scholarly journals POS1146 NONCODING RNA CONTRIBUTE TO PATHOGENESIS IN PRIMARY GOUTY ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 852.1-852
Author(s):  
Q. B. Zhang ◽  
Y. Q. Huang ◽  
F. N. Xiao ◽  
G. L. Jian ◽  
Y. P. Tang ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Current Knowledge ◽  
Science And Technology ◽  
Gouty Arthritis ◽  
Noncoding Rnas ◽  
Acute Gout ◽  
Research Support ◽  
Expression Levels ◽  
Significant Difference

Background:Gout is an arthritic disease caused by the deposition of monosodium urate crystal (MSU) in the joints, which can lead to acute inflammation and damage adjacent tissue [1].Over the past decade, noncoding RNAs (ncRNAs) have been shown to have crucial importance in health and disease[2,3]. However, studies evaluating the function of ncRNAs in gout are scarce, and current knowledge of the role of ncRNAs in gout is still limited.Objectives:To assess the contribution of noncoding RNAs to gout and the clinical importance of these genes in primary gouty arthritis (GA).Methods:The mRNA expression levels of noncoding RNAs (LINC00173, LINC00963, LINC01330 and miRNA-182-5p) were measured in peripheral blood mononuclear cells (PBMCs) from 60 gout patients(including 30 acute gout patients, 30 intercritical gout patients) and 40 healthy subjects. The relationship between noncoding RNA expression levels and laboratory features was analyzed in GA patients.Results:The expression levels of LINC00173, LINC00963 and miRNA-182-5p were much lower in the AG and IG group than in the HC groups (p<0.05), and no significant difference was detected between AG and IG groups(P>0.05). The expression levels of LINC01330 were much lower in the AG group than in the IG and HC groups (p<0.05), and no significant difference was detected between AG and IG groups(P>0.05). In GA patients, the levels of noncoding RNAs mRNA correlated with laboratory inflammatory and metabolic indexes.Conclusion:Altered noncoding RNAs expression suggests that noncoding RNAs is involved in the pathogenesis of GA and participates in regulating inflammation and metabolism.References:[1]Xu Yi-Ting,Leng Ying-Rong,Liu Ming-Ming et al. MicroRNA and long noncoding RNA involvement in gout and prospects for treatment.[J].Int Immunopharmacol, 2020, 87: 106842.doi:10.1016/j.intimp.2020.106842[2]Yu Yunfang,Zhang Wenda,Li Anlin et al. Association of Long Noncoding RNA Biomarkers With Clinical Immune Subtype and Prediction of Immunotherapy Response in Patients With Cancer.[J].JAMA Netw Open, 2020, 3: e202149.doi:10.1001/jamanetworkopen.2020.2149[3]Zou Yaoyao,Xu Siqi,Xiao Youjun et al. Long noncoding RNA LERFS negatively regulates rheumatoid synovial aggression and proliferation.[J].J Clin Invest, 2018, 128: 4510-4524.doi:10.1172/JCI97965Figure 1.Relative Expression of noncoding RNAs in the PBMCs of Patients.Disclosure of Interests:Quan-Bo Zhang Grant/research support from: the National Natural Science Foundation of China(General Program) (no.81974250) and Science and Technology Plan Project of Sichuan Province (no.2018JY0257), Yu-Qin Huang: None declared, Fan-Ni Xiao: None declared, gui-lin jian: None declared, Yi-Ping Tang: None declared, Fei Dai: None declared, Jian-Xiong Zheng: None declared, Yu-Feng Qing Grant/research support from: Science and Technology Project of Nanchong City (no.18SXHZ0522).

scholarly journals POS0136 ROLES OF AUTOPHAGY IN THE PATHOGENESIS OF PRIMARY GOUTY ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 280.1-280
Author(s):  
Y. Q. Huang ◽  
Q. B. Zhang ◽  
J. X. Zheng ◽  
G. L. Jian ◽  
T. H. Liu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Science And Technology ◽  
Gouty Arthritis ◽  
The Other ◽  
Sirtuin 1 ◽  
Neutrophil Extracellular Trap ◽  
Acute Gout ◽  
Research Support ◽  
Crystal Deposition ◽  
Expression Levels

Background:Gout is a chronic autoinflammatory disease caused by monosodium urate (MSU) crystal deposition [1].Acute gout is characterized by an acute inflammatory reaction that resolves spontaneously within a few days[2], which is one of the distinguishing features of gout compared to other arthropathies or self-inflammatory diseases. Autophagy is a lysosomal degradation pathway that is essential for cellular growth, survival, differentiation, development and homeostasis [3]. Studies have demonstrated that autophagy might play a key role in the pathogenesis of primary gouty arthritis (GA) [4-7]. However, the roles of autophagy in the development of gout have not yet been elucidated.Objectives:The aim of our study was to investigate the changes in autophagy-related gene (ATG) mRNA and protein in patients and the clinical importance of these genes in primary gouty arthritis (GA) and to explore the roles of autophagy in the pathogenesis of GA.Methods:The mRNA and protein expression levels of ATGs (ATG3, ATG7, ATG10, ATG5, ATG12, ATG16L1, ATG4B and LC3-2) were measured in peripheral blood mononuclear cells (PBMCs) from 196 subjects, including 57 acute gout patients (AG group), 57 intercritical gout patients (IG group) and 82 healthy control subjects (HC group). The relationship between ATG expression levels and laboratory features was analyzed in GA patients.Results:The expression levels of ATG4B, ATG5, ATG12, ATG16L1, ATG10 and LC3-2 mRNA were much lower in the AG group than in the IG and HC groups (p<0.05), while the ATG7 mRNA level was much higher in the AG group than in the IG and HC groups (p<0.05). The protein expression levels of LC3-2, ATG3, ATG7 and ATG10 were much higher in the AG group than in the other groups, while those of ATG5, ATG12, ATG16L1 and ATG4B were far lower in the AG group than in the other groups (p<0.05). In GA patients, the levels of ATG mRNA and protein correlated with laboratory inflammatory and metabolic indexes.Conclusion:Altered ATG expression suggests that autophagy is involved in the pathogenesis of GA and participates in regulating inflammation and metabolism.References:[1]Dalbeth N, Choi HK, Joosten LAB, Khanna PP, Matsuo H, Perez-Ruiz F, et al. Gout. Nat Rev Dis Primers. 2019;5: 69.doi:10.1038/s41572-019-0115-y.[2]Schauer C, Janko C, Munoz LE, Zhao Y, Kienhöfer D, Frey B, et al. Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines. Nat Med. 2014;20: 511-517.doi:10.1038/nm.3547.[3]Han Y, Zhang L, Xing Y, Zhang L, Chen X, Tang P, et al. Autophagy relieves the function inhibition and apoptosis-promoting effects on osteoblast induced by glucocorticoid. Int J Mol Med. 2018;41: 800-808. doi:10.3892/ijmm.2017.3270.[4]Yang QB, He YL, Zhong XW, Xie WG, Zhou JG. Resveratrol ameliorates gouty inflammation via upregulation of sirtuin 1 to promote autophagy in gout patients. Inflammopharmacology. 2019;27: 47-56.doi:10.1007/s10787-018-00555-4.[5]Mitroulis I, Kambas K, Chrysanthopoulou A, Skendros P, Apostolidou E, Kourtzelis I, et al. Neutrophil extracellular trap formation is associated with IL-1β and autophagy-related signaling in gout. PLoS One. 2011;6: e29318.doi: 10.1371/journal.pone.0029318.[6]Crişan TO, Cleophas MCP, Novakovic B, Erler K, van de Veerdonk FL, Stunnenberg HG, et al. Uric acid priming in human monocytes is driven by the AKT-PRAS40 autophagy pathway. Proc Natl Acad Sci U S A. 2017;114: 5485-5490.doi:10.1073/pnas.1620910114.[7]Lee SS, Lee SW, Oh DH, Kim HS, Chae SC, Kim SK. Genetic analysis for rs2241880(T > C) in ATG16L1 polymorphism for the susceptibility of Gout. J Clin Rheumatol. 2019;25: e113-e115.doi:10.1097/rhu.0000000000000685.Disclosure of Interests:Yu-Qin Huang: None declared, Quan-Bo Zhang Grant/research support from: National Natural Science Foundation of China(General Program) (no.81974250) and Science and Technology Plan Project of Sichuan Province (no.2018JY0257), Jian-Xiong Zheng: None declared, gui-lin jian: None declared, tao-hong liu: None declared, Xin He: None declared, fan-ni xiao: None declared, qin xiong: None declared, Yu-Feng Qing Grant/research support from: Science and Technology Project of Nanchong City (no.18SXHZ0522)

scholarly journals Antifungal Effect of Long Noncoding RNA 9708-1 in the Vulvovaginal Candidiasis Murine Model

2021 ◽  
Vol 186 (2) ◽  
pp. 177-188
Author(s):  
Ying Wu ◽  
Lisha Jiang ◽  
Lingling Zhang ◽  
Xia Liu ◽  
Lina Yan ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Basal Layer ◽  
Vulvovaginal Candidiasis ◽  
Control Group ◽  
Therapeutic Effects ◽  
Blank Control Group ◽  
Candida Spp ◽  
Expression Levels ◽  
Gene And Protein Expression

AbstractVulvovaginal candidiasis (VVC) caused by Candida spp. affects 70–75% of women at least once during their lives. We aim to elucidate the potential mechanism of VVC and investigate the therapeutic effects of long noncoding RNA 9708-1. Female BALB/c mice were randomized to four treatment groups, including the blank control group, VVC control group, vehicle control group and lncRNA 9708-1-overexpressed group. Mice were euthanized on Day 4, Day 7 and Day 14 after treatment. Colony-forming unit (CFU) was measured, and the inflammation was detected by hematoxylin and eosin (H&E). Gene and protein expression levels of lncRNA 9708-1 and FAK were determined by real-time PCR, Western blot and immunohistochemistry. The overexpression of lncRNA 9708-1 significantly decreased the fungal load from Day 4 to 7. H&E staining indicated that the impaired histological profiles were improved in lncRNA 9708-1-overexpressed group. LncRNA 9708-1 led to a significant increase in FAK level of vagina tissue which is expressed mainly in epithelial basal layer. This study suggests that lncRNA 9708-1 played a protective role on murine experimental VVC by upregulating the expression levels of FAK.

THU0078 EXPRESSION PROFILE ANALYSIS OF LONG NONCODING RNAS INDUCED BY IL-1ß IN RHEUMATOID ARTHRITIS FIBROBLAST-LIKE SYNOVIOCYTES

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 251.1-251
Author(s):  
J. M. Kim ◽  
H. J. Kang ◽  
S. J. Jung ◽  
B. W. Song ◽  
H. J. Jeong ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Expression Profile ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Aberrant Expression ◽  
Iκb Kinase ◽  
Ngs Data ◽  
Fibroblast Like Synoviocytes

Background:Long noncoding RNAs (lncRNAs) have recently emerged as important biological regulators and the aberrant expression of lncRNAs has been reported in various diseases including cancer, cardiovascular disease, and diabetes mellitus. However, the role of lncRNAs in the pathogenesis of rheumatoid arthritis (RA) remains unknown.Objectives:Thus, we studied lncRNAs influenced by IL-1, which is one of the key mediators in the pathogenesis of RA, and also investigated whether regulation of NF-κB activation, which is known to be induced by IL-1, could lead to the changes of expression of those lncRNAs.Methods:Fibroblast-like synoviocytes (FLS) were obtained from the knee joints of the patients with RA. The next-generation sequencing (NGS) data were analyzed to identify differentially expressed lncRNAs between unstimulated RA FLS and IL-1-stimulated RA FLS. The expression levels of the top 5 candidates in NGS data were validated by RT-qPCR using extended number of unstimulated RA FLS and IL-1-stimulated RA FLS. IMD-0560, an inhibitor of IκB kinase (IKK) was used for the regulation of NF-κB activation. Activation and inhibition of NF-κB were confirmed by Western blotting. Changed expressions of the lncRNAs were identified by RT-qPCR.Results:NGS analysis revealed up-regulated 30 lncRNAs and down-regulated 15 lncRNAs in IL-1-treated RA FLS compared with unstimulated RA FLS. Top 5 lncRNAs were selected among 30 lncRNAs up-regulated by IL-1 in RA FLS based on fold-change with P-value cutoff. The up-regulated lncRNAs including NR_046035, NR_027783, NR_033422, NR_003133, and NR_049759 were validated by RT-qPCR. IMD-0560 inhibited phosphorylation of IκBα induced by IL-1 in RA FLS. Overexpression of lncRNAs induced by IL-1 was also inhibited by IMD-0560 in RA FLS.Conclusion:Our study revealed that IL-1 increased the expression of NR_046035, NR_027783, NR_033422, NR_003133, and NR_049759 in RA FLS. In addition, the expression of these lncRNAs was regulated by inhibition of NF-κB activation. Thus, our data suggest that the lncRNAs might be involved in the pathogenesis of RA through NF-κB signaling pathway.References:[1]Long noncoding RNAs and human disease. Trends Cell Biol. 2011 Jun;21(6):354-61.[2]A long noncoding RNA mediates both activation and repression of immune response genes. Science. 2013 Aug 16;341(6147):789-92.[3]Long noncoding RNA expression profile in fibroblast-like synoviocytes from patients with rheumatoid arthritis. Arthritis Res Ther. 2016 Oct 6;18(1):227.Disclosure of Interests:None declared

scholarly journals Long Noncoding RNA CTBP1-AS Regulates Ovarian Granulosa Cells Proliferation and Autophagy and Participates in Polycystic Ovary Syndrome

2021 ◽  
Author(s):  
Kaixuan Sun ◽  
Yinling Xiu ◽  
Jianbo Song ◽  
Yuexin Yu
Keyword(s):  
Granulosa Cells ◽  
Peripheral Blood ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Polycystic Ovary ◽  
Blood Leukocytes ◽  
Expression Levels ◽  
Ovarian Granulosa Cells ◽  
Related Proteins ◽  
Ovarian Syndrome

Abstract ObjectiveThis study aims to investigate the expression of long noncoding RNA CTBP1-AS in patients with polycystic ovarian syndrome (PCOS) and its effects on the proliferation and autophagy of ovarian granulosa cells. MethodsReal-time polymerase chain reaction assay was used to analyze the expression levels of CTBP1-AS in peripheral blood leukocytes of 40 PCOS patients and 40 non-PCOS women and the CTBP1-AS expression in ovarian granulosa cells and transfect ovarian granulosa cells with pcDNA3.1-CTBP1-AS and si-CTBP1-AS, respectively. Consequently, the CCK-8 kit was used to analyze the effect of CTBP1-AS on the proliferation of ovarian granulosa cells. Moreover, Western blotting was used to detect the expression levels of autophagy-related proteins LC3II/I and P62. ResultThe CTBP1-AS expression in the peripheral blood of PCOS patients was higher compared with non-PCOS patients (P < 0.05). Furthermore, the CTBP1-AS expression of ovarian granulosa cells in PCOS patients was higher compared with non-PCOS patients (P < 0.05). Consequently, CTBP1-AS overexpression in ovarian granulosa cells promotes the proliferation of ovarian granulosa cells and autophagy levels (P < 0.05). The CTBP1-AS expression interference in ovarian granulosa cells can inhibit the proliferation of ovarian granulosa cells and autophagy levels (P < 0.05). ConclusionThe CTBP1-AS expression in peripheral blood and ovarian granulosa cells of PCOS patients significantly increased, and CTBP1-AS could promote the proliferation of ovarian granulosa cells and the level of autophagy.

Unique Archaeal Small RNAs

2018 ◽  
Vol 52 (1) ◽  
pp. 465-487 ◽  
Author(s):  
José Vicente Gomes-Filho ◽  
Michael Daume ◽  
Lennart Randau
Keyword(s):  
Noncoding Rna ◽  
Genome Rearrangement ◽  
Rna Binding ◽  
Elevated Temperatures ◽  
Rna Binding Proteins ◽  
Current Knowledge ◽  
Extreme Environments ◽  
Noncoding Rnas ◽  
Hyperthermophilic Archaea ◽  
Rna Modification

Advances in genome-wide sequence technologies allow for detailed insights into the complexity of RNA landscapes of organisms from all three domains of life. Recent analyses of archaeal transcriptomes identified interaction and regulation networks of noncoding RNAs in this understudied domain. Here, we review current knowledge of small, noncoding RNAs with important functions for the archaeal lifestyle, which often requires adaptation to extreme environments. One focus is RNA metabolism at elevated temperatures in hyperthermophilic archaea, which reveals elevated amounts of RNA-guided RNA modification and virus defense strategies. Genome rearrangement events result in unique fragmentation patterns of noncoding RNA genes that require elaborate maturation pathways to yield functional transcripts. RNA-binding proteins, e.g., L7Ae and LSm, are important for many posttranscriptional control functions of RNA molecules in archaeal cells. We also discuss recent insights into the regulatory potential of their noncoding RNA partners.

scholarly journals Long noncoding RNA ANRIL protects cardiomyocytes against hypoxia/reoxygenation injury by sponging miR-195-5p and upregulating Bcl-2

RSC Advances ◽  
2019 ◽  
Vol 9 (61) ◽  
pp. 35624-35635 ◽  
Author(s):  
Hui Zhao ◽  
Li Meng ◽  
Chengyang Xu ◽  
Bin Lin ◽  
Xiangming Zheng ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

Long noncoding RNAs have been widely accepted to play important roles in acute myocardial infarction (AMI).

scholarly journals Silencing of Long Noncoding RNA Nespas Aggravates Microglial Cell Death and Neuroinflammation in Ischemic Stroke

Stroke ◽  
2019 ◽  
Vol 50 (7) ◽  
pp. 1850-1858 ◽  
Author(s):  
Yiming Deng ◽  
Duanduan Chen ◽  
Luyao Wang ◽  
Feng Gao ◽  
Bo Jin ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Noncoding Rnas ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Oxygen Glucose Deprivation ◽  
Cerebral Artery Occlusion

Background and Purpose— Ischemic stroke is one of the leading causes of morbidity and mortality worldwide and a major cause of long-term disability. Recently, long noncoding RNAs have been revealed, which are tightly associated with several human diseases. However, the functions of long noncoding RNAs in ischemic stroke still remain largely unknown. In the current study, for the first time, we investigated the role of long noncoding RNA Nespas in ischemic stroke. Methods— We used in vivo models of middle cerebral artery occlusion and in vitro models of oxygen-glucose deprivation to illustrate the effect of long noncoding RNA Nespas on ischemic stroke. Results— We found expression of Nespas was significantly increased in ischemic cerebral tissues and oxygen-glucose deprivation–treated BV2 cells in a time-dependent manner. Silencing of Nespas aggravated middle cerebral artery occlusion operation–induced IR injury and cell death. In addition, proinflammatory cytokine production and NF-κB (nuclear factor-κB) signaling activation were inhibited by Nespas overexpression. TAK1 (transforming growth factor-β–activated kinase 1) was found to directly interact with Nespas, and TAK1 activation was significantly suppressed by Nespas. At last, we found Nespas-inhibited TRIM8 (tripartite motif 8)-induced K63-linked polyubiquitination of TAK1. Conclusions— We showed that Nespas played anti-inflammatory and antiapoptotic roles in cultured microglial cells after oxygen-glucose deprivation stimulation and in mice after ischemic stroke by inhibiting TRIM8-related K63-linked polyubiquitination of TAK1.

Implication of regulatory networks of long noncoding RNA/circular RNA-miRNA-mRNA in diabetic cardiovascular diseases

Epigenomics ◽  
2020 ◽  
Vol 12 (21) ◽  
pp. 1929-1947
Author(s):  
Wei Xiong ◽  
Mengran Yao ◽  
Yuqiao Yang ◽  
Yan Qu ◽  
Jinqiao Qian
Keyword(s):  
Diabetes Mellitus ◽  
Cardiovascular Diseases ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Regulatory Networks ◽  
Noncoding Rnas ◽  
Circular Rna ◽  
Competing Endogenous Rna ◽  
Prognostic Evaluation ◽  
Functional Roles

Diabetic cardiovascular diseases (DCVDs) are the most common complications of diabetes mellitus and are considered to be one of the most important threats to global health and an economic burden. Long noncoding RNA (lncRNA), circular RNA (circRNA), and miRNA are a novel group of noncoding RNAs that are involved in the regulation of various pathophysiological processes, including DCVDs. Interestingly, both lncRNA and circRNA can act as competing endogenous RNA of miRNA, thereby regulating the expression of the target mRNA by decoying or sponging the miRNA. In this review, we focus on the mechanistic, pathological and functional roles of lncRNA/circRNA-miRNA-mRNA networks in DCVDs and further discuss the potential implications for early detection, therapeutic intervention and prognostic evaluation.

scholarly journals Long Noncoding RNA Plays a Key Role in Metastasis and Prognosis of Hepatocellular Carcinoma

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Guangbing Li ◽  
Haohai Zhang ◽  
Xueshuai Wan ◽  
Xiaobo Yang ◽  
Chengpei Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Regulation Of Gene Expression ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Comprehensive Review ◽  
Cellular Processes

Long noncoding RNAs (lncRNAs) have been attracting immense research interests. However, only a handful of lncRNAs had been thoroughly characterized. They were involved in fundamental cellular processes including regulation of gene expression at epigenetics as well as tumorogenesis. In this paper, we give a systematic and comprehensive review of existing literature about lncRNA involvement in hepatocellular carcinoma. This review exhibited that lncRNAs played important roles in tumorigenesis and subsequent prognosis and metastasis of hepatocellular carcinoma and elucidated the role of some specific lncRNAs such as MALAT1 and HOTAIR in the pathophysiology of hepatocellular carcinoma and their potential of being therapeutic targets.

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