RAW264.7 cells. The luciferase report assay was performed to detect the target relationship between NORAD and miR-410-3p and the association between them was revealed by Pearson correlation. Results The expression of NORAD was at a higher level in the NS group than in the pneumonia controls. The levels of NORAD could sever as a diagnostic marker on discriminating NS patients from pneumonia neonates. The expression of IL-6, IL-8, and TNF-α was enhanced in the macrophage cells under LPS circumstances, while NORAD knockdown reversed the overexpression of these pro-inflammatory cytokines. Besides, miR-410-3p was a possible ceRNA of NORAD by the finding that the luciferase activity fell in the co-transfection of miR-410-3p mimics and WT-NORAD group. In vitro, LPS management could inhibit the expression of miR-410-3p, while silenced NORAD ameliorated the suppressed miR-410-3p levels. Decreased expression of miR-410-3p was discovered in NS patients and the changes of miR-410-3p expression were correlated with the levels of NORAD in the NS patients. Conclusion We found a raised level of NORAD in the NS patients and it might be a diagnostic indicator for NS patients. NORAD elimination meliorated the inflammation actions steered by LPS. MiR-410-3p was a target of NORAD and lowly expressed in the NS patients.

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Knockdown of lncRNA NORAD inhibits the proliferation, inflammation and fibrosis of human mesangial cells under high‑glucose conditions by regulating the miR‑485/NRF1 axis

Cited by 16 publications

References 31 publications

lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis

lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis

Lnc90386 Sponges miR-33-5p to Mediate Mycoplasma gallisepticum-Induced Inflammation and Apoptosis in Chickens via the JNK Pathway

Clinical Significance of the Serum lncRNA NORAD Expression in Patients with Neonatal Sepsis and Its Association with miR-410-3p

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