miR-485 suppresses inflammation and proliferation of mesangial cells in an in vitro model of diabetic nephropathy by targeting NOX5

Wu, Jian; Lu, Kan V.; Zhu, Mingying; Xie, Xin; Ding, Yaqin; Shao, Xiaorong; Chen, Yiyue; Liu, Jibo; Xu, Mengzhu; Xu, Yi; Zhou, Jing; Shen, Xiaoyu; Zhu, Chunling

doi:10.1016/j.bbrc.2019.11.020

Cited by 36 publications

(26 citation statements)

References 29 publications

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“…Similarly, the upregulation of NOX4 and reduction of its direct regulator, miR-25, was reported in kidneys of diabetic rat model, HG-treated mesangial cells and upon diabetic peripheral neuropathy [267,268]. Expression of another NOX, NOX5, was proved to be rescued by HG-reduced miR-485, its direct regulator, in human mesangial cells, thus enhancing their proliferation and inflammation [269]. NOX4 was also found to be targeted by miR-146a in diabetic nephropathy, while overexpression of miR-146a was accompanied by amelioration of both inflammation and OxS [270,271].…”

Section: Mirnas In Mets-a Link With Obesity and Insulin Resistance/hymentioning

confidence: 53%

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Włodarski

Strycharz

Wróblewski

et al. 2020

IJMS

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Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS.

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Section: Mirnas In Mets-a Link With Obesity and Insulin Resistance/hymentioning

confidence: 53%

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Włodarski

Strycharz

Wróblewski

et al. 2020

IJMS

View full text Add to dashboard Cite

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“…Increasing and emerging evidence has illustrated that miRNAs are vital regulators in the development of DN by binding to the 3′-UTR of the target gene, which causes mRNA cleavage or translational repression [23,39]. To explore the target genes of miR-144, starBase v2.0 software was used and predicted SOCS2 as one of the targets of miR-144.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that miRNAs are closely related to the development of DN [22]. For example, miR-485 inhibits inflammation and expansion of mesangial cells in vitro by targeting NOX5 [23]. It has also been reported that miR-218 regulates DN by targeting IKK-β and modulating NF-κB-mediated inflammation [24].…”

Section: Introductionmentioning

confidence: 99%

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

Min

Xie

2020

Kidney Blood Press Res

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Background: Diabetic nephropathy constitutes a large proportion of end-stage kidney failure in diabetic patients. However, the underlying molecular mechanisms remain unclear. Methods: Db/db diabetic mouse models and high glucose (HG)-induced human renal mesangial cells (HRMCs) were used as research models in vivo and in vitro. The expression of cancer susceptibility candidate 2 (CASC2) was quantified by qRT-PCR. The regulatory role of CASC2 in cell apoptosis, inflammatory factor release, and fibrosis was verified by flow cytometry, qRT-PCR, and Western blot assay, respectively. The bioinformatics prediction software DIANA and starBase v2.0 were used to predict the putative binding sites. The interactions among CASC2, miR-144, and SOCS2 were explored by the luciferase assay and Western bolt assay. Results: The expression of CASC2 in diabetic mouse models and HG-induced HRMCs was lower than that in the control (p < 0.05). Overexpression of CASC2 resulted in a decrease in the apoptosis rate, inflammatory factor release (TNF-α, IL-6, and IL-1β), expression of cleaved caspase-3, and fibrotic proteins (fibronectin, Col-IV, and TGF-β1) and an increase in Bcl-2 expression. Inhibition of CASC2 caused increased expression of miR-144. Furthermore, mechanistic investigations confirmed that activation of the miR-144/SOCS2 regulatory loop by overexpression of miR‐144 reversed the in vitro effects of CASC2 on inhibiting cell apoptosis, inflammatory factor release, and fibrosis. In addition, simultaneous overexpression of miR-144 and SOCS2 further increased the inhibition of cell apoptosis, inflammatory factor release, and fibrosis by CASC2. Conclusion: CASC2 could alleviate the degree and process of apoptosis, inflammation, and fibrosis in diabetic nephropathic models by regulating the miR-144/SOCS2 axis.

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“…It has been reported that AGE expression can significantly inhibit the viability of cells, such as fibroblasts, in a time-dependent manner ( 44 ). AGEs may destroy stability of the internal environment by enhancing intracellular oxidative stress, thus inhibiting cell viability ( 45 ).…”

Section: Discussionmentioning

confidence: 99%

Inhibitor of RAGE and glucose‑induced inflammation in bone marrow mesenchymal stem cells: Effect and mechanism of action

Jiang

Wang

et al. 2020

Mol Med Rep

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The occurrence and development of hyperglycemia-induced inflammation is associated with increased expression of receptor for advanced glycation end products (RAGE) and inflammatory factors, including IL-1β, TnF-α and il-6. Previous studies have reported that the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome interacts with thioredoxin-interacting protein (TXNIP) and serves a crucial role in inflammation. FPS-ZM1 has been identified as target inhibitor of RAGE and has been shown to exert an anti-inflammatory effect in vitro. However, the underlying mechanism by which FPS-ZM1 impacts high glucose (HG)-induced inflammation in bone marrow mesenchymal stem cells (BMScs) remains unclear. The present study explored the regulatory effect of FPS-ZM1 on HG-induced inflammation in BMSCs. Furthermore, the role of the TXNIP/NLRP3 inflammasome signaling pathway in the regulatory effects of FPS-ZM1 on HG-induced inflammation was studied. cell viability was determined using cell counting Kit-8 and western blotting was used to assess the protein expression levels of raGe. eliSa was used to determine the levels of inflammatory markers. Reverse transcription-quantitative Pcr and western blotting were used to measure the mrna and protein expression levels of TXniP, caspase-1, thioredoxin (TRX), NLRP3 and apoptosis-related speck-like protein containing card (aSc). The results revealed that in BMScs, raGe expression was stimulated by HG, an effect which was reversed by treatment with FPS-ZM1. in addition, HG activated inflammatory factors, such as TnF-α, IL-1β and il-6; however, their levels were suppressed when cells were treated with FPS-ZM1 or the TXNIP/NLRP3 pathway inhibitor, resveratrol (Res). Furthermore, FPS-ZM1 inhibited the mrna and protein expression levels of TXniP, caspase-1, NLRP3 and ASC, and promoted TRX expression, which was consistent with the effects of res. These findings indicated that FPS-ZM1 may attenuate HG-induced inflammation in BMSCs. Furthermore, the TXNIP/NLRP3 inflammasome signaling pathway mediated the molecular mechanism underlying this effect.

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miR-485 suppresses inflammation and proliferation of mesangial cells in an in vitro model of diabetic nephropathy by targeting NOX5

Cited by 36 publications

References 29 publications

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

Inhibitor of RAGE and glucose‑induced inflammation in bone marrow mesenchymal stem cells: Effect and mechanism of action

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