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Persistent organic pollutants and plasma microRNAs: A community-based profiling analysis

ENVIRONMENT INTERNATIONAL 2025年 197卷 109328页

作者： Qu, Jingli Li, Wending Jia, Chengyong Jiang, Qin Tang, Rui Yin, Yu Wang, Xi Long, Pinpin wu, tangchun Yuan, Yu Huazhong Univ Sci & Technol Tongji Med Coll Dept Occupat & Environm Hlth Sch Publ HlthMinist EducKey Lab Environm & Hlth Wuhan 430030 Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth State Key Lab Environm Hlth Incubating Wuhan 430030 Peoples R China Columbia Univ Mailman Sch Publ Hlth Dept Environm Hlth Sci New York NY 10032 USA

Background: Whether exposure to persistent organic pollutants (POPs) may incur microRNAs (miRNAs) dysregulation remains largely unclear. Objectives: We aim to identify the miRNA signature and related pathways of low-level POPs exposure in a community-based population. Methods: We used general linear regression to model the association of POPs with plasma miRNAs, adjusting for age, gender, smoking, alcohol consumption, body mass index, triglyceride, and total cholesterol levels. We performed pathway enrichment analysis based on 11 experimentally validated and prediction-based databases, and performed tissue specificity analysis. Results: We identified 19 POPs significantly associated with 23 miRNAs at false discovery rate-adjusted P value < 0.2, most of which were related to organophosphorus and organochlorine pesticides. Pathway enrichment of the associated miRNAs highlighted chromosome segregation, RNA splicing, autophagy regulation, lipid metabolism, cell growth, development and differentiation, cell cycle regulation, neural network construction, and signal transduction. Notably, 13 POPs were positively associated with miR-6810-3p, a miRNA enriched in temporal lobe with high tissue specificity (Tissue Specificity Index = 0.78). Pathway analysis revealed that miR-6810-3p contributes to the positive regulation of autophagy and multiple cellular functions related to the nervous system such as transport along microtubules, maintenance of cell polarity, and synaptic transmission. Conclusion: In conclusion, we identified POPs-related miRNA signatures in community-dwelling adults, and highlighted miR-6810-3p in association with multiple POPs, with a potential role in nervous system regulation.

关键词： Persistent organic pollutants MicroRNAs Pathway enrichment Gene ontology enrichment analysis Neurological function

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Circulating MicroRNAs in association with urinary arsenic: A community-based multi-center study in China

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ENVIRONMENTAL RESEARCH 2025年 274卷 121354页

作者： Li, Wending Li, Zhaoyang Ma, Jixuan Xu, Xuedan Wang, Bin Long, Pinpin Jiang, Qin You, Yutong Qu, Jingli Wang, Yufei Wang, Yaxin He, Meian Chen, Weihong Yuan, Yu wu, tangchun Huazhong Univ Sci & Technol Minist Educ Dept Occupat & Environm Hlth Key Lab Environm & Hlth Wuhan 430030 Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth State Key Lab Environm Hlth Incubating Wuhan 430030 Peoples R China Columbia Univ Mailman Sch Publ Hlth Dept Environm Hlth Sci New York NY 10032 USA

The profile of plasma miRNAs in association with arsenic exposure remains largely unclear. We aim to identify plasma miRNAs assoicated with urinary arsenic using a two-stage design in Chinese population. The discovery group, Shimen panel, consists of 19 high vs. low arsenic-exposed pairs selected from 1095 residents in an arsenic- contaminated area. The validation group, wuhan-Zhuhai panel, consists of 53 community-dwelling participants with moderate arsenic exposure. Plasma miRNAs were measured by microarray in the Shimen panel and by sequencing in the wuhan-Zhuhai panel. Arsenic levels in urine and plasma were quantified using inductively coupled plasma mass spectrometry. During the discovery stage, 16 miRNAs were found to be differentially expressed between high and low urinary arsenic groups in the Shimen panel (fold change >2, P < 0.05). Seven miRNAs (miR-101-3p, miR-142-3p, miR-148a-3p, miR-15a-5p, miR-199a-3p, miR-27b-3p, and miR-340-5p) were validated to have a positive association with log-transformed urinary arsenic levels in the wuhan-Zhuhai panel (P < 0.05). Furthermore, five of the seven miRNAs were also associated with arsenic in plasma. The identified miRNAs were primarily associated with cancer-related pathways. These identified miRNAs would serve as crucial biomarkers for arsenic exposure, elucidating the epigenetic mechanisms underlying arsenic- induced toxicity and carcinogenesis.

关键词： Circulating microRNAs Arsenic Multi-center study Cancer-related pathways Two-stage design

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Persistence of humoral and cellular immune response after SARS-CoV-2 infection: opportunities and challenges

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Frontiers of Medicine 2020年第6期14卷 816-819页

作者： tangchun wu School of Public Health Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

The emerging COVID-19 pandemic caused by SARSCoV-2 infection has created a global *** the circumference of no effective treatment or vaccine,the Chinese government has implemented multifaceted measures of social distancing,home isolation,and centralized quarantine,which achieved a remarkable result of controlling the COVID-19 outbreak[1].However,the personal,psychological,economic,and societal consequences of the shutdown and physical distancing make it difficult to sustain these public health interventions for a long time[2].To find a new balance between curbing the pandemic and minimizing the indirect effects on society,a better understanding of adaptive immunity in response to SARS-CoV-2 infection is required.

关键词： infection immunity vaccine

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Effectiveness of inactivated COVID-19 vaccine against the severity of Omicron variant

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Frontiers of Medicine 2023年第3期17卷 576-580页

作者： Hao Wang Li Liu tangchun wu Ministry of Education and State Key Laboratory of Environmental Health(Incubating) School of Public HealthTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

The COVID-19 pandemic has led to unprecedented levels of morbidity,mortality,and economic disruption *** non-pharmaceutical interventions have been implemented worldwide to curb the spread of SARS-CoV-2,including social distancing,home isolation,and centralized quarantine[1].Nevertheless,these interventions cannot be sustained over the *** hopes of controlling the pandemic rely heavily on vaccination,which remains the best tool available for preventing infection and symptomatic illness.

关键词： sustained mortality severity

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Road traffic and air pollution: Evidence from a nationwide traffic control during coronavirus disease 2019 outbreak

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SCIENCE OF THE TOTAL ENVIRONMENT 2021年 781卷 146618-146618页

作者： Jia, Chengyong Li, Wending wu, tangchun He, Meian Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth Dept Occupat & Environm HlthMinist Educ 13 Hangkong Rd Wuhan 430030 Hubei Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth State Key Lab Environm Hlth Incubating 13 Hangkong Rd Wuhan 430030 Hubei Peoples R China

Existing estimations of air pollution from automobile sources are based on either experiments or small-scale governmental interventions. China's nationwide traffic control during the coronavirus disease 2019 outbreak provided us a unique opportunity to assess the direct dose-effect relationship between vehicle density and air pollution. We found that, during the coronavirus disease 2019 outbreak, the nationwide reduced air pollution (except for O-3) could be largely explained by traffic control measures. During the traffic control period, every doubling of vehicle density was associated with a decrease of 4.2 (2.0, 6.4) mu g/m(3) in PM2.5, 5.5 (2.9, 8.1) mu g/m(3) in PM10, 1.5 (0.9, 2.0) mu g/m(3) in NO2, and 0.04 (0.02, 0.07) mg/m(3) in CO comparing cities with different vehicle densities. Similarly, for every 10% increase in the truck proportion, PM2.5 decreased by 12.3 (4.1, 20.6) mu g/m(3) , PM10 decreased by 14.3 (4.6, 23.9) mu g/m(3), and CO decreased by 0.14 (0.05, 023) mg/m(3). Moreover, the associations between vehicle density and reduction in PM2.5, PM10, and CO during the traffic control period were stronger and showed near-complete linearity in cities with low green coverage rate (All P < 0.05 for interaction). According to our estimation, PM2.5 emissions from every doubling of vehicle density can lead to over 8000 excess deaths per year, 66% of which were caused by cardiopulmonary diseases. This natural experiment study is the first to observe the dose-effect relationship between on-road traffic and traffic-generated air pollution, as well as the mitigating effect of urban greening. Findings provide key evidence to the assessment and control of traffic-generated air pollution and its public health impact. (C) 2021 Elsevier B.V. All rights reserved.

关键词： Air pollution Traffic Intervention COVID-19 Mortality Urban greening

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Genetic variations of CYP2B6 gene were associated with plasma BPDE-Alb adducts and DNA damage levels in coke oven workers

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TOXICOLOGY LETTERS 2012年第3期211卷 232-238页

作者： Huang, Guoxiang Guo, Huan wu, tangchun Huazhong Univ Sci & Technol Inst Occupat Med Tongji Med Coll Sch Publ Hlth Wuhan 430030 Hubei Peoples R China Huazhong Univ Sci & Technol Minist Educ Key Lab Environm & Hlth Sch Publ Hlth Tongji Med Coll Wuhan 430030 Hubei Peoples R China

Polycyclic aromatic hydrocarbons (PAHs), the main components of coke oven emissions, can induce activation of cytochrome P450 (CYP) enzymes, which metabolize PAHs and result in DNA damage by forming adducts. This study was designed to know whether genetic variants of CYP genes are associated with plasma benzo[a]pyrene-7,8-diol-9,10-epoxide-albumin (BPDE-Alb) adducts and DNA damage in coke oven workers. In this study, 298 workers were divided into four groups according to the environmental PAHs exposure levels. The concentrations of plasma BPDE-Alb adducts were detected by reverse-phase high-performance liquid chromatography and the DNA damage levels were measured using comet assay. Twelve tag single nucleotide polymorphisms (tagSNPs) of 4 GYP genes were selected and genotyped by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. In the top group, workers with CYP2B6 rs3760657GA genotype have lower BPDE-Alb adducts and DNA damage levels than those with rs3760657GG genotype (P < 0.05). In the control group, the DNA damage levels of subjects with CYP1A1 rs4646421AA or GA + AA genotypes were lower than those with GG genotype (P < 0.05). However, no such effects were shown for the other tagSNPs. These results suggested that genetic variations of CYP2B6 might be associated with low BPDE-Alb adducts and DNA damage levels in worker with high exposure to PAHs. (c) 2012 Elsevier Ireland Ltd. All rights reserved.

关键词： Genetic variations CYP2B6 BDPE-Alb adducts DNA damage PAHs

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Nickel promotes the invasive potential of human lung cancer cells via TLR4/MyD88 signaling

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TOXICOLOGY 2011年第1-2期285卷 25-30页

作者： Xu, Zengguang Ren, Tao Xiao, Chunyi Li, Huiyi wu, tangchun Huazhong Univ Sci & Technol Inst Occupat Med Sch Publ Hlth Tongji Med Coll Wuhan 430030 Hubei Peoples R China Huazhong Univ Sci & Technol Key Lab Environm & Hlth Sch Publ Hlth Tongji Med CollMinist Educ Wuhan 430030 Hubei Peoples R China Tongji Univ Sch Med East Hosp Dept Sci Res Shanghai 200120 Peoples R China Tongji Univ Sch Med East Hosp Dept Resp Med Shanghai 200120 Peoples R China

Epidemiological studies have demonstrated a close correlation between nickel exposure and the incidence of lung cancer. Several studies have suggested that nickel contributes to tumor progression of human lung cancer. In this in vitro study, we found that nickel, as nickel chloride, could significantly enhance the invasive potential of human lung cancer cells, accompanied by elevated expression of IL-8, TGF-beta, MMP2 and MMP9 in human lung cancer cells. Importantly, we demonstrated that nickel could activate TLR4 signaling in human lung cancer cells. Further studies showed that the TLR4/MyD88 signaling conferred the enhanced invasive potential of human lung cancer cells induced by nickel. Finally, we revealed that the p38MAPK pathway and NF-kB pathway were necessary for the enhanced invasive potential of human lung cancer cells induced by nickel. Our data provide a mechanistic explanation for nickel induced invasion of human lung cancer, and they suggest new strategies for nickel-related lung cancer clinical biotherapies. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

关键词： TLR4 Nickel Human lung cancer Invasive potential

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The role of natriuretic peptide precursor A gene polymorphism in the development of coronary heart disease in Chinese Han population

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Frontiers of Medicine 2009年第4期3卷 437-442页

作者： Ripen NSENGA Longxian CHENG Mei’an HE tangchun wu Department of Cardiology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Institute of Occupational Medicine Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

Natriuretic peptide precursor A(NPPA)is synthesized,stored,and released by atrial *** studies have shown that NPPA plays a signiﬁcant role in the regulation of coronary circulation and in ***5065 NPPA gene polymorphism leads to the translation of NPPA with two additional arginines and has been suggested to be associated with salt-sensitive *** purpose of the present study was to investigate the relationship between the rs5065 NPPA gene polymorphism and the risk of coronary heart disease(CHD)in Chinese Han *** genotyped the single nucleotide polymorphism(SNP)rs5065 NPPA in the human NPPA gene in 1861 sex-and age-matched subjects,comprising of 904 CHD cases and 957 controls of Chinese Han *** of SNP was performed with Taqman SNP allelic discrimination assays by means of an ABI *** study showed that the frequencies of rs5065 NPPA C allele in the case and the control groups were 0.012 and 0.005,*** was signiﬁcant difference in C allele frequency distribution between the two groups(OR=2.607,95%CI:1.197–5.678,P=0.012).In the case group,there was signiﬁcant difference between smokers and nonsmokers with subjects carrying C allele(P=0.037),and no signiﬁcant difference in gender,age,fasting total cholesterol(TC),triglycerides(TG),fasting plasma glucose(FPG),body mass index(BMI),and blood pressure(BP)between the cases and the controls(P>0.05).Our results suggest that the C allele of rs5065 NPPA gene polymorphism may be associated with the risk of CHD.

关键词： natriuretic peptide precursor A coronary heart disease gene polymorphism allelic discrimination poly-morphism,single nucleotide

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Reconstruction of the full transmission dynamics of COVID-19 in wuhan

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NATURE 2020年第7821期584卷 420-+页

作者： Hao, Xingjie Cheng, Shanshan wu, Degang wu, tangchun Lin, Xihong Wang, Chaolong Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth Minist EducKey Lab Environm & HlthState Key Lab Wuhan Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth Dept Epidemiol & Biostat Wuhan Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Sch Publ Hlth Dept Occupat & Environm Hlth Wuhan Peoples R China Huazhong Univ Sci & Technol Natl Med Ctr Major Publ Hlth Events Wuhan Peoples R China Harvard TH Chan Sch Publ Hlth Dept Biostat Boston MA 02115 USA Harvard Univ Dept Stat Cambridge MA 02138 USA Broad Inst MIT & Harvard Cambridge MA 02142 USA

As countries in the world review interventions for containing the pandemic of coronavirus disease 2019 (COVID-19), important lessons can be drawn from the study of the full transmission dynamics of its causative agent-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)- in wuhan (China), where vigorous non-pharmaceutical interventions have suppressed the local outbreak of this disease(1). Here we use a modelling approach to reconstruct the full-spectrum dynamics of COVID-19 in wuhan between 1 January and 8 March 2020 across 5 periods defined by events and interventions, on the basis of 32,583 laboratory-confirmed cases(1). Accounting for presymptomatic infectiousness(2), time-varying ascertainment rates, transmission rates and population movements(3), we identify two key features of the outbreak: high covertness and high transmissibility. We estimate 87% (lower bound, 53%) of the infections before 8 March 2020 were unascertained (potentially including asymptomatic and mildly symptomatic individuals);and a basic reproduction number (R-0) of 3.54 (95% credible interval 3.40-3.67) in the early outbreak, much higher than that of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS)(4,5). We observe that multipronged interventions had considerable positive effects on controlling the outbreak, decreasing the reproduction number to 0.28 (95% credible interval 0.23-0.33) and-by projection-reducing the total infections in wuhan by 96.0% as of 8 March 2020. We also explore the probability of resurgence following the lifting of all interventions after 14 consecutive days of no ascertained infections;we estimate this probability at 0.32 and 0.06 on the basis of models with 87% and 53% unascertained cases, respectively-highlighting the risk posed by substantial covert infections when changing control measures. These results have important implications when considering strategies of continuing surveillance and interventions to eventually co

关键词： Epidemiology SARS-CoV-2 Viral infection

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The JNK signaling pathway is involved in sodium-selenite-induced apoptosis mediated by reactive oxygen in HepG2 cells

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CANCER BIOLOGY & THERAPY 2008年第5期7卷 689-696页

作者： Zou, Yunfeng Niu, Piye Yang, Jin Yuan, Jing wu, tangchun Chen, Xuemin Huazhong Univ Sci & Technol Tongji Med Coll Dept Occupat & Environm Key Lab Environm & HlthMinist EducSch Publ Hlth Wuhan 430030 Hubei Peoples R China

Selenium compounds as effective chemopreventive agents can induce apoptosis in tumor cells, and reactive oxygen species (ROS) are important mediators in apoptosis induced by various stimuli including chemopreventive agents. The major mitogen-activated protein kinases (MAPKs), c-JUN N-terminal kinase (JNK), p38 and extracelluar signal-regulated kinase (ERK) are three kinases that have been shown to regulate apoptosis. In this study, we showed that selenite-induced apoptosis in HepG2 cells was mediated by ROS that activated JNK to regulate apoptosis. The selenite-treated HepG2 cells showed a dose- and time-dependent decrease in cell viability that was coincident with increased the levels of the apoptosis rate. The levels of selenite-induced ROS as measured by 2', 7'-dichlorofluorescein diacetate (DCFH-DA) fluorescence also showed a dose- and time-dependent increase in HepG2 cells. The kinase activity of JNK was induced by selenite in a dose- dependent manner and HepG2 cells exposed to selenite (10 mu M) for 4 h showed increased levels of phosphorylated JNK, which decreased when exposed for additional 4 h. In contrast, Sp600125, a specific inhibitor of JNK, remarkably blocked the apoptosis of HepG2 exposed to selenite. Furthermore, N-acetylcysteine (NAC), a known antioxidant, increased cell viability and decreased ROS generation. Moreover, NAC effectively blocked apoptosis and decreased the levels of phosphorylated JNK induced by selenite. These results revealed that JNK might be involved in selenite-induced ROS-mediated apoptosis in HepG2 cells.

关键词： JNK apoptosis cell viability reactive oxygen species free radicals selenite HepG2

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