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Corrigendum to“3Cpro of FMDV inhibits type II interferon-stimulated JAK-stat signaling pathway by blocking STAT1 nuclear translocation”[Virol Sin 38(2023)387–397]

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Virologica Sinica 2024年第2期39卷 351-354页

作者： Xiangju Wu Lei Chen Chao Sui Yue Hu Dandan Jiang Fan Yang Laura C.Miller Juntong Li Xiaoyan Cong Nataliia Hrabchenko Changhee Lee Yijun Du Jing Qi Shandong Key Laboratory of Animal Disease Control and Breeding Key Laboratory of Livestock and Poultry Multi-omics of MARAInstitute of Animal Science and Veterinary MedicineInstitute of Crop Germplasm ResourcesShandong Academy of Agricultural SciencesJinan250100China College of Life Science Shandong Normal UniversityJinan250358China state Key Laboratory of Veterinary Etiological Biology National Foot and Mouth Disease Reference LaboratoryKey Laboratory of Animal Virology of Ministry of AgricultureLanzhou Veterinary Research InstituteChinese Academy of Agricultural SciencesLanzhou730050China Department of Diagnostic Medicine and Pathobiology College of Veterinary MedicineKansas State UniversityManhattanKS66506USA College of Veterinary Medicine and Virus Vaccine Research Center Gyeongsang National UniversityJinju52828Republic of Korea

Due to our negligence,the original version of this article,published online on Mar 14,2023,contained some mistakes in several Figs.In Fig.2D,the positions of the bands for protein 3A and 3B were incorrectly shifted.Th... 详细信息

关键词： STAT1 FMDV bands

3C^(pro)of FMDV inhibits type II interferon-stimulated JAK-stat signaling pathway by blocking STAT1 nuclear translocation

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Virologica Sinica 2023年第3期38卷 387-397页

作者： Xiangju Wu Lei Chen Chao Sui Yue Hu Dandan Jiang Fan Yang Laura C.Miller Juntong Li Xiaoyan Cong Nataliia Hrabchenko Changhee Lee Yijun Du Jing Qi Shandong Key Laboratory of Animal Disease Control and Breeding/Key Laboratory of Livestock and Poultry Multi-omics of MARA Institute of Animal Science and Veterinary MedicineInstitute of Crop Germplasm ResourcesShandong Academy of Agricultural SciencesJinan250100China College of Life Science Shandong Normal UniversityJinan250358China state Key Laboratory of Veterinary Etiological Biology/National Foot and Mouth Disease Reference Laboratory/Key Laboratory of Animal Virology of Ministry of Agriculture Lanzhou Veterinary Research InstituteChinese Academy of Agricultural SciencesLanzhou730050China Department of Diagnostic Medicine and Pathobiology College of Veterinary MedicineKansas State UniversityManhattanKS66506USA College of Veterinary Medicine and Virus Vaccine Research Center Gyeongsang National UniversityJinju52828Republic of Korea

Foot-and-mouth disease virus(FMDV)has developed various strategies to antagonize the host innate immunity.FMDV Lpro and 3Cpro interfere with type I IFNs through different mechanisms.The structural protein VP3 of FMDV degrades Janus kinase 1 to suppress IFN-γsignaling transduction.Whether non-structural proteins of FMDV are involved in restraining type II IFN signaling pathways is unknown.In this study,it was shown that FMDV replication was resistant to IFN-γtreatment after the infection was established and FMDV inhibited type II IFN induced expression of IFN-γ-stimulated genes(ISGs).We also showed for the first time that FMDV non-structural protein 3C antagonized IFN-γ-stimulated JAK-stat signaling pathway by blocking STAT1 nuclear translocation.3C^(pro)expression significantly reduced the ISGs transcript levels and palindromic gamma-activated sequences(GAS)promoter activity,without affecting the protein level,tyrosine phosphorylation,and homodimerization of STAT1.Finally,we provided evidence that 3C protease activity played an essential role in degrading KPNA1 and thus inhibited ISGs mRNA and GAS promoter activities.Our results reveal a novel mechanism by which an FMDV non-structural protein antagonizes host type II IFN signaling.

关键词： Foot-and-mouth disease virus(FMDV) 3C IFN-γ JAK-stat signaling pathway STAT1 KPNA1

Esculetin protects against early sepsis via attenuating inflammation by inhibiting NF-κB and STAT1/stat3 signaling

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Chinese Journal of Natural Medicines 2021年第6期19卷 432-441页

作者： CHENG Yao-Jun TIAN Xin-Lei ZENG Ya-Zhi LAN Nan GUO Ling-Feng LIU Ke-Feng FANG Hui-Long FAN Hong-Ye PENG Zhong-Lu Key Laboratory of Universities in Hunan Province on Cardiovascular and Cerebrovascular Natural Drugs Research Xiangnan UniversityChenzhou 423000China state Key Laboratory of Natural Medicines School of Life Science and TechnologyChina Pharmaceutical UniversityNanjing 210009China

Esculetin,a natural derivative from the traditional and widely-used Chinese medicinal herb Cortex Fraxini,has a variety of pharmacological effects,especially in anti-inflammation.However,it is not clear whether esculetin has a therapeutic effect on sepsis.This study aimed to investigate the anti-inflammatory and protective effects of esculetin on early sepsis.The results showed that the lung injury was significantly relieved with the treatment of esculetin,accompanied with the restrained production of inflammatory factors including IL-1β,IL-6,TNF-α,CCL2 and iNOS during the early phase of E.coli-induced sepsis.Of note,activation of NF-κB and STAT1/stat3 signals,the main upstream signals of many inflammatory factors,were attenuated by esculetin in both lung tissues from septic mice and LPS-stimulated macrophage.These findings suggested that the protection of esculetin against early sepsis should be related to its anti-inflammatory effect,which was at least partly due to its inhibition on NF-κB and STAT1/stat3 signaling pathway in macrophage.Thus,esculetin could serve as a potential therapeutic agent by rebalancing innate immune response in macrophage for the treatment of early sepsis.

关键词： Esculetin NF-κB STAT1 stat3 Early sepsis

IFN-β通过STAT1诱导SARI表达抑制AML细胞增殖及促进凋亡

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中国免疫学杂志 2022年

作者：林艳凤洪小颖黄莹莹王小花吴玮林东红薛龑福建医科大学医学技术与工程学院

目的：探讨IFN-β诱导SARI表达对AML细胞增殖、凋亡的作用，并筛选其潜在的调控分子。方法：qPCR、Western blot筛选SARI低表达的AML细胞作为实验细胞株；以不同浓度IFN-β干预AML细胞，于不同时间采用qPCR、Western blot检测SARI表达... 详细信息

目的：探讨IFN-β诱导SARI表达对AML细胞增殖、凋亡的作用，并筛选其潜在的调控分子。方法：qPCR、Western blot筛选SARI低表达的AML细胞作为实验细胞株；以不同浓度IFN-β干预AML细胞，于不同时间采用qPCR、Western blot检测SARI表达，选取IFN-β作用的适当浓度和时间；采用RNA-Seq转录组测序及KEGG富集分析，初步筛选IFN-β诱导AML细胞SARI表达的潜在调控分子；通过相应分子抑制剂联合IFN-β处理AML细胞，MTS法检测细胞增殖，流式细胞术检测细胞凋亡；明确该分子参与IFN-β诱导SARI表达对AML细胞增殖及凋亡作用。结果：HL60和NB4细胞的SARI表达量相对较低，选为实验细胞株；1ng/ml IFN-β作用12h后AML细胞SARI表达增高且细胞增殖抑制、凋亡增多；筛选STAT1为IFN-β诱导SARI表达潜在调控分子；抑制STAT1后，IFN-β对AML细胞SARI表达、增殖抑制、凋亡促进的作用被明显逆转。结论：IFN-β可通过STAT1诱导AML细胞的SARI表达，抑制细胞增殖，促进细胞凋亡。

关键词： IFN-β SARI STAT1 AML 增殖及凋亡

抑制GRK2异常转膜控制JAK1-STAT1信号转导减少CIA小鼠树突状细胞的成熟

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中国药理学通报 2022年第6期38卷 832-841页

作者：张春梅斯梦刘潇一杨雪枝姜玲魏伟安徽医科大学临床药理研究所、抗炎免疫药物教育部重点实验室、抗炎免疫药物安徽协同创新中心、安徽医科大学类风湿关节炎研究中心安徽合肥230032

目的G蛋白偶联受体激酶2(G protein-coupled receptor kinase 2,GRK2)异常活化和JAK1-STAT1信号转导异常参与类风湿关节炎(rheumatoid arthritis,RA)的免疫异常反应,但两者关系不清。该文研究了GRK2对胶原性关节炎(collagen-induced arthritis,CIA)小鼠树突状细胞(dendritic cells,DCs)JAK1-STAT1信号通路的作用和机制,为揭示RA的新机制提供依据。方法建立CIA模型,流式细胞术检测DCs共刺激分子水平,ELISA检测小鼠血浆细胞因子水平,免疫组化法检测脾脏组织中p-JAK1、p-STAT1、GRK2的表达。体外用骨髓细胞诱导成DCs,IFN-α和PGE2刺激48 h。流式细胞术检测DCs共刺激分子水平和吞噬能力,ELISA检测细胞上清中细胞因子水平。CO-IP法检测DCs中GRK2和JAK1共定位。Western blot法检测JAK1、STAT1、胞膜GRK2表达。成像流式细胞术检测p-STAT1入核率。结果CIA小鼠中DCs共刺激分子水平升高,脾脏中GRK2与p-JAK1、p-STAT1的表达呈正相关,且CIA组脾脏中GRK2与JAK1共定位明显下降。体外实验表明,GRK2抑制剂降低DCs共刺激分子表达、IL-6和TNF-α水平,JAK1、STAT1表达、GRK2胞膜表达、p-STAT1入核,增加DCs吞噬功能及GRK2与JAK1的共定位。结论DCs中GRK2转膜异常,介导了DCs的成熟和JAK1-STAT1信号通路活化,抑制GRK2转膜可恢复其对DCs的JAK1-STAT1信号转导的控制,减少DCs的成熟,在改善小鼠CIA中发挥重要作用。

关键词：树突状细胞 G蛋白偶联受体激酶2 JAK1 STAT1 IFN-α PGE2

Interactome profiling reveals interaction of SARS-CoV-2 NSP13 with host factor STAT1 to suppress interferon signaling

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Journal of Molecular Cell Biology 2021年第10期13卷 760-762页

作者： Kuan Feng Yuan-Qin Min Xiulian Sun Fei Deng Peiqing Li Hualin Wang Yun-jia Ning state Key Laboratory of Virology Wuhan Institute of VirologyChinese Academy of SciencesWuhan 430071China Department of Pediatric Emergency Guangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangzhou 510623China Center for Biosafety Mega-Science Chinese Academy of SciencesWuhan A30071China

Dear Editor,The on-going coronavirus disease 2019(COVID-19)pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)has resulted in u叩rece-dented medical and socioeconomic disruption globally.As of late September 2021,over 231 million confirmed cases have been reported worldwide.Although the viral pathogenesis remains largely unclear,impairment of interferon(IFN)responses likely contributes to disease progression and severity(Blanco-Melo et al.,2020;Meffre and Iwasaki,2020;Min et al.,2021).Indeed,several viral proteins are potential regulators of the IFN system(Min et al.,2021).However,the underlying mechanisms employed by SARS-CoV-2 IFN antagonist candidates,such as nonstructural protein 13(NSP13),still need to be determined.

关键词： NSP1 STAT1 al.

STAT1在PPARγ活化后抑制结核分枝杆菌感染巨噬细胞炎症反应中的作用

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免疫学杂志 2022年第9期38卷 768-774页

作者：刘冬梅彭少君韩晓群郑文昊陈嘉敏王烈浩刘云辉娄晓杰宜春学院化学与生物工程学院 336000 宜春学院医学院 336000

目的探讨STAT1在激活过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptorγ,PPARγ)后抑制结核分枝杆菌(Mycobacterium tuberculosis,MTB)感染巨噬细胞炎症反应中的作用。方法人单核细胞系THP-1细胞成功诱导分化为巨噬细胞后,建立结核分枝杆菌毒株H37Rv细胞感染模型,将细胞随机分为:1)Control组;2)PPARγ激动剂罗格列酮(Rosiglitazone,ROZ)组;3)PPARγ拮抗剂GW9662组;4)MTB感染组;5)MTB+ROZ组;6)MTB+GW9662组,分组干预48 h。采用ELISA法测定各组细胞上清液TNF-α、IL-6和IL-10的表达水平;CFU测定各组细菌负荷量;CCK-8法检测各组巨噬细胞增殖率情况;RT-PCR法检测细胞内PPARγ和磷酸化STAT1 mRNA表达水平;Western blotting法检测细胞内PPARγ和磷酸化STAT1蛋白水平。结果与对照组相比,激动剂ROZ组PPARγ、IL-10和巨噬细胞增殖率有所上调(P>0.05),TNF-α、IL-6和磷酸化STAT1则下调(P>0.05),拮抗剂GW9662组与之相反(P>0.05);而MTB感染各组中PPARγ、TNF-α、IL-6和IL-10的表达显著升高(P1),磷酸化STAT1和巨噬细胞增殖率明显降低(P10含量有所升高(P1),而TNF-α、IL-6、磷酸化STAT1和巨噬细胞增殖率则明显降低(PSTAT1表达,进而抑制巨噬细胞炎症反应,促进MTB的存活、复制,最终降低巨噬细胞增殖率。

关键词：结核分枝杆菌巨噬细胞 PPARγ STAT1 炎症

Di(2-ethylhexyl) phthalate Disorders Lipid Metabolism via TYK2/STAT1 and Autophagy in Rats

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Biomedical and Environmental Sciences 2019年第6期32卷 406-418页

作者： ZHANG Yue Zhu ZHANG Zhao Ming ZHOU Li Ting ZHU Jian ZHANG Xiao Han QI Wen DING Shuang XU Qi HAN Xu ZHAO Ya Ming SONG Xin Yue ZHAO Tian Yang YE Lin Department of Occupational and Environmental Health School of Public Health Jilin University

Objective Previous studies have indicated that the plasticizer di(2-ethylhexyl) phthalate(DEHP) affects lipid accumulation;however, its underlying mechanism remains unclear. We aim to clarify the effect of DEHP on lipid metabolism and the role of TYK2/STAT1 and autophagy. Methods In total, 160 Wistar rats were exposed to DEHP [0, 5, 50, 500 mg/(kg·d)] for 8 weeks. Lipid levels, as well as mRNA and protein levels of TYK2, STAT1, PPARγ, AOX, FAS, LPL, and LC3 were detected. Results The results indicate that DEHP exposure may lead to increased weight gain and altered serum lipids. We observed that DEHP exposure affected liver parenchyma and increased the volume or number of fat cells. In adipose tissue, decreased TYK2 and STAT1 promoted the expression of PPARγ and FAS. The mRNA and protein expression of LC3 in 50 and 500 mg/(kg·d) groups was increased significantly. In the liver, TYK2 and STAT1 increased compensatorily;however, the expression of FAS and AOX increased, while LPL expression decreased. Joint exposure to both a high-fat diet and DEHP led to complete disorder of lipid metabolism. Conclusion It is suggested that DEHP induces lipid metabolism disorder by regulating TYK2/STAT1. Autophagy may play a potential role in this process as well. High-fat diet, in combination with DEHP exposure, may jointly have an effect on lipid metabolism disorder.

关键词： DEHP TYK2 STAT1 High-fat diet Autophagy Lipid metabolism

High salt diet accelerates the progression of murine lupus through dendritic cells via the p38 MAPK and STAT1 signaling pathways

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Signal Transduction and Targeted Therapy 2020年第1期5卷 2082-2094页

作者： Ze Xiu Xiao Xiaojiang Hu Ximei Zhang Zhigang Chen Julie Wang Ke Jin Feng Lin Cao Baoqing Sun Joseph A.Bellanti Nancy Olsen Song Guo Zheng Department of Clinical Immunology The Third Affiliated Hospital at Sun Yat-sen University510630 GuangzhouChina Department of Internal Medicine Ohio State University College of Medicine and Wexner Medical CenterColumbusOH 43210USA Department of Medicine Penn State College of MedicineHersheyPA 17033USA Laboratory of Human Diseases and Immunotherapy West China HospitalSichuan UniversityChengduChina Department of Internal Medicine The First Hospital of Harbin Medical UniversityHarbinChina Department of Allergy and Clinical Immunology The First Affiliated Hospital of Guangzhou Medical UniversityGuangzhouChina Department of Pediatrics and Microbiology-Immunology Georgetown University Medical CenterWashingtonDCUSA

The increased incidence of systemic lupus erythematosus(SLE)in recent decades might be related to changes in modern dietary habits.Since sodium chloride(NaCl)promotes pathogenic T cell responses,we hypothesize that excessive salt intake contributes to the increased incidence of autoimmune diseases,including SLE.Given the importance of dendritic cells(DCs)in the pathogenesis of SLE,we explored the influence of an excessive sodium chloride diet on DCs in a murine SLE model.We used an induced lupus model in which bone marrow-derived dendritic cells(BMDCs)were incubated with activated lymphocyte-derived DNA(ALD-DNA)and transferred into C57BL/6 recipient mice.We observed that a high-salt diet(HSD)markedly exacerbated lupus progression,which was accompanied by increased DC activation.NaCl treatment also stimulated the maturation,activation and antigenpresenting ability of DCs in vitro.Pretreatment of BMDCs with NaCl also exacerbated BMDC-ALD-DNA-induced lupus.These mice had increased production of autoantibodies and proinflammatory cytokines,more pronounced splenomegaly and lymphadenopathy,and enhanced pathological renal lesions.The p38 MAPK–STAT1 pathway played an important role in NaClinduced DC immune activities.Taken together,our results demonstrate that HSD intake promotes immune activation of DCs through the p38 MAPK–STAT1 signaling pathway and exacerbates the features of SLE.Thus,changes in diet may provide a novel strategy for the prevention or amelioration of lupus or other autoimmune diseases.

关键词： STAT1 lupus prevention