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Lysosome and proteasome dysfunction in alcohol-induced liver injury

Liver Research 2019年第3期3卷 191-205页

作者： terrence m.donohue.jr Natalia A.Osna Kusum K.Kharbanda Paul G.Thomes Research Service Department of Veterans AffairsNebraska-Western Iowa Health Care SystemOmahaNEUSA Department of Internal medicine Section of Gastroenterology and HepatologyUniversity of Nebraska Medical CenterOmahaNEUSA Department of Biochemistry and molecular Biology University of Nebraska Medical CenterOmahaNEUSA Department of Pharmacology and Experimental Neuroscience University of Nebraska Medical CenterOmahaNEUSA College of Public Health University of Nebraska Medical CenterOmahaNEUSA

The review describes research findings on the influence of alcohol consumption on two crucial catabolic systems in hepatocytes:the lysosome and the ubiquitin-proteasome system(UPS).The lysosome is a membrane-bound organelle that degrades all aging and/or damaged organelles and hydrolyzes all forms of *** UPS is mostly *** carries out the majority of its functions in the soluble portion of the cytoplasm(cytosol)and degrades nearly all intracellular proteins,particularly those with short half-lives,so that their levels are tightly *** review will briefly discuss the epidemiology of alcohol abuse and the spectrum of alcohol-induced liver disease(AILD).We will explain why ethanol(EtOH)metabolism,but not EtOH alone,is ***,we will summarize how heavy drinking alters hepatic catabolic systems,resulting in liver enlargement that develops from hepatocyte swelling due,in part,to aberrant accumulation of undegraded lipid droplets(steatosis)and undegraded proteins(proteopathy).Our detailed description of each catabolic system will highlight its discoverer(s)and emphasize each system’s *** important,we will review the evidence that chronic EtOH consumption disrupts hepatic lysosome biogenesis and inhibits the UPS by impeding hepatic proteasome *** will become evident that each of these EtOH-induced defects has far-reaching functional ***,we will describe current and potential therapeutic interventions for alleviating EtOH-induced liver *** most effective intervention is the cessation of EtOH ***,there are other potential approaches using natural or synthetic compounds that activate autophagy or the proteasome to enhance the degradation of accumulated lipid droplets or proteins,respectively,which could alleviate *** approaches,now in their early stages of investigation,will also be discussed in this review.

关键词： Alcohol Lysosome Proteasome Ethanol Liver Proteostasis Lipostasis Alcohol-induced liver disease(AILD)

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Autophagy and ethanol-induced liver injury

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World Journal of Gastroenterology 2009年第10期15卷 1178-1185页

作者： terrence m.donohue.jr Liver Study Unit The Omaha Veterans Affairs Medical Center Department of Internal Medicine University of Nebraska Medical Center Omaha Nebraska 68105 United States

The majority of ethanol metabolism occurs in the liver. Consequently, this organ sustains the greatest damage from ethanol abuse. Ethanol consumption disturbs the delicate balance of protein homeostasis in the liver, causing intracellular protein accumulation due to a disruption of hepatic protein catabolism. Evidence indicates that ethanol or its metabolism impairs trafficking events in the liver, including the process of macroautophagy, which is the engulfment and degradation of cytoplasmic constituents by the lysosomal system. Autophagy is an essential, ongoing cellular process that is highly regulated by nutrients, endocrine factors and signaling pathways. A great number of the genes and gene products that govern the autophagic response have been characterized and the major metabolic and signaling pathways that activate or suppress autophagy have been identified. This review describes the process of autophagy, its regulation and the possible mechanisms by which ethanol disrupts the process of autophagic degradation. The implications of autophagic suppression are discussed in relation to the pathogenesis of alcohol-induced liver injury.

关键词： Autophagy Autophagosome Ethanolmetabolism Hepatomegaly Lysosomes Signal transduction

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Alcohol-induced steatosis in liver cells

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World Journal of Gastroenterology 2007年第37期13卷 4974-4978页

作者： terrence m.donohue.jr Liver Study Unit The Omaha Veterans Affairs Medical Center the Department of Internal Medicine University of Nebraska Medical Center Omaha Nebraska 68105 United States

Alcohol-induced fatty liver (steatosis) was believed to result from excessive generation of reducing equivalents from ethanol metabolism, thereby enhancing fat accumulation. Recent findings have revealed a more complex picture in which ethanol oxidation is still required, but specific transcription as well as humoral factors also have important roles. Transcription factors involved include the sterol regulatory element binding protein 1 (SREBP-1) which is activated to induce genes that regulate lipid biosynthesis. Conversely, ethanol consumption causes a general down-regulation of lipid (fatty acid) oxidation, a reflection of inactivation of the peroxisome proliferator- activated receptor-alpha (PPAR-α) that regulates genes involved in fatty acid oxidation. A third transcription factor is the early growth response-1 (Egr-1), which is strongly induced prior to the onset of steatosis. The activities of all these factors are governed by that of the principal regulatory enzyme, AmP kinase. Important humoral factors, including adiponectin, and tumor necrosis factor-α (TNF-α), also regulate alcohol-induced steatosis. Their levels are affected by alcohol consumption and by each other. This review will summarize the actions of these proteins in ethanol-elicited fatty liver. Because steatosis is now regarded as a significant risk factor for advanced liver pathology, an understanding of the molecular mechanisms in its etiology is essential for development of effective therapies.

关键词： Ethanol metabolism Fatty liver Sterolregulatory element binding protein Peroxisomeproliferator activated receptor Early growth response-i Fatty acid toxicity Triglycerides Acetaldehyde Reactiveoxygen species

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Implication of altered proteasome function in alcoholic liverinjury

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World Journal of Gastroenterology 2007年第37期13卷 4931-4937页

作者： Natalia A Osna terrence m.donohue.jr Liver Study Unit The Omaha Veterans Affairs Medical Center the Department of Internal Medicine University of Nebraska Medical Center Omaha Nebraska 68105 United States

The proteasome is a major protein-degrading enzyme, which catalyzes degradation of oxidized and aged proteins, signal transduction factors and cleaves peptides for antigen presentation. Proteasome exists in the equilibrium of 26S and 20S particles. Proteasome function is altered by ethanol metabolism, depending on oxidative stress levels： low oxidative stress induces proteasome activity, while high oxidative stress reduces it. The proposed mechanisms for modulation of proteasome activity are related to oxidative modification of proteasomal proteins with primary and secondary products derived from ethanol oxidation. Decreased proteolysis by the proteasome results in the accumulation of insoluble protein aggregates, which cannot be degraded by proteasome and which further inhibit proteasome function. mallory bodies, a common signature of alcoholic liver diseases, are formed by liver cells, when proteasome is unable to remove cytokeratins. Proteasome inhibition by ethanol also promotes the accumulation of pro-apoptotic factors in mitochondria of ethanol-metabolizing liver cells that are normally degraded by proteasome. In addition, decreased proteasome function also induces accumulation of the negative regulators of cytokine signaling （I-~B and SOCS）, thereby blocking cytokine signal transduction. Finally, ethanol-elicited blockade of interferon type 2 and 2 signaling and decreased proteasome function impairs generation of peptides for mHC class Ⅰ-restricted antigen presentation.

关键词： 20S proteasome 26S proteasome, PA28, CYP2E1, Apoptosis, Liver

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一种新的肿瘤相关糖蛋白的纯化与分析

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细胞与分子免疫学杂志 1987年第4期 19-19页

作者： Thomas L.Klug,terrence F.Gerber,Vencent R.Zurawski jr.,Norman C.LeDonne jr,张明杰 Laboratory of Cancer Research Centoccr malvern PA 19355 Laboratory of Cancer Research Centoccr malvern PA 19355 Laboratory of Cancer Research Centoccr malvern PA 19355 Laboratory of Cancer Research Centoccr malvern PA 19355

为了从血清及悬浮组织培养上清提纯出高产量的人胃肠道相关糖蛋白抗原曾设计了一个方案。提纯的关键步骤是用单克隆抗体1116 TS-19-9进行亲和柱层析,接着使结合的蛋白诱导烷化,并进行第二次免疫亲和柱分步收集。诱导和烷化有利于打断含... 详细信息

为了从血清及悬浮组织培养上清提纯出高产量的人胃肠道相关糖蛋白抗原曾设计了一个方案。提纯的关键步骤是用单克隆抗体1116 TS-19-9进行亲和柱层析,接着使结合的蛋白诱导烷化,并进行第二次免疫亲和柱分步收集。诱导和烷化有利于打断含抗原的二硫化物稳

关键词：肿瘤相关糖蛋白粘蛋白培养上清

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温哥华公寓

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城市环境设计 2019年第2期118卷 210-219页

作者： Carl mcDonald melissa Bauld Aaron mark Alan Tansey Alex Wu Alexandra Gustafsson Alina Tamosiunaite Amina Blacksher Aran Coakley Arash Adel Ahmadian Armen menendian Barbora Srpkova Ben Zunkeler Benjamin Caldwell Benjamin Novacinski Bennett Gale Birk Daugaard Blake Theodore Smith Brian Foster Brian Rome Carolien Schippers Christopher James malcolm jr. Christopher Junkin Christopher Tron David Brown David Dottelonde Deborah Campbell Doug Stechschulte Douglass Alligood Edward Yung Elena Bresciani Filip milovanovic Francesca Portesine Gabriel Hernandez Solano Gabriel Jewell-Vitale Hector Garcia Ivy Hume Jan Leenknegt Janice Rim John Kim Josiah Poland Julian Liang Julianne Gola Julie Kaufman Karol Bogdan Borkowski Kurt Nieminen Lauren Turner Lorenz Krisai Lucio Santos marcella martinez martin Voelkle matthew Dlugosz megan Ng michael Robert Taylor Otilia Pupezeanu Paula Domka Phillip macDougall Ryan Yang Sean Franklin Sebastian Grogaard Simon Scheller Spencer Hayden Taylor Fulton terrence Chew Terry Lallak Thomas Smith Tianqi Zhang Tobias Hjortdal Tran Le Valentina mele Xinyu Wang Yaziel Juarbe Yoanna Shivarova Zach Walters Zhifei Xu Andrew Latreille Glotman Simpson Urban YVR 运小红

温哥华公寓的建成预示着这个年轻的城市正在打开城市政策制定的新局面。它将成为从Granville大桥进入温哥华市中心的城市大门。塔楼和群房的设计是对新城市主义地域类型中的"温哥华主义"建筑的全新解读,配合一座纤细的塔楼,试图保留城... 详细信息

温哥华公寓的建成预示着这个年轻的城市正在打开城市政策制定的新局面。它将成为从Granville大桥进入温哥华市中心的城市大门。塔楼和群房的设计是对新城市主义地域类型中的"温哥华主义"建筑的全新解读,配合一座纤细的塔楼,试图保留城市视觉通廊并激活步行通道。住宅塔楼借助高度和毗邻河流的地理位置,是唯一可以同时享受水景和山景的建筑,坐拥温哥华广袤的自然风光。

关键词：温哥华平面图 Dialog 立面图

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