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甘肃农业大学学报 2017年第1期52卷 7-12,20页

作者：孙业清庞云渭郝海生赵学明杜卫华朱化彬马友记甘肃农业大学动物科学技术学院甘肃兰州730070 中国农业科学院北京畜牧兽医研究所北京100193

【目的】研究Trx及其抑制因子txnip基因在牛卵母细胞及不同发育阶段体外受精胚胎中的表达变化.【方法】采用实时荧光定量PCR方法,检测牛GV期卵母细胞、MⅡ期卵母细胞、受精卵、2-4细胞胚胎、8-16细胞胚胎、桑椹胚和囊胚中Trx1、Trx2和TX... 详细信息

【目的】研究Trx及其抑制因子txnip基因在牛卵母细胞及不同发育阶段体外受精胚胎中的表达变化.【方法】采用实时荧光定量PCR方法,检测牛GV期卵母细胞、MⅡ期卵母细胞、受精卵、2-4细胞胚胎、8-16细胞胚胎、桑椹胚和囊胚中Trx1、Trx2和txnip基因mRNA的相对表达量.【结果】Trx1和Trx2基因在GV期卵母细胞和不同发育阶段的胚胎均有不同程度的表达.GV期卵母细胞Trx1mRNA表达量最高,随着卵母细胞的成熟及受精后胚胎的发育逐渐降低,囊胚期胚胎表达量又急速升高.Trx2基因在受精前的卵母细胞中高表达,受精后表达量逐渐下降,囊胚期胚胎Trx2 mRNA的表达量最低.内源性抑制因子txnip基因在2-4细胞胚胎阶段之前都是高表达,从8-16细胞胚胎阶段表达下降,在囊胚期胚胎表达量最低.【结论】牛卵母细胞及附植前胚胎自身的抗氧化能力在发育的不同阶段可能有所不同,而Trx1、Trx2及txnip基因在卵母细胞和不同发育阶段胚胎中的表达模式可能起到了重要的调控作用.

关键词：牛 Trx1 Trx2 txnip 胚胎表达体外试验

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Thioredoxin-interacting protein-activated intracellular potassium deprivation mediates the anti-tumour effect of a novel histone acetylation inhibitor HL23, a fangchinoline derivative, in human hepatocellular carcinoma

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JOURNAL OF ADVANCED RESEARCH 2023年 51卷 181-196页

作者： Lu, Yuanjun Liu, Yazhou Lan, Junjie Chan, Yau-Tuen Feng, Zixin Huang, Lan Wang, Ning Pan, Weidong Feng, Yibin Univ Hong Kong Sch Chinese Med Pok Fu Lam Hong Kong Peoples R China Guizhou Med Univ State Key Lab Funct & Applicat Med Plants Guiyang 550014 Peoples R China Key Lab Chem Nat Prod Guizhou Prov Guiyang 550014 Peoples R China Chinese Acad Sci Guiyang 550014 Peoples R China Chinese Acad Sci Chengdu Inst Biol Nat Prod Res Ctr Chengdu 610041 Peoples R China

Introduction: Hyperactivated histone deacetylases (HDACs) act as epigenetic repressors on gene transcription and are frequently observed in human hepatocellular carcinoma (HCC). Although multiple pharmacological HDAC inhibitors (HDACis) have been developed, none is available in human ***: To investigate the pharmacological effects of a fangchinoline derivative HL23, as a novel HDACi and its molecular mechanisms through txnip-mediated potassium deprivation in HCC. Methods: Both in vitro assays and orthotopic HCC mouse models were used to investigate the effects of HL23 in this study. The inhibitory activity of HL23 on HDACs was evaluated by in silico studies and cellular assays. Chromatin immunoprecipitation (ChIP) was conducted to confirm the regulation of HL23 on acetylation mark at txnip promoter. Genome-wide transcriptome analysis together with bioinformatic analysis were conducted to identify the regulatory mechanisms of HL23. The clinical significance of txnip and HDACs was evaluated by analysing publicly available ***: HL23 exerted compatible HDACs inhibition potency as Vorinostat (SAHA) while had superior anti-HCC effects than SAHA and sorafenib. Both in vitro and in vivo studies showed HL23 significantly suppressed HCC progression and metastasis. HL23 significantly upregulated txnip expression via regulating acetylation mark (H3K9ac) at txnip promoter. txnip was responsible for anti-HCC activity of HL23 through mediating potassium channel activity. HDAC1 was predicted to be the target of HL23 and HDAC1lowtxniphigh could jointly predict promising survival outcome of patients with HCC. Combination treatment with HL23 and sorafenib could significantly enhance sorafenib efficacy. Conclusion: Our study identified HL23 as a novel HDACi through enhancing acetylation at txnip promoter to trigger txnip-dependent potassium deprivation and enhance sorafenib efficacy in HCC treatment.(c) 2023 The Authors. Published by Elsevier B.V. on behalf of C

关键词： HDAC txnip Potassium deprivation Sorafenib Hepatocellular carcinoma

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NLRP3-mediated inflammation in cardio-oncology: sterile yet harmful

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TRANSLATIONAL RESEARCH 2023年 252卷 9-20页

作者： Mauro, Adolfo G. Mezzaroma, Eleonora Toldo, Stefano Melendez, Giselle C. Franco, R. Lee Lesnefsky, Edward J. Abbate, Antonio Hundley, W. Gregory Salloum, Fadi N. Virginia Commonwealth Univ Pauley Heart Ctr Dept Internal Med Cardiol Richmond VA USA Wake Forest Sch Med Dept Internal Med Dept Pathol Sect Cardiovasc MedSect Comparat Med Winston Salem NC USA Virginia Commonwealth Univ Coll Humanities & Sci Dept Kinesiol & Hlth Sci Richmond VA USA McGuire Vet Affairs Med Ctr Dept Med Serv Richmond VA USA Virginia Commonwealth Univ Pauley Heart Ctr 1101 East Marshall StRoom 7-070 Richmond VA 23298 USA Virginia Commonwealth Univ Div Cardiol Med & Physiol & Biophys Box 9802041101 East Marshall StRoom 7-070 Richmond VA 23298 USA

Despite significant advances and the continuous development of novel, effective therapies to treat a variety of malignancies, cancer therapy-induced cardiotoxicity has been identified as a prominent cause of morbidity and mortality, closely competing with secondary malignancies. This unfortunate limitation has prompted the incep-tion of the field of cardio-oncology with its purpose to provide the necessary knowledge and key information on mechanisms that support the use of the most efficacious cancer therapy with minimal or no interruption while paying close attention to preventing cardiovascular related morbidity and mortality. Several mechanisms that contribute to cancer therapy-induced cardiotoxicity have been proposed and studied. These mainly involve mito-chondrial dysfunction and reactive oxygen species-induced oxidative stress, lysosomal damage, impaired autoph-agy, cell senescence, DNA damage, and sterile inflammation with the formation and activation of the NLRP3 inflammasome. In this review, we focus on describing the principal mechanisms for different classes of cancer therapies that lead to cardiotoxicity involving the NLRP3 inflammasome. We also summarize current evidence of cardio-protection with inflammasome inhibitors in the context of heart disease in general, and further highlight the potential application of this evidence for clinical translation in at risk patients for the purpose of preventing cancer therapy associated cardiovascular morbidity and mortality.

关键词： AF Atrial fibrillation AICM Anthracycline-induced cardiomyopathy AKT Protein kinase B ALR AIM2-like receptor AMI Acute myocardial infarction ASC Apoptosis-associated speck-like protein containing a CARD domain BMDM Bone marrow-derived macrophages Ca 2+ Calcium CaMKIIδ Ca 2+/calmodulin-dependent protein kinase II δ CAPS Cryopyrin-associated periodic syndrome CARD Carboxy-terminal caspase recruitment domain CHF Congestive heart failure CVB3 Coxsackievirus B3 DAMPS Danger-associated molecular patterns DOX Doxorubicin EGFR Epidermal-grow factor receptor ER Endoplasmic reticulum FDA Food and Drug Administration FGFR Fibroblast grow factor receptor GDP Guanosine diphosphate GSDMD Gasdermin D H 2S Hydrogen sulfide HER2 Human epidermal growth factor receptor 2 HFpEF Heart failure with preserved ejection fraction HFrEF Heart failure with reduced ejection fraction ICI Immune checkpoint inhibitor IKKβ Inhibitor for kappa B kinase β IL-18 Interleukin-18 IL-1Ra Recombinant IL-1 receptor antagonist IL-1RI Interleukin-1 receptor type I IL-1β Interleukin-1β K + Potassium LDLR Low-density lipoprotein receptor LRR Leucine-rich repeats LV Left ventricular LVEF Left ventricular ejection fraction MAPK Mitogen-activated protein kinase mtDNA Mitochondrial DNA Na 2S Sodium sulfide NaHS Sodium hydrosulfide NEK NIMA-related kinases proteins NF-kB Nuclear factor kappa-light-chain-enhancer of activated B cells NLR (NOD)-like receptors NLRP3 Nod-like receptor protein 3 NOD Nucleotide-binding and oligomerization domain NRTK Non-receptor tyrosine kinase NTproBNP N-terminal-pro hormone B-type natriuretic peptide PAMPS Pathogen-associated molecular patterns PDGFR Platelet-derived grow factor receptor PI3K Phosphoinositide 3 Kinase PRR Pattern recognition receptor PYD Pyrin domain RAGE Receptor for advanced glycation end-products ROS Reactive oxygen species RT Radiation therapy RTK Receptor tyrosine kinases SGLT2 Sodium-glucose Cotransporter-2 TK Tyrosine kinases TKI Tyrosine kinase inhibitors TLR Toll-like receptors txnip Thioredoxin-interacting

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Structural basis for the regulatory role of the PPxY motifs in the thioredoxin-interacting protein txnip

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BIOCHEMICAL JOURNAL 2016年第2期473卷 179-187页

作者： Liu, Yanli Lau, Johnathan Li, Weiguo Tempel, Wolfram Li, Li Dong, Aiping Narula, Ashrut Qin, Su Min, Jinrong Cent China Normal Univ Coll Life Sci Hubei Key Lab Genet Regulat & Integrat Biol Wuhan 430079 Peoples R China Univ Toronto Struct Genom Consortium 101 Coll St Toronto ON M5G 1L7 Canada Cent China Normal Univ Coll Chem Key Lab Pesticide & Chem Biol Wuhan 430079 Peoples R China South Univ Sci & Technol China Mat Characterizat & Preparat Ctr Shenzhen 518055 Peoples R China South Univ Sci & Technol China Life Sci Res Ctr Shenzhen 518055 Peoples R China Univ Toronto Dept Physiol Med Sci Bldg Toronto ON M5S 1A8 Canada

txnip (thioredoxin-interacting protein) negatively regulates the antioxidative activity of thioredoxin and participates in pleiotropic cellular processes. Its deregulation is linked to various human diseases, including diabetes, acute myeloid leukaemia and cardiovascular diseases. The E3 ubiquitin ligase Itch (Itchy homologue) polyubiquitinates txnip to promote its degradation via the ubiquitin-proteasome pathway, and this Itch-mediated polyubiquitination of txnip is dependent on the interaction of the four WW domains of Itch with the two PPxY motifs of txnip. However, the molecular mechanism of this interaction of txnip with Itch remains elusive. In the present study, we found that each of the four WW domains of Itch exhibited different binding affinities for txnip, whereas multivalent engagement between the four WW domains of Itch and the two PPxY motifs of txnip resulted in their strong binding avidity. Our structural analyses demonstrated that the third and fourth WW domains of Itch were able to recognize both PPxY motifs of txnip simultaneously, supporting a multivalent binding mode between Itch and txnip. Interestingly, the phosphorylation status on the tyrosine residue of the PPxY motifs of txnip serves as a molecular switch in its choice of binding partners and thereby downstream biological signalling outcomes. Phosphorylation of this tyrosine residue of txnip diminished the binding capability of PPxY motifs of txnip to Itch, whereas this phosphorylation is a prerequisite to the binding activity of txnip to SHP2 [SH2 (Src homology 2) domain-containing protein tyrosine phosphatase 2] and their roles in stabilizing the phosphorylation and activation of CSK (c-Src tyrosine kinase).

关键词： Itch phosphotyroine PPxY motifs SHP2 txnip

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Potential Mechanisms and Effects of Chinese Medicines in Treatment of Diabetic Atherosclerosis by Modulating NLRP3 Inflammasome:A Narrative Review

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Chinese Journal of Integrative Medicine 2022年第8期28卷 753-761页

作者： YUAN Jia-yao FU Yu FENG Zhi-hai SANG Feng SHAO Ming-yi LI Lei-lei School of First Clinical Henan University of Chinese MedicineZhengzhou450000China Department of Endocrinology The First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou450000China Department of Key Laboratory of Viral Diseases Prevention and Treatment of Traditional Chinese Medicine of Henan Province The First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou450000China Department of Gastroenterology The First Affiliated Hospital of Henan University of Chinese MedicineZhengzhou450000China

Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3)is an intracellular sensor that detects endogenous danger signals and environmental irritants to assemble into the NLRP3 *** of the NLRP3 inflammasome leads to the secretion of the proinflammatory cytokines interleutkin(IL)-1β and IL-18 and induces *** studies have shown that the NLRP3 inflammasome participates in the initiation and progression of diabetic atherosclerosis through pathological mechanisms such as β-cell dysfunction,insulin resistance,endothelial cell dysfunction,monocyte adhesion and infiltration,and smooth muscle cell proliferation and *** diabetic atherosclerosis,Chinese medicine has been proven effective for the inflammatory response mediated by the NLRP3 *** review summarizes the latest progress on the NLRP3 inflammasome in the pathogenesis and potential Chinese medicine treatment of diabetic atherosclerosis.

关键词： Chinese medicine diabetic atherosclerosis NLRP3 inflammasome interleukin-1β txnip pyroptosis

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Melatonin alleviates cadmium-induced liver injury by inhibiting the txnip-NLRP3 inflammasome

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JOURNAL OF PINEAL RESEARCH 2017年第3期62卷 n/a-N.PAG页

作者： Cao, Zhengwang Fang, Yiliang Lu, Yonghui Tan, Dunxian Du, Changhong Li, Yuming Ma, Qinlong Yu, Junmei Chen, Mengyan Zhou, Chao Pei, Liping Zhang, Lei Ran, Haiying He, Mindi Yu, Zhengping Zhou, Zhou Third Mil Med Univ Dept Occupat Hlth Chongqing Peoples R China Univ Texas Hlth Sci Ctr Dept Cellular & Struct Biol San Antonio TX USA Chongqing Engn Res Ctr Nanomedicine Third Mil Med Univ Inst Combined Injury State Key Lab Trauma Chongqing Peoples R China Third Mil Med Univ Inst Hepatobiliary Surg XinQiao Hosp Chongqing Peoples R China Third Mil Med Univ Biomed Anal Ctr Chongqing Peoples R China Guangxi Univ Sch Med Dept Occupat Hlth Nanning Peoples R China Third Mil Med Univ Dept Occupat Hlth Chongqing Peoples R China

Cadmium (Cd) is a persistent environmental and occupational contaminant that -accumulates in the liver and induces oxidative stress and inflammation. Melatonin possesses potent hepatoprotective properties against the development and progression of acute and chronic liver injury. Nevertheless, the molecular mechanism underlying the protective effects of melatonin against Cd-induced hepatotoxicity remains obscure. In this study, we aimed to investigate the effects of melatonin on Cd-induced liver inflammation and hepatocyte death. Male C57BL/6 mice were intraperitoneally injected with melatonin (10 mg/kg) once a day for 3 days before exposure to CdCl2 (2.0 mg/kg). We found that Cd induced hepatocellular damage and inflammatory infiltration as well as increased serum ALT/AST enzymes. In addition, we showed that Cd triggered an inflammatory cell death, which is mediated by the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, melatonin treatment significantly alleviated Cd-induced liver injury by decreasing serum ALT/ AST levels, suppressing pro-inflammatory cytokine production, inhibiting NLRP3 inflammasome activation, ameliorating oxidative stress, and attenuating hepatocyte death. Most importantly, melatonin markedly abrogated Cd-induced txnip overexpression and decreased the interaction between txnip and NLRP3 in vivo and in vitro. However, treatment with siRNA targeting txnip blocked the protective effects of melatonin in Cd-treated primary hepatocytes. Collectively, our results suggest that melatonin confers protection against Cd-induced liver inflammation and hepatocyte death via inhibition of the txnip-NLRP3 inflammasome pathway.

关键词： cadmium liver injury melatonin NLRP3 inflammasome txnip

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Cytokines Regulate β-Cell Thioredoxin-interacting Protein (txnip) via Distinct Mechanisms and Pathways

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JOURNAL OF BIOLOGICAL CHEMISTRY 2016年第16期291卷 8428-8439页

作者： Hong, Kyunghee Xu, Guanlan Grayson, Truman B. Shalev, Anath Univ Alabama Birmingham Comprehens Diabet Ctr 1825 Univ BlvdSHEL 1206 Birmingham AL 35294 USA Univ Alabama Birmingham Dept Med Div Endocrinol Diabet & Metab 1825 Univ BlvdSHEL 1206 Birmingham AL 35294 USA

Thioredoxin-interacting protein (txnip) is a key regulator of diabetic beta-cell apoptosis and dysfunction, and txnip inhibition prevents diabetes in mouse models of type 1 and type 2 diabetes. Although we have previously shown that txnip is strongly induced by glucose, any regulation by the proinflammatory cytokines tumor necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), and interferon gamma (IFN gamma) has remained largely unexplored. Moreover, even though this three-cytokine mixture is widely used to mimic type 1 diabetes in vitro, the mechanisms involved are not fully understood. Interestingly, we have now found that this cytokine mixture increases beta-cell txnip expression;however, although TNF alpha had no effect, IL-1 beta surprisingly down-regulated txnip transcription, whereas IFN gamma increased txnip levels in INS-1 beta-cells and primary islets. Human txnip promoter analyses and chromatin immunoprecipitation studies revealed that the IL-1 beta effect was mediated by inhibition of carbohydrate response element binding protein activity. In contrast, IFN gamma increased pro-apoptotic txnip post-transcriptionally via induction of endoplasmic reticulum stress, activation of inositol-requiring enzyme 1 alpha (IRE1 alpha), and suppression of miR-17, a microRNA that targets and down-regulates txnip. In fact, miR-17 knockdown was able to mimic the IFN gamma effects on txnip, whereas miR-17 overexpression blunted the cytokine effect. Thus, our results demonstrate for the first time that the proinflammatory cytokines TNF alpha, IL-1 beta, and IFN gamma each have distinct and in part opposing effects on beta-cell txnip expression. These findings thereby provide new mechanistic insight into the regulation of txnip and beta-cell biology and reveal novel links between proinflammatory cytokines, carbohydrate response element binding protein-mediated transcription, and microRNA signaling.

关键词： beta cell (B-cell) cytokine microRNA (miRNA) pancreatic islet type 1 diabetes txnip

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Verapamil Inhibits Ser202/Thr205 Phosphorylation of Tau by Blocking txnip/ROS/p38 MAPK Pathway

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Pharmaceutical research 2018年第2期35卷 44页

作者： Mariarosa Anna Beatrice Melone Clemente Dato Simona Paladino Cinzia Coppola Claudia Trebini Maria Teresa Giordana Lorena Perrone Department of Medical Surgical Neurological Metabolic Sciences and Aging Second Division of Neurology Center for Rare Neurological e Neuromuscular Diseases and Interuniversity Center for Research in Neurosciences University of Campania Luigi Vanvitelli 80100 Naples Italy. Dipartimento di Medicina Molecolare e Biotecnologie Mediche Università degli Studi di Napoli Federico II 80100 Naples Italy. Department of Neuroscience University Hospital San Giovanni Battista di Torino 10126 Molinette Italy. Universite´Grenoble Alpes Grenoble France. perronelorena1@***. DKFZ Department of Functional and Structural Genomics Heidelberg Germany. perronelorena1@***.

PURPOSE:Oxidative stress is a hallmark of Alzheimer's Disease (AD) and promotes tau phosphorylation. Since Thioredoxin Interacting protein (txnip), the inhibitor of the anti-oxidant system of Thioredoxin, is up regulated in the hippocampus of AD patients, we investigated whether txnip plays a role in promoting tau phosphorylation and whether Verapamil, an inhibitor of txnip expression, prevents txnip downstream effects. METHODS:We analyzed txnip expression and tau phosphorylation in the hippocampus of the 5xFAD mice in the absence and presence of a pharmacological treatment with Verapamil. Using SH-SY5Y cells, we verified the causative role of txnip in promoting tau phosphorylation at Ser202/Thr205, by inducing txnip silencing. RESULTS:The amyloid beta peptide (Aβ) leads to txnip over-expression in SH-SY5Y cells, which in turns induces oxidative stress and the activation of p38 MAPK, promoting tau phosphorylation at Ser202/Thr205. Silencing of txnip abolishes Aβ-induced tau phosphorylation, p38 MAPK phosphorylation and subsequent tau phosphorylation. Verapamil prevents txnip expression as well as p38 MAPK and tau phosphorylation at Ser202/Thr205 in the hippocampus of the 5xFAD mice. CONCLUSIONS:Our study unveil a novel pathway involved in AD progression that is inhibited by Verapamil, shedding new light on the understanding of the therapeutic potential of Verapamil in AD.

关键词： Alzheimer’s disease Neuron Oxidative stress txnip Tau phosphorylation Verapamil p38 MAPK

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Structural basis for a novel interaction between txnip and Vav2

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FEBS LETTERS 2016年第6期590卷 857-865页

作者： Liu, Shasha Wu, Xue Zong, Minru Tempel, Wolfram Loppnau, Peter Liu, Yanli Cent China Normal Univ Coll Life Sci Hubei Key Lab Genet Regulat & Integrat Biol Wuhan 430079 Peoples R China Jilin Univ China Japan Union Hosp Changchun 130023 Peoples R China Univ Toronto Struct Genom Consortium 101 Coll St Toronto ON M5G 1L7 Canada

Thioredoxin-interacting protein (txnip) is a multifunctional protein involved in diverse cellular processes such as cell proliferation and apoptosis. txnip stability is controlled by the ubiquitin-proteasome pathway, and the E3 ubiquitin ligase Itch directly interacts with txnip via PPxY motifs of txnip. In a previously published study, we have shown that phosphorylation of the PPxY tyrosyl residue switches txnip selectivity between different binding partners. Here, we describe that tyrosine-phosphorylated PPxY motifs also bind to SH2 domains of Vav2 and Src with dissociation constants around 10 mu M and that phosphorylation is indispensable for these interactions as well. The crystal structure of the complex between a phosphorylated PPxY motif, and the SH2 domain of Vav2 reveals a conserved recognition mechanism.

关键词： SH2 domain txnip Tyrosine-phosphorylated PPxY motif Vav2

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MicroRNA-20a negatively regulates expression of NLRP3-inflammasome by targeting txnip in adjuvant-induced arthritis fibroblast-like synoviocytes

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JOINT BONE SPINE 2016年第6期83卷 695-700页

作者： Li, Xiao-Feng Shen, Wen-Wen Sun, Ying-Yin Li, Wan-Xia Sun, Zheng-Hao Liu, Yan-Hui Zhang, Lei Huang, Cheng Meng, Xiao-Ming Li, Jun Anhui Med Univ Anhui Key Lab Bioact Nat Prod Sch Pharm Meishan Rd 81 Hefei 230032 Peoples R China Anhui Med Univ Inst Liver Dis Meishan Rd 81 Hefei 230032 Peoples R China Anhui Inst Innovat Drugs Meishan Rd 81 Hefei 230032 Peoples R China

Objectives: Rheumatoid arthritis (RA) is a heterogenic and systemic autoimmune disease characterized by synovitis and joint structural damage. However, the pathogenesis of RA is still obscure. It has been reported microRNA-20a (miRNA-20a) was significantly associated with the regulation of pro inflammatory cytokines release in RA FLS. The purpose of this study was to explore the function and underlying mechanisms of miRNA-20a on NLRP3-inflammasome in adjuvant-induced arthritis (AA) fibroblast-like synoviocytes (FLSs) in vitro. Methods: In this study, using a combination of Western blotting, Q-PCR, and ELISA analysis, we investigated the influence and function of miRNA-20a on NLRP3-inflammasome by targeting txnip in AA FLSs. Results: In the present study, the expression of NLRP3-inflammasome was significant up-regulated in AA model in vitro. Our study indicated that silence of NLRP3 down-regulated the expression of NLRP3-inflammasome and the secretion of IL-1 beta and MMP-1. Moreover, over-expression of miR-20a decreased formation of NLRP3-inflammasome, including NLRP3, ASC and caspase-1, and suppressed the secretion of IL-1 beta and MMP-1, along with down-regulated the expressions of txnip in primary FLSs isolated from AA. With the combined use of prediction programs and luciferase assay, the rat txnip mRNA 3'UTR predicted to be targeted by miR-20a. Similarly, inhibitor txnip expression by txnip-siRNA markedly repressed formation of NLRP3-inflammasome and the secretion of IL-1 beta and MMP-1. Conclusion: Taken together, these results indicate that miR-20a may play a pivotal role in the NLRP3-inflammasome by targeted inhibit txnip expression in AA FLSs. (C) 2016 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.

关键词： MicroRNA-20a txnip NLRP3-inflammasome RA

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