Journal of Internal Medicine Concepts & Practice >

2023 , Vol. 18 >Issue 02: 92 - 98

DOI: https://doi.org/10.16138/j.1673-6087.2023.02.006

Research report

Expression of LINC01465 in gouty arthritis and its clinical significances

Expand
  • 1. Department of Rheumatology, Shenzhen Futian Hospital for Rheumatic Diseases, Shenzhen 518000, China
    2. Department of Rheumatology, Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai 200052, China

Received date: 2022-10-20

  Online published: 2023-05-15

Fold

Abstract

Objective To explore the potential pathogenesis-related long non-coding RNA (lncRNA) in gouty arthritis (GA) and the correlation with inflammatory factors. Methods GA microarray data were obtained from the Gene Expression Omnibus(GEO) database, and key lncRNA was identified and intersected by multiple machine learning methods. mRNAs co-expressed with lncRNAs were performed GO enrichment analysis. Kyoto encyclopedia of genes and genomes (KEGG) signaling pathway analysis was accomplished. The expression of key lncRNAs in GA patients was verified using quantitative real-time polymerase chain reaction(qRT-PCR) and the correlation between lncRNA and inflammatory factor levels was analyzed. The diagnostic value of LINC01465 expression levels in GA patients was analyzed by receiver operator characteristic(ROC) curves. Results One key lncRNA(LINC01465) was identified. GO enrichment analysis showed that the genes co-expressed with LINC01465 were enriched in RNA splicing, oxidative phosphorylation, reduced nicotinamide adenine dinucleotide (NADH ) dehydrogenase activity and other functions. KEGG signaling pathway analysis presented that it was mainly enriched in metabolic and inflammatory pathways such as nicotinate and nicotinamide metabolism, phosphoinositide 3-kinase(PI3K)-Akt, tumor necrosis factor signaling pathway. The qRT-PCR results exhibited that LINC01465 expression was upregulated in the patients with GA and was proportional to the expression of hematocrit, C-reactive protein and interleukin-6. The area under the receiver operator characteristic curve(AUC) was 0.86. Conclusions LINC01465 could be a potential diagnostic and therapeutic target for GA.

Key words： Gouty arthritis; LINC01465; Machine learning; Signaling pathway

Cite this article

XIAO Jianwei, CAI Xu, HUANG Xinmin, HONG Yiwei, WANG Rongsheng . Expression of LINC01465 in gouty arthritis and its clinical significances[J]. Journal of Internal Medicine Concepts & Practice, 2023 , 18(02) : 92 -98 . DOI: 10.16138/j.1673-6087.2023.02.006

References

[1] Kuo CF, Grainge MJ, Zhang W, et al. Global epidemiology of gout: prevalence, incidence and risk factors[J]. Nat Rev Rheumatol, 2015, 11(11): 649-662.
[2] Dehlin M, Jacobsson L, Roddy E. Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors[J]. Nat Rev Rheumatol, 2020, 16(7): 380-390.
[3] Major TJ, Dalbeth N, Stahl EA, et al. An update on the genetics of hyperuricaemia and gout[J]. Nat Rev Rheumatol, 2018, 14(6): 341-353.
[4] Jeong JH, Hong S, Kwon OC, et al. CD14+ cells with the phenotype of infiltrated monocytes consist of distinct populations characterized by anti-inflammatory as well as pro-inflammatory activity in gouty arthritis[J]. Front Immunol, 2017, 8:1260.
[5] Statello L, Guo CJ, Chen LL, et al. Gene regulation by long non-coding RNAs and its biological functions[J]. Nat Rev Mol Cell Biol, 2021, 22(2): 96-118.
[6] Engreitz JM, Ollikainen N, Guttman M. Long non-coding RNAs: spatial amplifiers that control nuclear structure and gene expression[J]. Nat Rev Mol Cell Biol, 2016, 17(12): 756-770.
[7] Fang L, Xu X, Lu Y, et al. Long noncoding RNA SNHG8 accelerates acute gouty arthritis development by upregulating AP3D1 in mice[J]. Bioengineered, 2021, 12(2): 9803-9815.
[8] Liu YF, Xing GL, Chen Z, et al. Long non-coding RNA HOTAIR knockdown alleviates gouty arthritis through miR-20b upregulation and NLRP3 downregulation[J]. Cell Cycle, 2021, 20(3): 332-344.
[9] Zhong X, Peng Y, Liao H, et al. Aberrant expression of long non-coding RNAs in peripheral blood mononuclear cells isolated from patients with gouty arthritis[J]. Exp Ther Med, 2019, 18(3): 1967-1976.
[10] Xiao J, Wang R, Cai X, et al. Coupling of co-expression network analysis and machine learning validation unearthed potential key genes involved in rheumatoid arthritis[J]. Front Genet, 2021, 12: 604714.
[11] Adamichou C, Genitsaridi I, Nikolopoulos D, et al. Lupus or not? SLE risk probability index(SLERPI): a simple, clinician-friendly machine learning-based model to assist the diagnosis of systemic lupus erythematosus[J]. Ann Rheum Dis, 2021, 80(6): 758-766.
[12] Noss MR, Saguil A. Gout: diagnosis and management[J]. Am Fam Physician, 2017, 96(10):668-670.
[13] Lodde V, Murgia G, Simula ER, et al. Long noncoding RNAs and circular RNAs in autoimmune diseases[J]. Biomolecules, 2020, 10(7): 1044.
[14] Zhang M, Jang H, Nussinov R. PI3K inhibitors: review and new strategies[J]. Chem Sci, 2020, 11(23): 5855-5865.
[15] Shi Y, Mucsi AD, Ng G. Monosodium urate crystals in inflammation and immunity[J]. Immunol Rev, 2010, 233(1): 203-217.
[16] Malumbres M, Barbacid M. RAS oncogenes: the first 30 years[J]. Nat Rev Cancer, 2003, 3(6): 459-465.
[17] Roskoski R Jr. RAF protein-serine/threonine kinases: structure and regulation[J]. Biochem Biophys Res Commun, 2010, 399(3): 313-317.
[18] Krygowska AA, Castellano E. PI3K: a crucial piece in the RAS signaling puzzle[J]. Cold Spring Harbor Perspect Med, 2018, 8(6): a031450.
[19] Pacold ME, Suire S, Perisic O, et al. Crystal structure and functional analysis of Ras binding to its effector phosphoinositide 3-kinase gamma[J]. Cell, 2000, 103(6): 931-943.
[20] Cavalcanti NG, Marques CD, Lins E Lins TU, et al. Cytokine profile in gout: inflammation driven by IL-6 and IL-18?[J]. Immunol Invest, 2016, 45(5): 383-395.
[21] Charles P, Terrier B, Perrodeau é, et al. Comparison of individually tailored versus fixed-schedule rituximab regimen to maintain ANCA-associated vasculitis remission[J]. Ann Rheum Dis, 2018, 77(8): 1143-1149.
[22] Nizet V, Johnson RS. Interdependence of hypoxic and innate immune responses[J]. Nat Rev Immunol, 2009, 9(9): 609-617.
[23] Van den Bossche J, O’Neill LA, Menon D. Macrophage immunometabolism: where are we (going)?[J]. Trends Immunol, 2017, 38(6): 395-406.
[24] Mian Wu, Zhang M, Ma Y, et al. Chaetocin attenuates gout in mice through inhibiting HIF-1α and NLRP3 inflammasome-dependent IL-1β secretion in macrophages[J]. Arch Biochem Biophys, 2019, 670: 94-103.
[25] Vallée A, Lecarpentier Y. Crosstalk between peroxisome proliferator-activated receptor gamma and the canonical Wnt/β-catenin pathway in chronic inflammation and oxidative stress during carcinogenesis[J]. Front Immunol, 2018, 9: 745.
[26] Lopes F, Coelho FM, Costa VV, et al. Resolution of neutrophilic inflammation by H2O2 in antigen-induced arthritis[J]. Arthritis Rheum, 2011, 63(9): 2651-2660.
[27] Galv?o I, Queiroz-Junior CM, et al. The inhibition of phosphoinositide-3 kinases induce resolution of inflammation in a Gout model[J]. Front Pharmacol, 2019, 9: 1505.
[28] Stewart DJ. Wnt signaling pathway in non-small cell lung cancer[J]. J Natl Cancer Inst, 2014, 106(1): djt356.
[29] Ke B, Shen XD, Kamo N, et al. β-catenin regulates innate and adaptive immunity in mouse liver ischemia-reperfusion injury[J]. Hepatology, 2013, 57(3): 1203-1214.
[30] Xiao Y, Peng H, Hong C, et al. PDGF promotes the warburg effect in pulmonary arterial smooth muscle cells via activation of the PI3K/AKT/mTOR/HIF-1α signaling pathway[J]. Cell Physiol Biochem, 2017, 42(4): 1603-1613.
[31] Zhong H, Chiles K, Feldser D, et al. Modulation of hypoxia-inducible factor 1alpha expression by the epidermal growth factor/phosphatidylinositol 3-kinase/PTEN/AKT/FRAP pathway in human prostate cancer cells: implications for tumor angiogenesis and therapeutics[J]. Cancer Res, 2000, 60(6): 1541-1545.
[32] Yang XM, Wang YS, Zhang J, et al. Role of PI3K/Akt and MEK/ERK in mediating hypoxia-induced expression of HIF-1α and VEGF in laser-induced Rat choroidal neovascularization[J]. Invest Ophthalmol Vis Sci, 2009, 50(4): 1873-1879.
[33] Karar J, Cerniglia GJ, Lindsten T, et al. Dual PI3K/mTOR inhibitor NVP-BEZ235 suppresses hypoxia-inducible factor (HIF)-1α expression by blocking protein translation and increases cell death under hypoxia[J]. Cancer Biol Ther, 2012, 13(11): 1102-1111.
[34] Semenza GL. HIF-1: upstream and downstream of cancer metabolism[J]. Curr Opin Genet Dev, 2010, 20(1): 51-56.
Options
Outlines

/

〈 〉