LncRNA SNHG12 downregulates RAGE to attenuate hypoxia-reoxygenation-induced apoptosis in H9c2 cells

Lu, Ping; Xiao, Shihui; Chen, Shaoze; Fu, Youlin; Zhang, Peng; Yao, Yaner; Chen, Feng

doi:10.1093/bbb/zbaa090

Cited by 9 publications

(9 citation statements)

References 32 publications

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“…In addition to cancer, SNHG12 has been shown to be involved in cerebral ischemia-reperfusion (I/R) injury; specifically, its upregulation protects against cerebral I/R injury ( 21 ). Recently, Lu et al pointed out that the lncRNA SNHG12 is effective in protecting against hypoxia/reoxygenation-induced injury in myocardial cells ( 22 ). Furthermore, SNHG12 is a kind of snoRNAs, and these snoRNAs were predicted to have roles in post-translational modifications and alternative splicing, processes differentially regulated in HCM ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

SNHG 12 and hsa-miR-140-5P may play an important role in the ceRNA network related to hypertrophic cardiomyopathy

Zhai¹,

Guo²,

Zhou³

et al. 2023

J Thorac Dis

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Background: Competing endogenous RNA (ceRNA) networks play important roles in the mechanism and development of a variety of diseases. This study aimed to construct a ceRNA network of hypertrophic cardiomyopathy (HCM). Methods:We searched the Gene Expression Omnibus (GEO) database and then analyzed the RNAs of 353 samples to explore differentially expressed lncRNAs (DELs), microRNAs (miRNAs; DEMs), and messenger RNAs (DEmRNAs) during the progression of HCM. Weighted gene co-expression network analysis (WGCNA), Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and transcription factor (TF) prediction of miRNAs were also performed, and the GO terms, KEGG pathway terms, protein-protein interaction (PPI) network, and Pearson correlation network of the DEGs were visualized with the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database and through Pearson analysis. In addition, a ceRNA network related to HCM was constructed on the basis of the DELs, DEMs, and DEs. Finally, the function of the ceRNA network was explored via GO and KEGG enrichment analyses.Results: Through our analysis, 93 DELs (77 upregulated and 16 downregulated), 163 DEMs (91 upregulated and 72 downregulated), and 432 DEGs (238 upregulated and 194 downregulated) were screened.The functional enrichment analysis results for miRNAs showed that the miRNAs were mainly related to the VEGFR signaling network and the INFr pathway and were mainly regulated by TFs such as SOX1, TEAD1, and POU2F1. Gene set enrichment analysis (GSEA), GO analysis, and KEGG enrichment analysis showed that the DEGs were enriched in the Hedgehog signaling pathway, IL-17 signaling pathway, and TNF signaling pathway. In addition, a ceRNA network including 8 lncRNAs (e.g., LINC00324, SNHG12, and ALMS1-IT1), 7 miRNAs (e.g., hsa-miR-217, hsa-miR-184, and hsa-miR-140-5p), and 52 mRNAs (e.g., IGFBP5, TMED5, and MAGT1) was constructed. The results revealed that SNHG12, hsa-miR-140-5p, hsa-miR-217, TFRC, HDAC4, TJP1, IGFBP5, and CREB5 may form an important network involved in the pathology of HCM. Conclusions:The novel ceRNA network that we have demonstrated will provide new research points about molecular mechanisms of HCM.

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Section: Discussionmentioning

confidence: 99%

SNHG 12 and hsa-miR-140-5P may play an important role in the ceRNA network related to hypertrophic cardiomyopathy

Zhai¹,

Guo²,

Zhou³

et al. 2023

J Thorac Dis

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“…28 Numerous studies have elaborated the essential functions of SNHG12 in human diseases, including atherosclerosis, 29 cerebral I/R injury, 30 and I/R-induced cardiac dysfunction. 31 Besides, Wu et al revealed that SNHG12 could relieve cerebral I/R injury by activating SIRT1/FOXO3a signaling through inhibition of autophagy and oxidative stress. 32 In addition, Yuan et al disclosed that SNHG12 promoted cell proliferation and reduced cell apoptosis in breast cancer via regulating the miR-15a-5/SALL4 cascade.…”

Section: Discussionmentioning

confidence: 99%

“…Yuan et al revealed that ZFAS1 attenuated BV-induced neurotoxicity via the miR-421/ZNF564 pathway 28. Numerous studies have elaborated the essential functions of SNHG12 in human diseases, including atherosclerosis,29 cerebral I/R injury,30 and I/Rinduced cardiac dysfunction 31. Besides, Wu et al revealed that SNHG12 could relieve cerebral I/R injury by activating…”

mentioning

confidence: 99%

LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497–5p to upregulate NLRX1

Sun

Yuan

2022

Hum Exp Toxicol

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Long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) has been reported to participate in the regulation of various nervous system disorders. Bupivacaine (BV), a commonly used local anesthetic, could generate neurotoxicity in neurons. This work intended to investigate the role and specific mechanism of SNHG12 in BV-induced neurotoxicity. In this study, we established an in vitro cell model of BV-induced neurotoxicity by exposing human neuroblastoma cells (SH-SY5Y) to BV. It was found that SNHG12 and NLRX1 levels were gradually downregulated, while miR-497–5p enrichment was upregulated accordingly with the increase of BV concentration. As indicated by functional assays, SNHG12 overexpression promoted cell viability but inhibited cell apoptosis and oxidative stress in BV-treated SH-SY5Y cells. In addition, it was identified that SNHG12 directly targeted miR-497–5p and attenuated BV-induced neurotoxicity via interaction with miR-497–5p. Besides, it was confirmed that SNHG12 could upregulate NLRX1 expression by absorbing miR-497–5p. Moreover, miR-497–5p decreased cell viability and induced cell apoptosis and oxidative stress, which was partly reversed by NLRX1 upregulation. In conclusion, our findings indicated that SNHG12 might relieve BV-associated neurotoxicity by upregulating NLRX1 via miR-497–5p in vitro, providing novel clues and biomarkers for the treatment and prevention of BV-associated neurotoxicity.

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“…In AGEs-induced endothelial cells, lncRNA MEG3 regulated cell viability, proliferation, and apoptosis through the lncRNA MEG3/MiR-93/p21 mediated pathway during the onset of diabetic vascular diseases [ 97 ]. In a cell-based study on hypoxia/reoxygenation-injured cardiomyocytes, lncRNA SNHG12 down-regulated RAGE, NF-κB expression, and pro-inflammatory responses [ 102 ]. In a different context, the lncRNA TP73-AS1-mediated RAGE-HMGB1 signaling pathway upregulated NF-κB expression and pro-inflammatory cytokine levels [ 12 , 103 ].…”

Section: Understanding the Role Of Lncrnas In Ages-related Dnmentioning

confidence: 99%

Glycation-Associated Diabetic Nephropathy and the Role of Long Noncoding RNAs

Durge

Sharma²,

Tupe³

2022

Biomedicines

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The glycation of various biomolecules is the root cause of many pathological conditions associated with diabetic nephropathy and end-stage kidney disease. Glycation imbalances metabolism and increases renal cell injury. Numerous therapeutic measures have narrowed down the adverse effects of endogenous glycation, but efficient and potent measures are miles away. Recent advances in the identification and characterization of noncoding RNAs, especially the long noncoding RNAs (lncRNAs), have opened a mammon of new biology to explore the mitigations for glycation-associated diabetic nephropathy. Furthermore, tissue-specific distribution and condition-specific expression make lncRNA a promising key for second-generation therapeutic interventions. Though the techniques to identify and exemplify noncoding RNAs are rapidly evolving, the lncRNA study encounters multiple methodological constraints. This review will discuss lncRNAs and their possible involvement in glycation and advanced glycation end products (AGEs) signaling pathways. We further highlight the possible approaches for lncRNA-based therapeutics and their working mechanism for perturbing glycation and conclude our review with lncRNAs biology-related future opportunities.

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LncRNA SNHG12 downregulates RAGE to attenuate hypoxia-reoxygenation-induced apoptosis in H9c2 cells

Cited by 9 publications

References 32 publications

SNHG 12 and hsa-miR-140-5P may play an important role in the ceRNA network related to hypertrophic cardiomyopathy

SNHG 12 and hsa-miR-140-5P may play an important role in the ceRNA network related to hypertrophic cardiomyopathy

LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497–5p to upregulate NLRX1

Glycation-Associated Diabetic Nephropathy and the Role of Long Noncoding RNAs

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