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Programmed cell death 5 correlates with disease activity and interleukin-17 in serum and synovial fluid of rheumatoid arthritis patients

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Chinese Medical Journal 2013年第2期126卷 296-299页

作者： WANG Jun-feng GUAN Zhen-peng ZHANG Shao-long PEI Zheng CHEN Ying-yu PAN Huan Arthritis clinic and research center Peking University People'sHospital Beijing 100044 China Peking University center for human Disease Genomics Beljing100191 China

Background Programmed cell death 5 （PDCD5） is a novel apoptotic regulatory gene that promotes apoptosis in various tumor cells. Studies have shown that PDCD5 accelerates the apoptosis of synoviocytes in vitro, implying a potential role in rheumatoid arthritis （RA） pathogenesis. This study examined the expression of PDCD5 in serum and synovial fluid of RA patients, its effect on the expression of inflammatory cytokine, interleukin-17 （IL-17）, and the assessment of disease activity in RA. Methods PDCD5 and IL-17 levels in serum and synovial fluid from 18 patients with RA and 22 patients with osteoarthritis （OA） were detected using enzyme-linked immunosorbent assay （ELISA）. Concentrations of serum PDCD5 in 40 healthy people were also detected as controls. As disease activity indices, C-reactive protein （CRP）, erythrocyte sedimentation rate （ESR）, rheumatoid factor （RF）, and X-ray grading scale were also evaluated. Results Serum and synovial fluid PDCD5 levels in RA patients were significantly higher than those in OA and healthy controls. Serum PDCD5 level was inversely correlated to CRP and ESR, and was significantly higher in the RF negative group than in the positive group. PDCD5 level was also negatively correlated with IL-17 levels both in serum and synovial fluid of RA patients. However, differences in synovial fluid PDCD5 level from RA patients at different Larsen stages were not detectable. Conclusions PDCD5 affects RA pathogenesis. Insufficient apoptosis of fibroblast-like synoviocytes and inflammatory cells in RA could increase the expression of PDCD5 protein. As PDCD5 levels correlated negatively with disease activity indices and IL-17 level, PDCD5 could become a target in the diagnosis and treatment of RA.

关键词： rheumatoid arthritis programmed cell death 5 interleukin-17 pathogenesis

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Inhibition of PARP1 Increases IRF-dependent gene Transcription in Jurkat Cells

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Current Medical Science 2019年第3期39卷 356-362页

作者： Cheng WANG Meng DU Dan HUANG Kun HUANG Kai HUANG Clinic Center of Human Gene Research Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Institution of Cardiology Union HospitalTongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

Poly(ADP-ribose) polymerase 1 (PARP1) plays important roles in the regulation of transcription factors. Mounting evidence has shown that inhibition of PARP1 influences the expression of genes associated with inflammatory response. Interferon regulatory factor 1 (IRF1) is a critical transcription factor for the development of both the innate and adaptive immune responses against infections. However, the molecular mechanism through which PARP1 mediates the effects has not been clearly demonstrated. Jurkat cells were exposed to dexamethasone (Dex) or PARP1 inhibitor PJ34. The expression levels of IL-12, LMP2, OAS1 and PKR were detected using real-time RT-PCR. The interactions between PARP1 and IRF1 were examined by coimmunoprecipitation (co-IP) assays. We further explored the mechanism of PARP1 suppressing IRF1 by assessing the activities of interferon stimulated response element (ISRE). The mRNA expression of IL-12, LMP2, OAS1 and PKR was obviously suppressed by Dex in Jurkat cells, which could be rescued by PJ34 treatment. Luciferase study revealed that poly(ADP-ribosyl)- ation suppressed IRF1-mediated transcription through preventing the binding of IRF1 to ISREs. PARP1 inhibited IRF1-mediated transcription in Jurkat cells by preventing IRF1 binding to ISREs in the promoters of target genes. It is suggested that PARP1 is a crucial regulator of IRF1-mediated immune response. This study provides experimental evidence for the possible application of PARP1 inhibitors in the treatment of IRF1-related immune anergy.

关键词： poly(ADP-ribose) polymerase 1 interferon regulatory factor 1 Jurkat cells gene transcription interferon stimulated response element

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Identification of a New Lamin A/C Mutation in a Chinese Family Affected with Atrioventricular Block as the Prominent Phenotype

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第1期30卷 103-107页

作者：吴小艳王擎桂乐刘木根张贤钦金润铭李伟闫露杜戎王秋芬祝建芳杨钧国 Department of Pediatrics Union HospitalTongji Medical CollegeHuazhong University of Science and Technology human Genome research center Union HospitalTongji Medical CollegeHuazhong University of Science and Technology center for human Genome research and College of Life Science and Technology Huazhong University of Science and Technology Department of Molecular Cardiology Cleveland ClinicCleveland Electrocardiogram Lab Jinshan Hospital

Even though mutations in LMNA have been reported in patients with typical dilated cardio-myopathy(DCM)and atrioventricular block(AVB)previously,the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval.Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2,where the LMNA gene was located.Direct DNA sequence analysis revealed a heterozygous G t...

关键词： atrioventricular block dilated cardiomyopathy LMNA

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STAT3 ameliorates cognitive deficits by positively regulatingthe expression of NMDARs in a mouse model of FTDP-17

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Signal Transduction and Targeted Therapy 2021年第1期6卷 158-170页

作者： Xiao-Yue Hong Hua-Li Wan Ting Li Bing-Ge Zhang Xiao-Guang Li Xin Wang Xiao Li Qian Liu Chong-Yang Chen Ying Yang Qun Wang Shu-Peng Li Hao Yu Jian-Zhi Wang Xi-Fei Yang Gong-Ping Liu Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China and Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Clinic Center of Human Gene Research Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina State Key Laboratory of Oncogenomics School of Chemical Biology and BiotechnologyPeking University Shenzhen Graduate SchoolShenzhenChina Bomedical Engineering Shenzhen PolytechnicShenzhen 518055China Key Laboratory of Modern Toxicology of Shenzhen Shenzhen Center for Disease Control and PreventionShenzhen 518055China Co-innovation center of Neuroregeneration Nantong UniversityNantongJiangsu 226001China

In tauopathies,memory impairment positively strongly correlates with the amount of abnormal tau aggregates;however,how tau accumulation induces synapse impairment is unclear.Recently,we found that human tau accumulation activated Signal Transduction and Activator of Transcription-1(STAT1)to inhibit the transcription of synaptic N-methyl-D-aspartate receptors(NMDARs).Here,overexpressing human P301L mutant tau(P301L-hTau)increased the phosphorylated level of Signal Transduction and Activator of Transcription-3(STAT3)at Tyr705 by JAK2,which would promote STAT3 translocate into the nucleus and activate STAT3.However,STAT3 was found mainly located in the cytoplasm.Further study found that P301L-htau acetylated STAT1 to bind with STAT3 in the cytoplasm,and thus inhibited the nuclear translocation and inactivation of STAT3.Knockdown of STAT3 in STAT3^(flox/flox) mice mimicked P301L-hTau-induced suppression of NMDARs expression,synaptic and memory impairments.Overexpressing STAT3 rescued P301L-hTau-induced synaptic and cognitive deficits by increasing NMDARs expression.Further study proved that STAT3 positively regulated NMDARs transcription through direct binding to the specific GAS element of NMDARs promoters.These findings indicate that accumulated P301L-hTau inactivating STAT3 to suppress NMDARs expression,revealed a novel mechanism for tau-associated synapse and cognition deficits,and STAT3 will hopefully serve as a potential pharmacological target for tauopathies treatment.

关键词： STAT3 inhibited expressing

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A 3D-printable device allowing fast and reproducible longitudinal preparation of mouse intestines

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Animal Models and Experimental Medicine 2022年第2期5卷 189-196页

作者： Beckey DeLucia Sergey Samorezov Megan T.Zangara Rachel L.Markley Lucas J.Osborn Karlee B.Schultz Christine McDonald Jan Claesen Department of Cardiovascular and Metabolic Sciences Lerner Research InstituteCleveland ClinicClevelandOhioUSA center for Microbiome and human Health Lerner Research InstituteCleveland ClinicClevelandOhioUSA Department of Biomedical Engineering Lerner Research InstituteCleveland ClinicClevelandOhioUSA Department of Molecular Medicine Cleveland Clinic Lerner College of Medicine of Case Western Reserve UniversityClevelandOhioUSA Department of Inflammation and Immunity Lerner Research InstituteCleveland ClinicClevelandOhioUSA College of Arts and Sciences John Carroll UniversityUniversity HeightsOhioUSA

Accurate and reproducible analysis of murine small and large intestinal tissue is key for preclinical models involving intestinal pathology.Currently,there is no easily ac-cessible,standardized method that allows researchers of different skill levels to con-sistently dissect intestines in a time-efficient manner.Here,we describe the design and use of the 3D-printed“Mouse Intestinal Slicing Tool”(MIST),which can be used to longitudinally dissect murine intestines for further analysis.We benchmarked the MIST against a commonly used procedure involving scissors to make a longitudinal cut along the intestines.Use of the MIST halved the time per mouse to prepare the intestines and outperformed alternative methods in smoothness of the cutting edge and overall reproducibility.By sharing the plans for printing the MIST,we hope to contribute a uniformly applicable method for saving time and increasing consistency in studies of the mouse gastrointestinal tract.

关键词： adenoma dissection i ntestines mice printing three-dimensional reproducibility of results

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REVA as A Well-curated Database for human Expressionmodulating Variants

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Genomics, Proteomics & Bioinformatics 2021年第4期19卷 590-601页

作者： Yu Wang Fang-Yuan Shi Yu Liang Ge Gao State Key Laboratory of Protein and Plant gene research School of Life SciencesBiomedical Pioneering Innovation Center(BIOPIC)&Beijing Advanced Innovation Center for Genomics(ICG)Center for Bioinformatics(CBI)Peking UniversityBeijing 100871China human Aging research Institute School of Life SciencesNanchang UniversityNanchang 330031.China

More than 90%of disease-and trait-associated human variants are noncoding.By systematically screening multiple large-scale studies,we compiled REVA,a manually curated database for over 11.8 million experimentally tested noncoding variants with expression-modulating potentials.We provided 2424 functional annotations that could be used to pinpoint the plausible regulatory mechanism of these variants.We further benchmarked multiple state-of-the-art computational tools and found that their limited sensitivity remains a serious challenge for effective large-scale analysis.REVA provides high-quality experimentally tested expression-modulating variants with extensive functional annotations,which will be useful for users in the noncoding variant community.REVA is freely available at http://***.

关键词： Noncoding variant Expression-modulating variant Massively parallel reporter assay Database Benchmark

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GSH-responsive camptothecin prodrug-based hybrid micellar nanoparticles enable antitumor chemo-immunotherapy by PD-L1 knockdown

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Nano research 2023年第1期16卷 834-848页

作者： Xi Tan Hong Zhou Chenhui Wang Xuhan Liu Xiangliang Yang Wei Liu College of Life Science and Technology Huazhong University of Science and TechnologyWuhan 430074China The Key Laboratory for human Disease gene Study of Sichuan Province and the Department of Laboratory Medicine Sichuan Provincial People’s HospitalUniversity of Electronic Science and Technology of ChinaChengdu 611731China Department of Emergency Medicine Shenzhen University General HospitalShenzhen University Clinical Medical AcademyShenzhen 518060China National Engineering research center for Nanomedicine Huazhong University of Science and TechnologyWuhan 430074China

The combinational chemo-immunotherapy as a novel treatment strategy has been widely studied and applied in clinic to enhance antitumor therapeutic efficacy and relieve side effects.RNA interference(RNAi)targeting PD-L1 via inhibiting novo production of PD-L1 will overcome the innate and adaptive PD-L1 expression during chemotherapy,thus enable sustained and efficient immune checkpoint blockade(ICB)to active antitumor immune response.Herein,we designed a glutathione(GSH)-responsive camptothecin(CPT)prodrug-based hybrid micellar nanoparticles(siPD-L1@HM-CPT)to achieve synergistic antitumor chemoimmunotherapy by PD-L1 knockdown.siPD-L1@HM-CPT derived from the one-step loading PD-L1 siRNA(siPD-L1)into the CPT prodrug-based hybrid micelles(HM-CPT)which were co-assembled from biodegradable polyphosphoesters-based prodrug CPT-ss-PAEEP15 and stabilizer DSPE-PEG,showed high loading efficiency,GSH-responsive drug release,and excellent stability and biosafety.siPD-L1@HM-CPT achieved simultaneously the co-delivery of CPT and siPD-L1 in vitro and in vivo,high accumulation at the tumor sites,and rapid intracellular release to promote antitumor efficacy via sensitizing CPT chemotherapy,inducing strong immunogenic cell death(ICD)and sustained ICB to improve intratumoral CD8+T cells infiltration.In addition,the antitumor immunity response limited by the differentiated immunogenicity,intrinsic PD-L1 expression,and intracellular GSH level was facilitated by efficient ICD and ICB from silencing PD-L1 and synergistic CPT chemosensitization in our experimental B16-F10 and 4T1 tumor models.Our study might offer a perspective on designing novel co-delivery nanoparticles by convenient and controllable preparation for antitumor chemo-immunotherapy.

关键词： camptothecin prodrug hybrid micellar nanoparticles glutathione(GSH)-responsive PD-L1 knockdown chemoimmunotherapy

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gene expression profiles of human adipose-derived mesenchymal stem cells dynamically seeded on clinically available processed nerve allografts and collagen nerve guides

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Neural Regeneration research 2021年第8期16卷 1613-1621页

作者： Femke Mathot Nadia Rbia Roman Thaler Allan B.Dietz Andre Jvan Wijnen Allen T.Bishop Alexander Y.Shin Department of Orthopedic Surgery Mayo ClinicRochesterMNUSA Department of Plastic Surgery RadboudumcNijmegenThe Netherlands Department of Dermatology Erasmus Medical CenterRotterdamThe Netherlands Department of Biochemistry and Molecular Biology Mayo ClinicRochesterMNUSA Department of Laboratory Medicine and Pathology Mayo ClinicRochesterMNUSA

It was hypothesized that mesenchymal stem cells(MSCs) could provide necessary trophic factors when seeded onto the surfaces of commonly used nerve graft substitutes. We aimed to determine the gene expression of MSCs when influenced by Avance■ Nerve Grafts or Neura Gen■ Nerve Guides. human adipose-derived MSCs were cultured and dynamically seeded onto 30 Avance■ Nerve Grafts and 30 Neura Gen■ Nerve Guides for 12 hours. At six time points after seeding, quantitative polymerase chain reaction analyses were performed for five samples per group. Neurotrophic [nerve growth factor(NGF), glial cell line-derived neurotrophic factor(GDNF), pleiotrophin(PTN), growth associated protein 43(GAP43) and brain-derived neurotrophic factor(BDNF)], myelination [peripheral myelin protein 22(PMP22) and myelin protein zero(MPZ)], angiogenic [platelet endothelial cell adhesion molecule 1(PECAM1/CD31) and vascular endothelial cell growth factor alpha(VEGFA)], extracellular matrix(ECM) [collagen type alpha I(COL1A1), collagen type alpha III(COL3A1), Fibulin 1(FBLN1) and laminin subunit beta 2(LAMB2)] and cell surface marker cluster of differentiation 96(CD96) gene expression was quantified. Unseeded Avance■ Nerve Grafts and Neura Gen■ Nerve Guides were used to evaluate the baseline gene expression, and unseeded MSCs provided the baseline gene expression of MSCs. The interaction of MSCs with the Avance■ Nerve Grafts led to a short-term upregulation of neurotrophic(NGF, GDNF and BDNF), myelination(PMP22 and MPZ) and angiogenic genes(CD31 and VEGFA) and a long-term upregulation of BDNF, VEGFA and COL1A1. The interaction between MSCs and the Neura Gen■ Nerve Guide led to short term upregulation of neurotrophic(NGF, GDNF and BDNF) myelination(PMP22 and MPZ), angiogenic(CD31 and VEGFA), ECM(COL1A1) and cell surface(CD96) genes and long-term upregulation of neurotrophic(GDNF and BDNF), angiogenic(CD31 and VEGFA), ECM genes(COL1A1, COL3A1, and FBLN1) and cell surface(CD96) genes. Analysis demonstrated MSCs seeded onto Neura Gen■ Nerve Guides expr

关键词： Avance■Nerve Grafts dynamic seeding mesenchymal stem cell NeuraGen■Nerve Guides peripheral nerve repair qPCR

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Silencing of Transposable Elements by piRNAs in Drosophila:An Evolutionary Perspective

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Genomics, Proteomics & Bioinformatics 2017年第3期15卷 164-176页

作者： Shiqi Luo Jian Lu State Key Laboratory of Protein and Plant gene research Center for BioinformaticsCollege of Life Sciences and Peking-Tsinghua Center for Life SciencesPeking University Beijing Advanced Innovation center for Food Nutrition and human Health College of Food Science and Nutritional EngineeringChina Agricultural University

Transposable elements （TEs） are DNA sequences that can move within the genome. TEs have greatly shaped the genomes, transcriptomes, and proteomes of the host organisms through a variety of mechanisms. However, TEs generally disrupt genes and destabilize the host genomes, which substantially reduce fitness of the host organisms. Understanding the genomic distribution and evolutionary dynamics of TEs will greatly deepen our understanding of the TE-mediated bio- logical processes. Most TE insertions are highly polymorphic in Drosophila melanogaster, providing us a good system to investigate the evolution of TEs at the population level. Decades of theoretical and experimental studies have well established ＂transposition-selection＂ population genetics model, which assumes that the equilibrium between TE replication and purifying selection determines the copy number of TEs in the genome. In the last decade, P-element-induced wimpy testis （PIW1）- interacting RNAs （piRNAs） were demonstrated to be master repressors of TE activities in Droso- phila, The discovery of piRNAs revolutionized our understanding of TE repression, because it reveals that the host organisms have evolved an adaptive mechanism to defend against TE invasion. Tremendous progress has been made to understand the molecular mechanisms by which piRNAs repress active TEs, although many details in this process remain to be further explored. The inter- action between piRNAs and TEs well explains the molecular mechanisms underlying hybrid dysge- nesis for the IoR and P-M systems in Drosophila, which have puzzled evolutionary biologists for decades. The piRNA repression pathway provides us an unparalleled system to study the co-evolutionary process between parasites and host organisms.

关键词： Transposable element piRNA Hybrid dysgenesis Evolution Drosophila

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Environmental factors and their role in the transmission of SARS-CoV-2

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Biosafety and Health 2021年第5期3卷 235-237页

作者： Dawid Maciorowski Divakar Sharma Adinarayana Kunamneni Grousbeck gene Therapy center Schepens Eye Research Institute and Massachusetts Eye and Ear InfirmaryBostonMAUSA Division of Medical Sciences Harvard UniversityBostonMAUSA Hericure Healthcare Pvt Ltd PuneIndia Department of Microbiology Maulana Azad Medical CollegeNew Delhi 110002India Division of Infectious Diseases Department of Internal MedicineMayo ClinicJacksonvilleFLUSA

In December of 2019,several cases of atypical pneumonia caused by an unknown agent were reported in Wuhan,the capital city of Hubei Province in China.In early January 2020,it was announced that these cases were caused by a novel coronavirus.The virus was later named Severe Acute Respiratory Syndrome Coronavirus 2(SARS-CoV-2),which causes a disease associated with atypical pneumonia termed Corona virus disease 2019(COVID-19).Several respiratory viruses,including coronaviruses and influenza viruses tend to have prominent peaks of infection during colder seasons,especially in temperate regions.The cold temperatures,along with accompanying dry conditions can drive respiratory tract infections by assisting with viral transmission,weakening the human immune system,and increasing viral molecular stability.Though the topic of SARS-CoV-2 transmission and warm weather has been associated with misinformation campaigns,it is worth investigating since an informative answer may give an indication of the future behavior of SARS-CoV-2.

关键词： COVID-19 SARS-CoV-2 Transmission of SARS-CoV-2 Environmental factors

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