The function of miR-199a-5p/Klotho regulating TLR4/NF-κB p65/NGAL pathways in rat mesangial cells cultured with high glucose and the mechanism

Wu, Can; Lv, Chuan; Chen, Fenqin; Ma, Xiaoyu; Shao, Ying; Wang, Qiuyue

doi:10.1016/j.mce.2015.09.024

Cited by 48 publications

(40 citation statements)

References 32 publications

(38 reference statements)

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“…25 Our results showed the expressions of two subunits of NF- κ B, p50 and p65 were significantly higher in H-MCs than those in L-MCs by qRT-PCR (Figure 3a). Moreover, overexpression of Gm4419 could increase the expressions of p50 and p65 in L-MCs, whereas Gm4419 knockdown could decrease the expressions of p50 and p65 in H-MCs (Figure 3b).…”

Section: Resultsmentioning

confidence: 69%

“…7 NF- κ B inhibitor alpha (I κ B α ) regulates activation of NF- κ B p50/p65 heterodimer, 8 and p50/p65 subunits translocate into the nucleus and bind to specific promoter sequence of the target inflammatory genes when I κ B α is degraded by immunoproteasome. 9, 10 Also, our previously study has shown that the activation of NF- κ B has a role in renal inflammation and fibrosis of the progression of DN. 3 In addition, recent researches have displayed that NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome directly participated in renal inflammatory processes, leading to the progression of diabetic glomerular damage, including glomerular fibrosis, hyperplasia of the extracellular matrix and glomerulosclerosis.…”

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confidence: 99%

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LincRNA-Gm4419 knockdown ameliorates NF-κB/NLRP3 inflammasome-mediated inflammation in diabetic nephropathy

et al. 2017

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Diabetic nephropathy (DN) as the primary cause of end-stage kidney disease is a common complication of diabetes. Recent researches have shown the activation of nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) and NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome are associated with inflammation in the progression of DN, but the exact mechanism is unclear. Long noncoding RNAs (lncRNAs) have roles in the development of many diseases including DN. However, the relationship between lncRNAs and inflammation in DN remains largely unknown. Our previous study has revealed that 14 lncRNAs are abnormally expressed in DN by RNA sequencing and real-time quantitative PCR (qRT-PCR) in the renal tissues of db/db DN mice. In this study, these lncRNAs were verified their expressions by qRT-PCR in mesangial cells (MCs) cultured under high- and low-glucose conditions. Twelve lncRNAs displayed the same expressional tendencies in both renal tissues and MCs. In particular, long intergenic noncoding RNA (lincRNA)-Gm4419 was the only one associating with NF-κB among these 12 lncRNAs by bioinformatics methods. Moreover, Gm4419 knockdown could obviously inhibit the expressions of pro-inflammatory cytokines and renal fibrosis biomarkers, and reduce cell proliferation in MCs under high-glucose condition, whereas overexpression of Gm4419 could increase the inflammation, fibrosis and cell proliferation in MCs under low-glucose condition. Interestingly, our results showed that Gm4419 could activate the NF-κB pathway by directly interacting with p50, the subunit of NF-κB. In addition, we found that p50 could interact with NLRP3 inflammasome in MCs. In conclusion, our findings suggest lincRNA-Gm4419 may participate in the inflammation, fibrosis and proliferation in MCs under high-glucose condition through NF-κB/NLRP3 inflammasome signaling pathway, and may provide new insights into the regulation of Gm4419 during the progression of DN.

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Section: Resultsmentioning

confidence: 69%

mentioning

confidence: 99%

LincRNA-Gm4419 knockdown ameliorates NF-κB/NLRP3 inflammasome-mediated inflammation in diabetic nephropathy

et al. 2017

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“…In addition, Singh, Boden and Rao reported that high glucose increased the expression of TLR-416. Moreover, other studies confirmed that high glucose could trigger the TLR4 signaling pathway to activate a related receptor1718. All of these studies showed that blood glucose is upstream of TLR4, and that the TLR4 inhibitor alone cannot change blood glucose content.…”

Section: Discussionmentioning

confidence: 87%

Effects of the TLR4 signaling pathway on apoptosis of neuronal cells in diabetes mellitus complicated with cerebral infarction in a rat model

Che

et al. 2017

Sci Rep

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This study aims to explore the effects of the TLR4 signaling pathway on the apoptosis of neuronal cells in rats with diabetes mellitus complicated with cerebral infarction (DMCI). A DMCI model was established with 40 Sprague Dawley rats, which were assigned into blank, sham, DM + middle cerebral artery occlusion (MCAO) and DM + MCAO + TAK242 groups. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. A TUNEL assay was applied for detecting cell apoptosis, and Western blotting was used for detecting the expression of TLR4, TNF-α, IL-1β and apoptosis-related proteins. Compared with the blank and sham groups, there was an increase in cell apoptosis, expression of Bcl-2, Bax, cleaved caspase-3, TNF-α, IL-1β and TLR4 proteins and MDA content and a decrease in SOD activity in the DM + MCAO and DM + MCAO + TAK242 groups. Compared with those in the DM + MCAO group, rats in the DM + MCAO + TAK242 group exhibited an increase in SOD activity and a decrease in cell apoptosis, expression of Bcl-2, Bax, cleaved caspase-3, TNF-α, IL-1β and TLR4 proteins and MDA content. Inhibition of the TLR4 signaling pathway reduces neuronal cell apoptosis and nerve injury to protect the brain.

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“…NF-kB inhibitor alpha (IkBa) regulated activation of NF-kB p50/p65 heterodimer, and p65 subunit translocated into the nucleus and bound to specific promoter sequence of the target genes when IkBa was degraded by immunoproteasome (Visekruna et al, 2006;Wu et al, 2015). Large multifunctional protease 7 (LMP7) is one the catalytic subunit of immunoproteasome (Akiyama et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

miR-451 suppresses the NF-kappaB-mediated proinflammatory molecules expression through inhibiting LMP7 in diabetic nephropathy

Sun

Peng

et al. 2016

Molecular and Cellular Endocrinology

106

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The function of miR-199a-5p/Klotho regulating TLR4/NF-κB p65/NGAL pathways in rat mesangial cells cultured with high glucose and the mechanism

Cited by 48 publications

References 32 publications

LincRNA-Gm4419 knockdown ameliorates NF-κB/NLRP3 inflammasome-mediated inflammation in diabetic nephropathy

LincRNA-Gm4419 knockdown ameliorates NF-κB/NLRP3 inflammasome-mediated inflammation in diabetic nephropathy

Effects of the TLR4 signaling pathway on apoptosis of neuronal cells in diabetes mellitus complicated with cerebral infarction in a rat model

miR-451 suppresses the NF-kappaB-mediated proinflammatory molecules expression through inhibiting LMP7 in diabetic nephropathy

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