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Inhibition of the Let-7 Family MicroRNAs Induces cardioprotection Against Ischemia-Reperfusion Injury in Diabetic Rats

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ANNALS OF THORAcIc SURGERY 2016年第3期102卷 829-835页

作者： Li, Juchen Ren, Yixing Shi, Enyi Tan, Zhibin Xiong, Jian Yan, Lihui Jiang, Xiaojing China Med Univ Affiliated Hosp 1 Dept Anesthesiol Shenyang 110001 Peoples R China China Med Univ Affiliated Hosp 1 Dept Cardiac Surg Shenyang Peoples R China Nanjing Univ Sch Med Nanjing Drum Tower Hosp Dept Anesthesiol Nanjing Jiangsu Peoples R China

Background. The expression of the let-7 family microRNAs in the myocardium of streptozotocin-induced diabetic rats was measured, and the cardioprotection of inhibition of let-7 microRNAs against ischemia-reperfusion injury was investigated. Methods. The diabetic rats and nondiabetic rats were subjected to 30 minutes of coronary artery occlusion followed by 120 minutes of reperfusion. The infarct size was determined by triphenyltetrazolium chloride staining. The expression of let-7 was measured by quantitative real-time polymerase chain reaction, and expressions of insulin receptor (InsR), insulin-like growth factor-1 receptor (IGF-1R), glucose transporter type 4 (GLUT4), and the phosphorylation states of Akt and the mammalian target of rapamycin (mTOR) were analyzed using Western blot. Inhibition of let-7 was performed by local transfection of lentivirus gene transfer vectors containing let-7 antimiR. Results. compared with nondiabetic rats, the expression of let-7 was enhanced in the myocardium of diabetic rats (p = 0.029), whereas expressions of InsR, IGF-1R, and GLUT4 were decreased after ischemia-reperfusion (p < 0.01). Local transfection of the let-7 antimiR markedly inhibited the expression of let-7 (p = 0.038) and improved expressions of InsR, IGF-1R, and GLUT4 in the myocardium of diabetic rats (p < 0.01). The infarct size of diabetic rats was much higher than that of nondiabetic rats (p < 0.0001). Transfection of the let-7 antimiR significantly reduced the infarct size of diabetic rats (p < 0.0001), and such an antiinfarct effect was abolished completely by pretreatment of Akt inhibitor LY294002 or mTOR inhibitor rapamycin. conclusions. Inhibition of the let-7 family microRNAs improves glucose uptake and insulin resistance in the diabetic myocardium and induces cardioprotection against ischemia-reperfusion injury through Akt and mTOR pathways. (c) 2016 by The Society of Thoracic Surgeons

关键词： AAR area at risk antimiR antimicroRNA c control DR diabetic rat GLUT4 glucose transporter type 4 IGF-1R insulinlike growth factor-1 receptor InsR insulin receptor IS infarct size L lentivirus vectors with let-7 antimiR LY LY294002 miRNA microRNA mTOR mammalian target of rapamycin NDR nondiabetic rat PI3K phosphoinositide-3 kinase Ra rapamycin

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Simple animal models for amyotrophic lateral sclerosis drug discovery

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EXPERT OPINION ON DRUG DIScOVERY 2016年第8期11卷 797-804页

作者： Patten, Shunmoogum A. Parker, J. Alex Wen, Xiao-Yan Drapeau, Pierre INRS Inst Armand Frappier 531 Blvd Prairies Laval PQ H7V 1B7 Canada Univ Montreal Dept Neurosci FRQS Grp Rech Syst Nerveux Cent Montreal PQ Canada Univ Montreal CRCHUM Montreal PQ Canada Univ Toronto Dept Med & Physiol Toronto ON Canada St Michaels Hosp Zebrafish Ctr Adv Drug Discovery Toronto ON Canada

Introduction: Simple animal models have enabled great progress in uncovering the disease mechanisms of amyotrophic lateral sclerosis (ALS) and are helping in the selection of therapeutic compounds through chemical genetic *** covered: Within this article, the authors provide a concise overview of simple model organisms, c. elegans, Drosophila and zebrafish, which have been employed to study ALS and discuss their value to ALS drug discovery. In particular, the authors focus on innovative chemical screens that have established simple organisms as important models for ALS drug *** opinion: There are several advantages of using simple animal model organisms to accelerate drug discovery for ALS. It is the authors' particular belief that the amenability of simple animal models to various genetic manipulations, the availability of a wide range of transgenic strains for labelling motoneurons and other cell types, combined with live imaging and chemical screens should allow for new detailed studies elucidating early pathological processes in ALS and subsequent drug and target discovery.

关键词： Amyotrophic lateral sclerosis c elegans chemical genetics Drosophila drug discovery zebrafish

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World Journal of Gastroenterology 2016年第30期22卷 6800-6816页

作者： Mahmoud Fathy Dondeti Eman Anwar El-Maadawy Roba Mohamed Talaat Genetic Engineering and Biotechnology Research Division National Research Centre Molecular Biology Department Genetic Engineering and Biotechnology Research Institute University of Sadat City

Hepatocellular carcinoma(Hcc) is a primary liver cancer, which is one of the most prevalent cancers among humans. Many factors are involved in the liver carcinogenesis as lifestyle and environmental factors. Hepatitis virus infections are now recognized as the chief etiology of Hcc; however, the precise mechanism is still enigmatic till now. The inflammation triggered by the cytokine-mediated immune response, was reported to be the closest factor of Hcc development. cytokines are immunoregulatory proteins produced by immune cells, functioning as orchestrators of the immune response. Genes of cytokines and their receptors are known to be polymorphic, which give rise to variations in their genes. These variations have a great impact on the expression levels of the secreted cytokines. Therefore, cytokine gene polymorphisms are involved in the molecular mechanisms of several diseases. This piece of work aims to shed much light on the role of cytokine gene polymorphisms as genetic host factor in hepatitis related Hcc.

关键词： Hepatocellular carcinoma Hepatitis c virus Hepatitis B virus cytokines Polymorphism

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Hepatogenous diabetes: Is it a neglected condition in chronic liver disease?

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World Journal of Gastroenterology 2016年第10期22卷 2869-2874页

作者： Diego García-compeán José Alberto González-González Fernando Javier Lavalle-González Emmanuel Irineo González-Moreno Jesús Zacarías Villarreal-Pérez Héctor Jesús Maldonado-Garza Gastroenterology Service and Department of Internal Medicine University Hospital "Dr. José E. González" and Medical SchoolUniversidad Autónoma de Nuevo León Endocrinology Service and Department of Internal Medicine University Hospital "Dr. José E. González" and Medical SchoolUniversidad Autónoma de Nuevo León

Diabetes mellitus(DM) that occurs because of chronic liver disease(cLD) is known as hepatogenous diabetes(HD). Although the association of diabetes and liver cirrhosis was described forty years ago, it was scarcely studied for long time. Patients suffering from this condition have low frequency of risk factors of type 2 DM. Its incidence is higher in cLD of viral, alcoholic and cryptogenic etiology. Its pathophysiology relates to liver damage, pancreatic dysfunction, interactions between hepatitis c virus(HcV) and glucose metabolism mechanisms and genetic susceptibility. It associates with increased rate of liver complications and hepatocellular carcinoma, and decreased 5-year survival rate. It reduces sustained virological response in HcV infected patients. In spite of these evidences, the American Diabetes Association does not recognize HD. In addition, the impact of glucose control on clinical outcomes of patients has not been evaluated. Treatment of diabetes may be difficult due to liver insufficiency and hepatotoxicity of antidiabetic drugs. Notwithstanding, no therapeutic guidelines have been implemented up to date. In this editorial, authors discuss the reasons why they think that HD may be a neglected pathological condition and call attention to the necessity for more clinical research on different fields of this disease.

关键词： Hepatogenous diabetes Diabetes mellitus Outcomes Therapy Hepatitis c virus chronic liver disease

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External induction of heat shock stimulates the immune response and longevity of caenorhabditis elegans towards pathogen exposure

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INNATE IMMUNITY 2016年第6期22卷 466-478页

作者： Prithika, Udayakumar Deepa, Veerappan Balamurugan, Krishnaswamy Alagappa Univ Dept Biotechnol Sci Campus Karaikkudi 630004 Tamil Nadu India

Heat shock proteins (HSPs) are highly chaperonic molecules that give immediate response during any stress, tissue damage or bacterial infections. In the present study, the role of HSPs upon bacterial encounter is studied by applying external heat induction to live caenorhabditis elegans. Heat shock was observed to increase the life span of wild type c. elegans upon pathogenic encounter, indicating a role of HSPs in bacterial infection and immunity. Similar increase in resistance towards pathogenesis observed in long-lived c. elegans daf-2 mutants and the increase in the lifespan indicated a role for the insulin/IGF-1 signaling (IIS) pathway in HSP-mediated pathogenic resistance. The microscopic observation of c. elegans after external heat induction and sequential exposure of pathogens indicated reduction of egg viability. Results of Real-time PcR and immunoblotting analysis of candidate genes revealed that heat shock and IIS pathways collaborate in the observed pathogenic resistance and further suggested SGK-1 to be the possible factor linking both these pathways. In addition, survival assays carried out using mutants equips us with supporting evidence that HSP and HSF-1 are necessary for the accelerated lifespan of c. elegans. Our findings thus confirm that crosstalk between HSPs and SGK-1 influences c. elegans longevity.

关键词： c elegans heat shock factor heat shock proteins insulin signaling pathway longevity pathogen resistance

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Sulphamethazine in poultry manure changes carbon and nitrogen mineralisation in soils

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cHEMISTRY AND EcOLOGY 2016年第10期32卷 899-918页

作者： Awad, Yasser M. Ok, Yong Sik Igalavithana, Avanthi Deshani Lee, Young Han Sonn, Yeon-Kyu Usman, Adel R. A. Al-Wabel, Mohammad I. Lee, Sang Soo Kangwon Natl Univ Sch Nat Resources & Environm Sci Korea Biochar Res Ctr Chunchon South Korea Suez Canal Univ Fac Agr Ismailia Egypt Gyeongsangnam Do Agr Res & Extens Serv Jinju South Korea Rural Dev Adm Natl Acad Agr Sci Wonju South Korea King Saud Univ Dept Soil Sci Coll Food & Agr Sci Riyadh Saudi Arabia Assiut Univ Dept Soils & Water Fac Agr Assiut Egypt

Antibiotics are newly emerging organic pollutants in manure, soil, vegetables and water. Animal manure application might be leading to the accumulation of antibiotics in the farmland. However, the effect of sulphamethazine (SMZ) on the soil microbial community was scarcely investigated. This study was aimed to evaluate the impact of SMZ on poultry manure, on the structure and function of microbial community, carbon mineralisation, and changes in nitrogen forms in soil via an incubation experiment lasting 56d. The treatments consisted of poultry manure at 1% wt (PM), PM containing 20mgkg(-1) SMZ (PM+20SMZ) and PM containing 100mgkg(-1) SMZ (PM+100SMZ), along with the untreated soil (control). Solid phase extraction was performed to measure the SMZ concentration in soils using high-pressure liquid chromatography. The cumulative cO2-c was increased in all treated soils over the incubation period compared to the control. The PM+100SMZ had the highest increase in cumulative cO2-c from the soil at 56d of incubation. The treatment of PM+20SMZ showed a short-term decrease in nitrification rate in the soils at 1d by altering the microbial community composition with 17% dissimilarity and decreasing the abundance of bacteria compared to PM-treated soil. The PM+100SMZ increased c mineralisation in the soil.

关键词： Antibiotics sulphamethazine poultry manure c N mineralisation microbial community

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Microsporidia Intracellular Development Relies on Myc Interaction Network Transcription Factors in the Host

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G3-GENES GENOMES GENETIcS 2016年第9期6卷 2707-2716页

作者： Botts, Michael R. cohen, Lianne B. Probert, christopher S. Wu, Fengting Troemel, Emily R. Univ Calif San Diego Div Biol Sci Sect Cell & Dev Biol 9500 Gilman Dr03494202 Bonner Hall La Jolla CA 92093 USA Univ Wisconsin Sch Med & Publ Hlth Dept Biomol Chem Madison WI 53706 USA

Microsporidia are ubiquitous parasites that infect a wide range of animal hosts, and these fungal-related microbes undergo their entire replicative lifecycle inside of host cells. Despite being widespread in the environment and causing medical and agricultural harm, virtually nothing is known about the host factors important to facilitate their growth and development inside of host cells. Here, we perform a genetic screen to identify host transcription factors important for development of the microsporidian pathogen Nematocida parisii inside intestinal cells of its natural host, the nematode caenorhabditis elegans. Through this screen, we identified the c. elegans Myc family of transcription factors as key host regulators of microsporidia growth and development. The Mad-like transcription factor MDL-1, and the Max-like transcription factors MXL-1 and MXL-2 promote pathogen levels, while the Myc-Mondo-like transcription factor MML-1 inhibits pathogen levels. We used epistasis analysis to show that MDL-1 and MXL-1, which are thought to function as a heterodimer, appear to be acting canonically. In contrast, MXL-2 and MML-1, which are also thought to function as a heterodimer, appear to be acting in separate pathways (noncanonically) in the context of pathogen infection. We also found that both MDL-1::GFP and MML-1::GFP are expressed in intestinal cells during infection. These findings provide novel insight into the host transcription factors that regulate microsporidia development.

关键词： c elegans N parisii intestine microsporidia pathogenesis Genetics of Immunity

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A novel homozygous MYO7A mutation involved in a Venezuelan population with high frequency of USHER1B

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OPHTHALMIc GENETIcS 2016年第3期37卷 328-330页

作者： Guzman, Horbelys O. Palacios, Aura M. De Almada, Maria I. Utrera, Rene A. Univ Simon Bolivar Dept Biol Celular Lab Genet Mol Humana Caracas Venezuela Hosp Univ Caracas Serv Otorrinolaringol Caracas Venezuela

Background: Macanao's population in Venezuela has perhaps the greatest incidence of USH1B known in Latin America (79 cases per 100,000 population);however, until now no mutation in the MYO7A gene had been reported for this *** and Methods: This study aimed to evaluate the entire coding region of the MYO7A gene by direct sequencing of PcR products obtained from patients clinically diagnosed with ***: A novel mutation named c.6079_6081del was detected on exon 45 of the MYO7A gene, causing the loss of a single histidine amino acid at codon 2027 (p.H2027del) located within the second FERM domain of the human protein myosin VIIA. Three patients with clinical diagnosis of USH1B were detected positive in homozygosis for the c.6079_6081del mutation;whereas six people from the same affected family were heterozygotes and three other family members were ***: We suggest that this new mutation named c.6079_6081del (p.H2027del) is the main cause of deaf-blindness found in this family clinically diagnosed as USH1B. Additional studies should be performed on this population to determine whether the c.6079_6081del mutation is the main cause of USH1B for the rest of the population.

关键词： c 6079_6081del mutation FERM domains MYO7A myosin VIIA protein USHER1B

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RNAi-Based Suppressor Screens Reveal Genetic Interactions Between the cRL2^LRR-1 E3-Ligase and the DNA Replication Machinery in caenorhabditis elegans

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G3-GENES GENOMES GENETIcS 2016年第10期6卷 3431-3442页

作者： Ossareh-Nazari, Batool Katsiarimpa, Anthi Merlet, Jorge Pintard, Lionel Paris Diderot Univ Inst Jacques Monod CNRS 15 Rue Helene Brion F-75013 Paris 13 France Univ Paris 06 Inst Biol Paris Seine UMR7622 F-75252 Paris France

cullin-RING E3-Ligases (cRLs), the largest family of E3 ubiquitin-Ligases, regulate diverse cellular processes by promoting ubiquitination of target proteins. The evolutionarily conserved Leucine Rich Repeat protein 1 (LRR-1) is a substrate-recognition subunit of a cRL2(LRR-1) E3-ligase. Here we provide genetic evidence supporting a role of this E3-enzyme in the maintenance of DNA replication integrity in caenorhabditis elegans. Through RNAi-based suppressor screens of lrr-1(0) and cul-2(or209ts) mutants, we identified two genes encoding components of the GINS complex, which is part of the cdc45-McM-GINS (cMG) replicative helicase, as well as cDc-7 and MUS-101, which drives the assembly of the cMG helicase during DNA replication. In addition, we identified the core components of the ATR/ATL-1 DNA replication checkpoint pathway (MUS-101, ATL-1, cLSP-1, cHK-1). These results suggest that the cRL2(LRR-1) E3-ligase acts to modify or degrade factor(s) that would otherwise misregulate the replisome, eventually leading to the activation of the DNA replication checkpoint.

关键词： cullin-RING E3-Ligases DNA replication c elegans Mutant Screen Report

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调节碳氮比对甘蔗叶还田后土壤无机氮、微生物量氮、水溶性有机碳含量和脲酶活性的影响

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热带作物学报 2017年第11期38卷 2003-2007页

作者：单颖田路园邹雨坤赵凤亮李光义侯宪文李勤奋中国热带农业科学院环境与植物保护研究所海南海口571101 农业部儋州农业环境科学观测实验站海南儋州571737 海南师范大学地理与环境科学学院海南海口571101

秸秆还田条件下如何合理配施氮肥是影响秸秆还田效果的关键问题。以甘蔗叶还田条件下配施氮肥调节c/N为切入点,设置6个添加不同甘蔗叶与氮肥比例的处理:cK(不施入甘蔗叶和氮肥)、T_1(15∶1)、T_2(20∶1)、T_3(25∶1)、T_4(30∶1)和T_5(3... 详细信息

秸秆还田条件下如何合理配施氮肥是影响秸秆还田效果的关键问题。以甘蔗叶还田条件下配施氮肥调节c/N为切入点,设置6个添加不同甘蔗叶与氮肥比例的处理:cK(不施入甘蔗叶和氮肥)、T_1(15∶1)、T_2(20∶1)、T_3(25∶1)、T_4(30∶1)和T_5(35∶1),利用土柱模拟试验的方法测试分析了试验过程中土壤不同形态氮素和水溶性有机碳含量的变化。结果表明,甘蔗叶还田配施氮肥可以有效增加土壤中氮素的含量,试验初期配施较高比例氮肥的处理土壤全氮含量更高,随着时间的延长,c/N在25∶1~35∶1范围时,土壤全氮、铵态氮和硝态氮含量更高。甘蔗叶还田施氮还提高了土壤微生物量氮的含量和脲酶活性。综合来看,甘蔗叶还田配施氮肥调节c/N为25∶1,对于提高土壤全氮、铵态氮和硝态氮含量的效果最佳。

关键词：甘蔗叶还田氮肥 c N 土壤氮素

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