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2012全国临床微生物与感染免疫学术研讨会

作者： xu yong,gao lifen,liang xiaohong,ma chunhong~* key laboratory for experimental teratology of ministry of education and institute oflmmunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china

Diabetes has become a major global problem threatening public health,however,no curative medicine is found to reduce the prevalence rate of it,especially the type 1 diabetes(T1D).T1D is a chronic autoimmune disorder mediated mainly by effector T cells(Th1),but the factors inducing clinical disease remain largely *** studies have indicated a positive relationship between T1D and viruses such as Coxsackie B virus and Cytomegalvirus. However,reports on whether Hepatisis B virus(HBV) take roles in T1D are limited and controvercial. Clinical data showed an increasing number of T1D patients in developed countries where with much low incidence of HBV infection,but there are relative few T1D patients in china with nearly 150 million HBV carriers, indicating the potential effect of HBV on *** the contrary,other reports found no correlation between T1D and ***,some studies have implied a protective role of HBV in the initiation or development of T1D,which may be explained by the hygiene hypothesis,although the immune mechanism is still *** order to address the role of HBV in T1D development,we used streptozotocin(STZ) to induce T1D in BALB/c HBV-transgenic(HBV-Tg) *** results suggested that HBV may delay the onset of T1D and may finally reduce the incidence of it.100%of mice in normal BALB/c group were diagnosed as T1D at the end of observation period,comparing with 87.5%of mice in HBV-Tg group(p=0.0106).And the onset of diabetes is also earlier in normal group after five consecutive STZ *** protective role of HBV might be due to the presense of Tregs in HBV-Tg *** studies are necessary to confirm how could these changes be involved in the diabetogenisis.

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role of ZHX2 in regulating human lipoprotein lipase

Role of ZHX2 in regulating human lipoprotein lipase

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2012全国临床微生物与感染免疫学术研讨会

作者： ma Hongxin,liang xiaohong,gao lifen,Yue xuetian,Zhang Zhenyu,Liu peng,Guo Min,Yan Wenjiang, ma chunhong~* key laboratory for experimental teratology of ministry of education and institute of Immunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china

Background & Aims Dyslipidemia is a major risk factor for many chronic diseases such as cardiovascular and cerebrovascular diseases,chronic liver disease,diabetes mellitus,*** report identified zinc-fingers and homeoboxes 2(ZHX2),one member of ZHX family,as a potential regulator of lipoprotein *** has been well recognized that ZHX2 works as a transcriptional repressor by interaction with *** lipase (LpL),one of the key enzymes in plasma lipid metabolism,can be regulated by ***,we hypothesized that ZHX2 might regulate lipoprotein metabolism by transcriptional repression on LpL ***,we investigate the role and mechanisms in which ZHX2 regulated LpL. Methods To confirm the effect of ZHX2 on LpL,ZHX2 overexpressing plasmid and specific sirNA were transfected into different hepatoma cell *** blot(WB) and rT-pCr were used to analyze the expression of *** reporter assays were introduced to observe the influence of ZHX2 on serial truncated and mutational human LpL *** immunoprecipitation(ChIp) assays were involved to identify the binding inteaction between ZHX2 and LpL promoter. results Overexpression of ZHX2 significantly repressed the expression of LpL in CHO and HepG2 cell,while ZHX2 knockdown increased LpL expression in SMMC7721 and QSG7701 cell *** reporter assays proved that ZHX2 suppressed the activity of LpL promoter in a dose-dependent manner,suggesting that ZHX2 inhibits the transcription of *** lucierase reporter assay with serial truncated LpL promoters identified the region from -96 to -38 of LpL promoter as critical region responsible for ZHX2 *** of ChIp assays presented that ZHX2 could bind to this region of LpL promoter. Conclusions For the first time,we demonstrated that ZHX2 suppresse the expression of LpL by binding its promoter *** findings may give new light on lipoprotein regulation and provide a new target for dyslipid

关键词： ZHX2 dyslipidemia LpL NF-YA

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TIpE1 is down-regulated in human hepatocellular cancer and inhibits cell proliferation

TIPE1 is down-regulated in human hepatocellular cancer and i...

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2012全国临床微生物与感染免疫学术研讨会

作者： Zhang Zhenyu,liang xiaohong,gao lifen,ma Hongxin,Liu xiao,pan Yingfang,Yue xuetian,Yan Wenjiang,Sun Wensheng,ma chunhong~* key laboratory for experimental teratology of ministry of education and institute of Immunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china

TIpEl(TNFAIp8L1) is a member of tumor necrosis factor alpha-induced protein 8 family(TIpE),which contains four members,TIpE,TIpE1,TIpE2 and *** is the first identified member and is considered to be connected with apoptosis and carcinogenesis,while TIpE2 is considered as a negative regulator of innate immunity and cellular immunity,but little is known about *** only research about TIpEl by professor Junying Yuan proved that knockdown of TIpEl inhibits necroptosis and apoptosis in L929 cells,besides this,there is no research about TIpEl and human ***,we for the first time,reported the expression and role of TIpEl in *** analysis of TIpEl in 100 hepatocellular cancer samples and their corresponding noncancerous tissues identified the decreased expression of TIpEl inHCC tissues compared with their corre-

关键词： TIpE1 HCC Cell growth

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Transcriptional up-regulation of FOXp3 by Ap-1/HBx:a novel mechanism for tumour growth in hepatocellular carcinoma

Transcriptional up-regulation of FOXP3 by AP-1/HBx:a novel m...

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2012全国临床微生物与感染免疫学术研讨会

作者： Zhang xiaoning,gao lifen,Yue xuetian,Zhang Feng,Liu peng,pan Yingfang,Zhang Zhenyu,Liu xiao, Gai xiaoxiao,liang xiaohong,ma chunhong~* key laboratory for experimental teratology of ministry of education and institute of Immunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china

Backgroud & Aims Transcription factor forkhead box protein 3(FOXp3) has been identified in different cancer cells where it plays contradict *** strongly suggests the urgency to study the expression pattern and function of FOXp3 in different types of ***,we aim to explore the expression and biological functions of FOXp3 in hepatocellular carcinoma(HCC) and to uncover the role of HBx in regulating FOXp3 expression. Methods FOXp3 expression in malignant hepatocytes was detected by immunohistochemical ***-mediated transcriptional regulation of FOXp3 was studied by cotransfection and luciferase reporter *** biological function of FOXp3 in vitro was analyzed by CCK-8,colony formation assay and cell cycle analysis. results Augmented FOXp3 expression is detected in liver cells from cancer *** FOXp3 staining in malignant hepatocytes from patients with HBV infection was significantly stronger than that from non-HBV infection (p=0.0268).In accordance,HBx enhance FOXp3 expression by up-regulating FOXp3 promoter activity in HCC cell *** Ap-1 binding site at -465 bp to -445 bp of FOXp3 promoter is responsible for HBx-induced FOXp3 transcriptional *** vitro assays show that enhanced expression of FOXp3 significantly promotes HCC cell growth and colony formation *** down of FOXp3 dampen the HBx-mediated acceleration of cell growth in HepG2. Conclusion Our data provides the first molecular mechanism describing the HBx-mediated transcriptional upregulation of FOXp3 which might play important role in the development of HBV related HCC by promoting the growth and proliferation of liver cancer cells.

关键词： Forkhead box protein 3 HBV X protein Ap-1 Transcription regulation Hepatocellular carcinoma

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role of TIpE in the development of Hepatocellular Carcinoma

Role of TIPE in the development of Hepatocellular Carcinoma

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2012全国临床微生物与感染免疫学术研讨会

作者： pan Yingfang~1,Shan Haixia~1,Zhang Zhenyu~1,Sun Wensheng~1,gao lifen~1,ma chunhong~1,liang xiaohong~(1*) key laboratory for experimental teratology of ministry of education and institute of Immunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china

Background Tumor necrosis factor(TNF)-alpha-induced protein 8(TNFAIp8 or TIpE),one member of TIpE family,was recently identified to be associated with ***,it is still unknown about the roles of TNFAIp8 inthe development of hepatocellular carcinoma(HCC).Therefore,the present study was designed to characterize the expression pattern of TNFAIp8 inthe HCC and to explore its possible roles in the development and progression of HCC. Methods Firstly,we investigated TIpE expression of cancerous and their paired paracancerous tissues from 98 HCC patients by rT-pCr and immunohistochemistry(IHC) and analyzed its correlation with clinicopathological ***,the effects of TIpE on cell proliferation and migration were examined in cultured HCC cell line by cell growth curve assay and transwell assay ***,we preliminarily explored the mechanisms of TIpE in the inhibited HCC invasion and migration. results We first analyzed TIpE mrNA expression in 16 HCC ***-pCr analysis showed that 69% (11/16) of patients exhibited decreased TIpE mrNA expression in cancerous tissues when compared with their corresponding paracancerous ***,downregulated TIpE protein level in HCC tissues were also confirmed by IHC analysis in 98 of paired paraffin ***,TIpE expression in HCC tissues was negatively correlated with tumor size,tumor differentiation,TNM stage,and lymphatic and venous ***,we analyzed the biological functions of TIpE in HCC cell *** growth curve assay showed that TIpE sirNA accelerated the growth of both BEL7402 and HepG2 ***,transwell assay demonstrated that TIpE knockdown also promoted cell migration and invasion,while TIpE overexpression played inhibitory ***, Western blot analysis revealed that TIpE knockdown led to epithelial-mesenchymal transition of HCC cell lines by downregulating E-cadherin expression and upregulating N-cadherin and Vimentin expression. Conclusi

关键词： TIpE HCC cell growth cell migration and invasion EMT

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Novel tumor suppressor gene ZHX2 enhances cisplatin sensitivity in hepato-cellular carcinoma cells

Novel tumor suppressor gene ZHX2 enhances cisplatin sensitiv...

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2012全国临床微生物与感染免疫学术研讨会

作者： Yue xuetian,liang xiaohong,ma Hongxin,Guo Min,Liu peng,Zhao Di,Zhang Zhenyu,Liu xiao,Gai xiaoxiao,pan Yingfang,gao lifen ma chunhong~* key laboratory for experimental teratology of ministry of education and institute of Immunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china

Zinc-fingers and homeoboxes 2(ZHX2) repress transcription of several genes associated with liver cancer,including a-fetoprotein(AFp),glypican 3 and ***,little is known about the role of ZHX2 indevelopment of hepatocellular carcinoma(HCC).We recently identified the tumor suppressor role of ZHX2 in *** of ZHX2 was significantly decreased in clinical hepatocellular carcinoma(HCC) tissues which correlated with reduced overall survival time of patients,high levels of tumor microvascularization,and hepatocyte *** analysis demonstrated that ZHX2 inhibits HCC cell proliferation,by preventing expression of cyclins A and E,and reduces growth of xenograft tumors in *** data indicated that loss of nuclear ZHX2 might be an early step in the development of HCC(Gastroenterology 2012). In this report,we examined the effect of a combination treatment using ZHX2 gene transfer and chemotherapeutic drug cisplatin(CDDp) on HCC and explored the underlying *** demonstrated that the combination of ZHX2 gene transfer and CDDp induced enhanced growth inhibition and increased apoptosis in HCC cell lines. Consistently,ZHX2 plus CDDp led to augmented cytochrome c release,more cleaved caspase-9 and ***, combination of ZHX2 with CDDp suppressed the growth of HepG2.2.15 xenograft in nude mice with more efficiency than ZHX2 gene transfer or CDDp *** findings suggest that the combination of ZHX2 gene transfer and cisplatin might represent a promising strategy for treating HCC.

关键词： ZHX2 tumor suppressor gene,CDDp combination chemotherapy HCC

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Zinc fingers and homeoboxes 2 involves in oncogenic activation of glypican 3 in human hepatocellular carcinoma

Zinc fingers and homeoboxes 2 involves in oncogenic activati...

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2012全国临床微生物与感染免疫学术研讨会

作者： Luan Fang~(1,2),Yue xuetian~1,Liu peng~1,Liu Jun~3,liang xiaohong~1,Shi Wei~1,gao lifen~1,Spear Brett~4,ma chunhong~1 1.key laboratory for experimental teratology of ministry of education and institute of Immunology,shandong university school of medicine,44 wenhua xi road,jinan,shandong,250012 p.r.china. 2.Department of Clinical laboratory,provincial Hospital affiliated to shandong university,324 Jingwu road,jinan,shandong,250021 p.r.china. 3.Department of Surgery,provincial Hospital affiliated to shandong university,324 Jingwu road,jinan,shandong,250021 p.r.china. 4.Department of Microbiology,Immunology,&Molecular Genetics and markey Cancer Center,university of Kentucky College of medicine,Lexington,KY,USA.

Background & Aims Glypican 3(GpC3) expresses abundantly in fetal liver and is silent in normal adult liver but becomes reactivated in hepatocellular carcinoma(HCC).And recently GpC3 has been the focus of particular interests because of its potential usefulness as a specific marker for *** study the mechanisms regulating the reactivation of GpC3 in HCC appears to be clinically ***-fingers and homeoboxes 2(ZHX2) are ubiquitously expressed and localized to the nuclei of cells,and appear to function as transcriptional repressors. previous data have shown that ZHX2 protein is involved in postnatal repression of GpC3 ***,we hypothesized ZHX2 might regulate GpC3 expression in HCC. Methods ZHX2 and GpC3 expression were analyzed by rT-pCr,Western blot and immunohistochemistry to evaluate the correlation of ZHX2 and GpC3 *** effects of ZHX2 overexpressed and sh-rNA mediated ZHX2 knockdown in different HCC cell lines were examined in regard to GpC3 *** assay of ZHX2 in HCC and cytoplasmic/nuclear ZHX2 staining in HCC and adjacent non-tumor sections were carried out to reveal the mechanism of GpC3 reactivation in *** reporter assays and chromatin immunoprecipitation were used to measure effects of ZHX2 on GpC3 promoter. rGSUltS Inverse correlation of ZHX2 and GpC3 expression was demonstrated not only in cultured liver cell lines but also in HCC *** of ZHX2 inHepG2,Hep3B and HepG2.2.15 cells,which express lower endogenous ZHX2,significantly decreases GpC3 *** contrast,ZHX2 knockdown increases GpC3 levels in SMMC7721 and *** these results represent the first direct evidence that ZHX2 represses GpC3 expression in *** assay of ZHX2 inHCC and cytoplasmic/nuclear ZHX2 staining in HCC and adjacent non-tumor sections reveal that decreased nuclear ZHX2 levels in HCC tissues is responsible for GpC3 reactivation. Co-transfections of ZHX2 and GpC3-luciferase reporter genes demon

关键词： ZHX2 GpC3 HCC Negative regulation

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Increased Tim-3 expression alleviates liver injury by regulating macrophage activation in MCD-induced NASH mice

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Cellular & Molecular Immunology 2019年第11期16卷 878-886页

作者： xianhong Du Zhuanchang Wu yong xu Yuan Liu Wen Liu Tixiao Wang Chunyang Li Cuijuan Zhang Fan Yi lifen gao xiaohong liang chunhong ma key laboratory for experimental teratology of ministry of education Department of ImmunologyShandong University School of Basic Medical ScienceJinanShandong 250012PR China Department of radiation Oncology Qilu Hospital of Shandong UniversityJinanShandongPR China key laboratory for experimental teratology of ministry of education Department of Histology and EmbryologyShandong University School of Basic Medical ScienceJinanShandongPR China institute of pathology and pathophysiology Shandong University School of MedicineJinanPR China key laboratory of Infection and Immunity of shandong province School of Basic Medical SciencesShandong UniversityJinanChina

As an immune checkpoint,Tim-3 plays roles in the regulation of both adaptive and innate immune cells including macrophages and is greatly involved in chronic liver ***,the precise roles of Tim-3 in nonalcoholic steatohepatitis(NASH)remain *** the current study,we analyzed Tim-3 expression on different subpopulations of liver macrophages and further investigated the potential roles of Tim-3 on hepatic macrophages in methionine and choline-deficient diet(MCD)-induced NASH *** results of flow cytometry demonstrated the significantly increased expression of Tim-3 on all detected liver macrophage subsets in MCD mice,including F4/80^(+)CD11b^(+),F4/80^(+)CD68^(+),and F4/80^(+)CD169^(+)***,Tim-3 knockout(KO)significantly accelerated MCD-induced liver steatosis,displaying higher serum ALT,larger hepatic vacuolation,more liver lipid deposition,and more severe liver ***,compared with wild-type C57BL/6 mice,Tim-3 KO MCD mice demonstrated an enhanced expression of NOX2,NLrp3,and caspase-1 p20 together with increased generation of IL-1βand IL-18 in *** vitro studies demonstrated that Tim-3 negatively regulated the production of reactive oxygen species(rOS)and related downstream pro-inflammatory cytokine secretion of IL-1βand IL-18 in *** administration of N-Acetyl-L-cysteine(NAC),a small molecular inhibitor of rOS,remarkably suppressed caspase-1 p20 expression and IL-1βand IL-18 production in livers of Tim-3 KO mice,thus significantly reducing the severity of steatohepatitis induced by *** conclusion,Tim-3 is a promising protector in MCD-induced steatohepatitis by controlling rOS and the associated pro-inflammatory cytokine production in macrophages.

关键词： macrophage NASH rOS Tim-3

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Deleterious variants in rNF111 impair female fertility and induce premature ovarian insufficiency in humans and mice

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Science china(Life Sciences) 2024年第7期67卷 1325-1337页

作者： Chengcheng Song Yingying Qin Yan Li Bingyi Yang Ting Guo Wenqing ma Dian xu keyan xu Fangfang Fu Li Jin Yanhua Wu Shuyan Tang xiaojun Chen Feng Zhang Obstetrics and Gynecology Hospital State Key Laboratory of Genetic EngineeringInstitute of Medical Genetics and GenomicsFudan UniversityShanghai 200011China Human phenome institute Zhangjiang Fudan International Innovation CenterFudan UniversityShanghai 201203China Center for reproductive medicine Cheeloo College of MedicineShandong UniversityJinan 250021China State key laboratory of reproductive medicine and Offspring Health Key Laboratory of Reproductive Endocrinology of Ministry of EducationNational Research Center for Assisted Reproductive Technology and Reproductive GeneticsShandong Key Laboratory of Reproductive MedicineShandong Provincial Clinical Research Center for Reproductive HealthShandong UniversityJinan 250021China Department of Obstetrics and Gynecology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China National Demonstration Center for experimental Biology education School of Life SciencesFudan UniversityShanghai 200433China Department of Gynecology the Tenth People’s Hospital of Tongji UniversityShanghai 200072China Soong Ching Ling institute of maternity and Child Health International Peace Maternity and Child Health Hospital of China Welfare InstituteShanghai 200030China

premature ovarian insufficiency(pOI)is a heterogeneous female disorder characterized by the loss of ovarian function before the age of *** represents a significant detriment to female ***,the known pOI-causative genes currently account for only a fraction of *** elucidate the genetic factors underlying pOI,we conducted whole-exome sequencing on a family with three fertile pOI patients and identified a deleterious missense variant in *** a subsequent replication study involving 1,030 pOI patients,this variant was not only confirmed but also accompanied by the discovery of three additional predicted deleterious rNF111 *** variants collectively account for eight cases,representing 0.78%of the study cohort.A further study involving 500 patients with diminished ovarian reserve also identified two additional rNF111 ***,rNF111 encodes an E3 ubiquitin ligase with a regulatory role in the TGF-β/BMp signaling *** analysis revealed that rNF111/rNF111 is predominantly expressed in the oocytes of mice,monkeys,and *** further investigate the functional implications of rNF111 variants,we generated two mouse models:one with a heterozygous missense mutation(rnf111+/M)and another with a heterozygous null mutation(rnf111^(+/-)).Both mouse models exhibited impaired female fertility,characterized by reduced litter sizes and small ovarian ***,rNA-seq and quantitative proteomics analysis unveiled that rnf111 haploinsufficiency led to dysregulation in female gonad development and negative regulation of the BMp signaling pathway within mouse *** conclusion,our findings strongly suggest that monoallelic deleterious variants in rNF111 can impair female fertility and induce pOI in both humans and mice.

关键词： pOI rNF111 female fertility ovarian reserve

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CUL4B facilitates HBV replication by promoting HBx stabilization

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Cancer Biology & medicine 2022年第1期19卷 120-131页

作者： Haixia Shan Bo Wang xiaodong Zhang Hui Song xi Li yongxin Zou Baichun Jiang Huili Hu Hao Dou Changshun Shao lifen gao chunhong ma xiaoyun Yang xiaohong liang Yaoqin Gong key laboratory for experimental teratology of the ministry of education Key Laboratory of Infection and Immunity of Shandong Province and Department of ImmunologySchool of Basic Medical SciencesShandong UniversityJinan 250012China Department of laboratory Diagnosis Cangzhou Combination of Traditional Chinese and Western Medicine Hospital of Hebei ProvinceCangzhou 061000China Division of Gastroenterology and Hepatology Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai Institute of Digestive DiseaseShanghai 200120China ministry of education key laboratory of experimental teratology and institute of Molecular medicine and Genetics School of Basic Medical SciencesShandong UniversityJinan 250012China Collaborative Innovation Center of Technology and Equipment for Biological Diagnosis and Therapy in Universities of shandong Jinan 250012China Department of Gastroenterology Qilu HospitalShandong UniversityJinan 250012China

Objective:Hepatitis B virus(HBV)infection is a major public health problem ***,the regulatory mechanisms underlying HBV replication remain *** 4 B-rING ubiquitin E3 ligase(CrL4 B)is involved in regulating diverse physiological and pathophysiological *** our study,we aimed to explain the role of CUL4 B in HBV ***:Cul4 b transgenic mice or conditional knockout mice,as well as liver cell lines with CUL4 B overexpression or knockdown,were used to assess the role of CUL4 B in HBV *** assays and immunofluorescence staining were performed to study the interaction between CUL4 B and *** chase assays and in vivo ubiquitination assays were performed to evaluate the half-life and the ubiquitination status of ***:The hydrodynamics-based hepatitis B model in Cul4 b transgenic or conditional knockout mice indicated that CUL4 B promoted HBV replication(preover,the overexpression or knockdown system in human liver cell lines validated that CUL4 B increased HBV replication in an HBx-dependent ***,immunoprecipitation assays and immunofluorescence staining showed an interaction between CUL4 B and ***,CUL4 B upregulated HBx protein levels by inhibiting HBx ubiquitination and proteasomal degradation(ppositive correlation between CUL4 B expression and HBV pg rNA level was observed in liver tissues from HBV-positive patients and HBV transgenic ***:CUL4 B enhances HBV replication by interacting with HBx and disrupting its ubiquitin-dependent proteasomal ***4 B may therefore be a potential target for anti-HBV therapy.

关键词： CUL4B HBV ubiquitination HBx HCC

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