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40
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M116.737015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M116.737015</a>
Pages
22482–22495
Issue
43
Volume
291
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
MitoNEET Deficiency Alleviates Experimental Alcoholic Steatohepatitis in Mice by Stimulating Endocrine Adiponectin-Fgf15 Axis.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
*adiponectin; *alcohol; *intestine; *iron; *liver injury; *Signal Transduction; Adiponectin/genetics/*metabolism; Alcoholic/genetics/*metabolism/pathology; Animals; Fatty Liver; Fibroblast Growth Factors/genetics/*metabolism; Humans; Iron-Binding Proteins/metabolism; Knockout; Male; Membrane Proteins/*deficiency/metabolism; Mice; NF-kappa B/genetics/metabolism; Sirtuin 1/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Hu Xudong; Jogasuria Alvin; Wang Jiayou; Kim Chunki; Han Yoonhee; Shen Hong; Wu Jiashin; You Min
Description
An account of the resource
MitoNEET (mNT) (CDGSH iron-sulfur domain-containing protein 1 or CISD1) is an outer mitochondrial membrane protein that donates 2Fe-2S clusters to apo-acceptor proteins. In the present study, using a global mNT knock-out (mNTKO) mouse model, we investigated the in vivo functional role of mNT in the development of alcoholic steatohepatitis. Experimental alcoholic steatohepatitis was achieved by pair feeding wild-type (WT) and mNTKO mice with Lieber-DeCarli ethanol-containing diets for 4 weeks. Strikingly, chronically ethanol-fed mNTKO mice were completely resistant to ethanol-induced steatohepatitis as revealed by dramatically reduced hepatic triglycerides, decreased hepatic cholesterol level, diminished liver inflammatory response, and normalized serum ALT levels. Mechanistic studies demonstrated that ethanol administration to mNTKO mice induced two pivotal endocrine hormones, namely, adipose-derived adiponectin and gut-derived fibroblast growth factor 15 (Fgf15). The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNTKO mice. Other potential mechanisms such as reduced oxidative stress, activated Sirt1 signaling, and diminished NF-kappaB activity also contribute to hepatic improvement in the ethanol-fed mNTKO mice. In conclusion, the present study identified adiponectin and Fgf15 as pivotal adipose-gut-liver metabolic coordinators in mediating the protective action of mNT deficiency against development of alcoholic steatohepatitis in mice. Our findings may help to establish mNT as a novel therapeutic target and pharmacological inhibition of mNT may be beneficial for the prevention and treatment of human alcoholic steatohepatitis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M116.737015" target="_blank" rel="noreferrer noopener">10.1074/jbc.M116.737015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*adiponectin
*alcohol
*intestine
*iron
*liver injury
*Signal Transduction
2016
Adiponectin/genetics/*metabolism
Alcoholic/genetics/*metabolism/pathology
Animals
Department of Pharmaceutical Sciences
Fatty Liver
Fibroblast Growth Factors/genetics/*metabolism
Han Yoonhee
Hu Xudong
Humans
Iron-Binding Proteins/metabolism
Jogasuria Alvin
Kim Chunki
Knockout
Male
Membrane Proteins/*deficiency/metabolism
Mice
NEOMED College of Pharmacy
NF-kappa B/genetics/metabolism
Shen Hong
Sirtuin 1/genetics/metabolism
The Journal of biological chemistry
Wang Jiayou
Wu Jiashin
You Min
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/IAI.00369-17" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/IAI.00369-17</a>
Issue
11
Volume
85
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Impairment of Hematopoietic Precursor Cell Activation during the Granulopoietic Response to Bacteremia in Mice with Chronic-Plus-Binge Alcohol Administration.
Publisher
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Infection and immunity
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-11
Subject
The topic of the resource
*Alcohol; *bacteremia; *cell signaling; *granulocytes; *granulopoietic response; *stem cells; Animal; Animals; Antigens; Bacteremia/genetics/*immunology/pathology; Binge Drinking/genetics/*immunology/pathology; Bone Marrow Cells/drug effects/immunology/pathology; CCAAT-Enhancer-Binding Protein-beta/genetics/immunology; Cyclin D1/genetics/immunology; Disease Models; Escherichia coli Infections/genetics/*immunology/pathology; Escherichia coli/growth & development/immunology; Ethanol/*pharmacology; Gene Expression Regulation/*drug effects/immunology; Granulocytes/drug effects/immunology/pathology; Hematopoiesis/*drug effects/genetics/immunology; Inbred BALB C; Ly/genetics/immunology; Male; Membrane Proteins/genetics/immunology; Mice; Mitogen-Activated Protein Kinase 1/genetics/immunology; Mitogen-Activated Protein Kinase 3/genetics/immunology; Nucleotidyltransferases/deficiency/genetics/immunology; Proto-Oncogene Proteins c-kit/genetics/immunology; Signal Transduction/*drug effects/immunology; Toll-Like Receptor 4/genetics/immunology
Creator
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Shi Xin; Lin Yuan-Ping; Gao Bin; Zhang Ping
Description
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Alcohol abuse impairs immune defense. To study the effect of chronic-plus-binge alcohol exposure on the granulopoietic response, acute alcohol intoxication (intraperitoneal injection of 5 g alcohol/kg body weight) was introduced to mice chronically fed on the Lieber-DeCarli low-fat liquid alcohol diet for 5 weeks. Bacteremia was induced by intravenous injection of Escherichia coli Bacteremia caused a remarkable increase in marrow lin(-) c-kit(+) Sca-1(+) cells. Activation of cell proliferation supported the increase in marrow lin(-) c-kit(+) Sca-1(+) cells. Alcohol administration inhibited this activation of lin(-) c-kit(+) Sca-1(+) cells. The bone marrow of pair-fed control mice receiving intraperitoneal saline stored a large number of mature granulocytes expressing a high level of Gr1 (Gr1(hi) cells). The proportion of Gr1(hi) cells and the total number of Gr1(+) cells were markedly reduced in the bone marrow, along with an increase in the ratio of Gr1(+) granulocytes in peripheral white blood cells following bacteremia. E. coli infection stimulated proliferation of granulopoietic precursor cells, resulting in a marked increase in the ratio of immature Gr1(lo) cells in the bone marrow. Alcohol administration itself triggered marrow release of Gr1(+) cells, resulting in reduction of the marrow granulocyte reserve with an elevation of granulocytes in the circulation. Alcohol also impaired activation of granulopoietic precursor proliferation following bacteremia. Alcohol disrupted lipopolysaccharide (LPS)-TLR4-ERK1/2-cyclin D1 signaling and inhibited upregulation of Sca-1 and C/EBPbeta expression by lineage-negative marrow cells in response to bacteremia. These results indicate that chronic-plus-binge alcohol exposure inhibits the granulopoietic response by disrupting key cell signaling for hematopoietic precursor cell activation and commitment to granulocyte lineage development.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/IAI.00369-17" target="_blank" rel="noreferrer noopener">10.1128/IAI.00369-17</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*alcohol
*bacteremia
*cell signaling
*granulocytes
*granulopoietic response
*Stem cells
2017
Animal
Animals
Antigens
Bacteremia/genetics/*immunology/pathology
Binge Drinking/genetics/*immunology/pathology
Bone Marrow Cells/drug effects/immunology/pathology
CCAAT-Enhancer-Binding Protein-beta/genetics/immunology
Cyclin D1/genetics/immunology
Department of Integrative Medical Sciences
Disease Models
Escherichia coli Infections/genetics/*immunology/pathology
Escherichia coli/growth & development/immunology
Ethanol/*pharmacology
Gao Bin
Gene Expression Regulation/*drug effects/immunology
Granulocytes/drug effects/immunology/pathology
Hematopoiesis/*drug effects/genetics/immunology
Inbred BALB C
Infection and immunity
Lin Yuan-Ping
Ly/genetics/immunology
Male
Membrane Proteins/genetics/immunology
Mice
Mitogen-Activated Protein Kinase 1/genetics/immunology
Mitogen-Activated Protein Kinase 3/genetics/immunology
NEOMED College of Medicine
Nucleotidyltransferases/deficiency/genetics/immunology
Proto-Oncogene Proteins c-kit/genetics/immunology
Shi Xin
Signal Transduction/*drug effects/immunology
Toll-Like Receptor 4/genetics/immunology
Zhang Ping