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Infection-stimulated Anemia Results Primarily from Interferon Gamma-dependent, signal transducer and activator of transcription 1-independent Red Cell Loss

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Chinese Medical Journal 2015年第7期128卷 948-955页

作者： Zheng Wang Dong-Xia Zhang Qi Zhao Department of Pediatric Surgery General Hospital of Chinese People's Liberation Army Beijing 100037 China Department of Immunology Yuhuangding Hospital Yantai Shandong 264000 China

Background： Although the onset of anemia during infectious disease is commonly correlated with production of inflammatory cytokines, the mechanisms by which cytokines induce anemia are poorly defined. This study focused on the mechanism research. Methods： Different types of mice were infected perorally with Toxoplasma gondii strain ME49. At the indicated times, samples fi＇om each mouse were harvested, processed, and analyzed individually. Blood samples were analyzed using a Coulter Counter and red blood cell （RBC） survival was measured by biotinylation. Levels of tumor necrosis factor-α （TNF-α）, inducible nitric oxide synthase （iNOS）, and inducible protein 10 （IP-10） mRNA in liver tissue were measured by real-time polymerase chain reaction. Results： T. gondii-infected mice exhibited anemia due to a decrease in both erythropoiesis and survival time of RBC in the circulation （P 〈 0.02）. In addition, infection-stimulated anemia was associated with fecal occult, supporting previous literature that hemorrhage is a consequence of T. gondii infection in mice. Infection-induced anemia was abolished in interferon gamma （IFNy） and I FNy receptor deficient mice （P 〈 0.05） but was still evident in mice lacking TNF-α, iNOS, phagocyte NADPH oxidase or IP-10 （P 〈 0.02）. Neither signal transducer and activator of transcription 1 （STAT1） deficient mice nor 129S6 controls exhibited decreased erythropoiesis, but rather suffered from an anemia resulting solely from increased loss of circulating RBC. Conclusions： Infection-stimulated decrease in erythropoiesis and losses of RBC have distinct mechanistic bases. These results show that during T. gondii infection, IFNγ is responsible foran anemia that results from both a decrease in erythropoiesis and a STAT1 independent loss of circulating RBC.

关键词： Anemia Helnorrhage signal transducer and activator of transcription 1 Tmot)lasma gondii

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LncRNA ZFPM2-AS1 promotes phyllodes tumor progression by binding to CDC42 and inhibiting STAT1 activation

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Acta Pharmaceutica Sinica B 2024年第7期14卷 2942-2958页

作者： Shishi He Guowei Huang Rong Lei Rurong Jia Zhanghai He Jiewen Chen Hongyan Huang Zixian Huang Ailifeire Yilihamu Xun Li Zilin Zhuang Mengjia Han Xueman Chen Di Huang Yan Nie Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Guangdong-Hong Kong Joint Laboratory for RNA MedicineMedical Research CenterSun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510120China Breast Tumor Center Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510120China Department of Pathology Shantou University Medical CollegeShantou 515041China School of Basic Medical Science Southern Medical UniversityGuangzhou 510515China Department of Pathology Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510120China Department of Breast Medicine Affiliated Foshan Maternity and Child Healthcare HospitalSouthern Medical UniversityFoshan 528000China Department of Breast Surgery Zhujiang HospitalSouthern Medical UniversityGuangzhou 510282China Department of Oral and Maxillofacial Surgery Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510120China

Breast phyllodes tumor(PT)is a rare fibroepithelial neoplasm with potential malignant *** non-coding RNAs(lncRNAs)play multifaceted roles in various cancers,but their involvement in breast PT remains largely *** this study,microarray was leveraged for the first time to investigate the role of lncRNA in *** identified lncRNA ZFPM2-AS1 was significantly upregulated in malignant PT,and its overexpression endowed PT with high tumor grade and adverse ***,we elucidated that ZFPM2-AS1 promotes the proliferation,migration,and invasion of malignant PT in *** ZFPM2-AS1 through nanomaterial-mediated siRNA delivery in patient-derived xenograft(PDX)model could effectively inhibit tumor progression in ***,our findings showed that ZFPM2-AS1 is competitively bound to CDC42,inhibiting ACK1 and STAT1 activation,thereby launching the transcription of *** conclusion,our study provides evidence that ZFPM2-AS1 plays a pivotal role in the pathogenesis of breast PT,and suggests that ZFPM2-AS1 could serve as a prognostic indicator for patients with PT as well as a promising novel therapeutic target.

关键词： LncRNA Phyllodes tumor ZFPM2-AS1 Cell division cycle 42 Activated cdc42 kinase 1 signal transducer and activator of transcription 1 TNF receptor superfamily member 19 Nano particles

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The m6A reader YTHDF2 alleviates the inflammatory response by inhibiting IL-6R/JAK2/STAT1 pathway-mediated high-mobility group box-1 release

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Burns & Trauma 2023年第1期11卷 524-535页

作者： Zhuo Zeng Yingying Lan Lijuan Zhang Yu Chen Yali Gong Fangqing Zuo Junda Li Gaoxing Luo Yizhi Peng Zhiqiang Yuan Institute of Burn Research State Key Laboratory of TraumaBurns and Combined InjurySouthwest HospitalArmy Medical University(Third Military Medical University)Chongqing 400038China

Background:Sepsis is a common severe complication in major burn victims and is characterized by a dysregulated systemic response to *** domain family 2(YTHDF2),a wellstudied N6-methyladenosine(m6A)reader that specifically recognizes and binds to m6A-modified transcripts to mediate their degradation,is connected to pathogenic and physiological processes in eukaryotes,but its effect on sepsis is still *** aimed to discover the effects and mechanisms of YTHDF2 in ***:Quantitative reverse transcription-polymerase chain reaction(qRT-PCR)and western blot analyses were used to measure the expression of YTHDF2,the interleukin 6 receptor(IL-6R),high-mobility group box-1(HMGB1),Janus kinase 2(JAK2)and signal transducer and activator of transcription 1(STAT1)under different in vitro ***-linked immunosorbent assays were utilized to evaluate the expression of HMGB1,IL-6,IL-1βand tumor necrosis factor-α.To confirm that YTHDF2 specifically targets IL-6R mRNA,RNA immunoprecipitation and dual-luciferase reporter assays were ***,we utilized a mouse model of lipopolysaccharide(LPS)-induced sepsis to verify the effects of YTHDF2 in ***:According to our findings,YTHDF2 was expressed at a low level in peripheral blood mononuclear cells from septic mice and patients as well as in LPS-induced RAW264.7 *** of YTHDF2 alleviated the inflammatory response by inhibiting HMGB1 release and JAK2/STAT1 signalling in LPS-stimulated ***,YTHDF2 suppressed JAK2/STAT1 signalling by directly recognizing the m6A-modified site in IL-6R and decreasing the stability of IL-6R mRNA,thereby inhibiting HMGB1 *** vivo experiments showed that YTHDF2 played a protective role in septic mice by suppressing the IL-6R/JAK2/STAT1/HMGB1 ***:In summary,these findings demonstrate that YTHDF2 plays an essential role as an inhibitor of inflammation to reduce the release of HMGB1 by inhibiting the IL-6R/J

关键词： YTH domain family 2 high-mobility group box-1 interleukin 6 receptor Janus kinase 2 signal transducer and activator of transcription 1 Inflammation Sepsis

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Hemophagocytic lymphohistiocytosis caused by STAT1 gain-offunction mutation is not driven by interferon-γ:A case report

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World Journal of Clinical Cases 2020年第23期8卷 6130-6135页

作者： Nan Liu Fen-Ying Zhao Xiao-Jun Xu Department of Hematology-oncology Children’s HospitalZhejiang University School of MedicineHangzhou 310003Zhejiang ProvinceChina

BACKGROUND Hemophagocytic lymphohistiocytosis(HLH)is a life-threatening hyperinflammatory syndrome caused by many genetic ***1 is a DNAbinding factor that regulates gene *** caused by STAT1 gain-offunction(GOF)mutations has rarely been reported and its clinical manifestations and mechanisms are not clearly *** SUMMARY A 2-year-old boy presented to our hospital with recurrent fever for>20 *** patient had a personal history of persistent oral candidiasis and inoculation site infection during the past 2 *** was *** blood cell count showed severe anemia,thrombocytopenia and *** laboratory tests showed liver dysfunction,hypertriglyceridemia and decreased *** was found in the bone *** computed tomography showed a cavitary *** for fungal infection were *** T helper(Th)1/Th2 cytokine determination demonstrated moderately elevated levels of interleukin(IL)-6 and IL-10 with normal interferon(IFN)-γ*** bovis was identified in bronchoalveolar lavage fluid by polymerase chain *** testing identified a heterozygous mutation of c.1154C>T causing a T385M amino acid substitution in *** antibacterial and antifungal therapy,the febrile disease was not *** signs of HLH were relieved after HLH-94 protocol administration,except *** was not resolved until he received anti-tuberculosis *** stem cell transplantation was refused and the patient died six months later due to severe *** Patients with STAT1 GOF mutation have broad clinical manifestations and may develop *** form of HLH presents with normal IFN-γlevel without cytokine storm.

关键词： Hemophagocytic lymphohistiocytosis signal transducer and activator of transcription 1 Gain-of-function Interferon gamma Mycobacterial disease Case report

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Effects of MIF on proliferation,migration,and STAT1 pathway of colon cancer cells

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Oncology and Translational Medicine 2020年第3期6卷 121-125页

作者： Feng Liu Jianxin Zhong Jianbin Sun Hailong Wu Department of Thyroid and Breast Surgery Wuhan Puai HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430000China

Objective This study aimed to investigate how macrophage migration inhibitory factor(MIF)regulates the interaction of signal transducer and activator of transcription 1(STAT1)with CD74,and affects colon cancer proliferation and *** After transfecting MIF small interfering RNA into the SW480 cell line,the expression of STAT1 and CD74 mRNA was detected by qRT-PCR and western *** and MTT assays were performed to detect the colon cancer cell invasion and proliferation ***-immunoprecipitation was used to detect the interaction between CD74 and STAT1 proteins in the treated and control *** The cellular biological assays(MTT and Transwell)showed that the proliferation and invasion ability of colon cancer cells decreased after MIF knockdown;the results showed significant statistical difference(P1 proteins;statistical difference was observed between the two groups(P1.

关键词： colon cancer migration inhibitory factor signal transducer and activator of transcription 1 cell proliferation cell migration

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