Bioinformatics Analysis of the Inflammation-Associated lncRNA-mRNA Coexpression Network in Type 2 Diabetes

Huang, Linjuan; Xiong, Shengxi; Liu, Hanshuang; Li, Min; Zhang, Ranran; Liu, Yan; Hu, Xiaolei

doi:10.1155/2023/6072438

Cited by 3 publications

(2 citation statements)

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“…Recent studies have shown that SNHG16 exacerbates diabetic nephropathy through stabilizing TLR4/NF-κB pathway activation [ 25 ]. Furthermore, our previous LncRNA microarray results show that SNHG16 is highly expressed in diabetic patients [ 10 ]. Therefore, the aim of this study was to investigate the mechanism of the SNHG16 in regulating diabetic inflammation and diabetic nephropathy, providing new ideas for the treatment of diabetes.…”

Section: Discussionmentioning

confidence: 99%

“…Another study has reported that SNHG16 exacerbates high glucose-induced foot cell injury in diabetic nephropathy [ 9 ]. Based on our previous findings, we extracted Peripheral blood mononuclear cells from type 2 diabetic patients and normal person, and after LncRNA microarray sequencing, we found that SNHG16 was upregulated in diabetic patients [ 10 ]. The pathological mechanism of diabetic nephropathy is also an inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

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Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway

Huang

Xiong

Liu

et al. 2023

Diabetol Metab Syndr

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Background Long noncoding RNAs (LncRNAs) have been identified to play an important role in diabetes. The aim of the present study was to determine the expression and function of small nucleolar RNA host gene 16 (SNHG16) in diabetic inflammation. Methods For the in vitro experiments, quantitative real-time PCR (qRT-PCR), Western blotting and immunofluorescence were used to detect LncRNA SNHG16 expression in the high-glucose state. The potential microRNA sponge target of LncRNA SNHG16, miR-212-3p, was detected by dual-luciferase reporter analysis and qRT-PCR. For the in vivo experiments, glucose changes in mice were detected after si-SNHG16 treatment, and SNHG16 and inflammatory factor expression in kidney tissues were detected by qRT-PCR and immunohistochemistry. Results LncRNA SNHG16 was upregulated in diabetic patients, HG-induced THP-1 cells, and diabetic mice. Silencing SNHG16 inhibited the diabetic inflammatory response and the development of diabetic nephropathy. miR-212-3p was found to be directly dependent on LncRNA SNHG16. miR-212-3p could inhibitor P65 phosphorylation in THP-1 cells. The miR-212-3p inhibitor reversed the action of si-SNHG16 in THP-1 cells and induced an inflammatory response in THP-1 cells. LncRNA SNHG16 was also found to be higher in the peripheral blood of diabetic patients than in the normal person. The area under the ROC curve is 0.813. Conclusion These data suggested that silencing LncRNA SNHG16 suppresses diabetic inflammatory responses by competitively binding miR-212-3p to regulate NF-κB. LncRNA SNHG16 can be used as a novel biomarker for patients with type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%