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  1. Article ; Online: Impaired T cell-mediated hepatitis in peroxisome proliferator activated receptor alpha (PPARα)-deficient mice.

    Hines, Ian N / Kremer, Michael / Moore, Sherri M / Wheeler, Michael D

    Biological research

    2018  Volume 51, Issue 1, Page(s) 5

    Abstract: Background: Peroxisome proliferator activated receptor alpha (PPARα), a regulator of enzymes involved in β oxidation, has been reported to influence lymphocyte activation. The purpose of this study was to determine whether PPARα plays a role in T cell- ... ...

    Abstract Background: Peroxisome proliferator activated receptor alpha (PPARα), a regulator of enzymes involved in β oxidation, has been reported to influence lymphocyte activation. The purpose of this study was to determine whether PPARα plays a role in T cell-mediated hepatitis induced by Concanavalin A (ConA).
    Methods: Wild type (wt) or PPARα-deficient (PPARα
    Results: Ten and 24 h following ConA administration, wt mice had significant liver injury as demonstrated by serum transaminase levels, inflammatory cell infiltrate, hepatocyte apoptosis, and expression of several cytokines including interleukin 4 (IL4) and interferon gamma (IFNγ). In contrast, PPARα
    Conclusion: Taken together, these data suggest that PPARα within the liver plays an important role in ConA-mediated liver injury through regulation of NKT cell recruitment and/or survival.
    MeSH term(s) Animals ; Cytokines/immunology ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Galactosylceramides/immunology ; Hepatitis, Autoimmune/etiology ; Hepatitis, Autoimmune/immunology ; Immunohistochemistry ; Macrolides/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; PPAR alpha/immunology ; Real-Time Polymerase Chain Reaction ; T-Lymphocytes/immunology
    Chemical Substances Cytokines ; Galactosylceramides ; Macrolides ; PPAR alpha ; concanamycin A (80890-47-7)
    Language English
    Publishing date 2018-02-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 1138990-4
    ISSN 0717-6287 ; 0716-9760
    ISSN (online) 0717-6287
    ISSN 0716-9760
    DOI 10.1186/s40659-018-0153-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Fas Regulates Macrophage Polarization and Fibrogenic Phenotype in a Model of Chronic Ethanol-Induced Hepatocellular Injury.

    Isayama, Fuyumi / Moore, Sherri / Hines, Ian N / Wheeler, Michael D

    The American journal of pathology

    2016  Volume 186, Issue 6, Page(s) 1524–1536

    Abstract: The role of Fas-mediated apoptosis and its effect on proinflammatory cytokine production in early alcoholic liver disease has not been addressed. Wild-type mice (C57Bl/6) or mice with a functional mutation in the Fas ligand (B6.gld) were given either ... ...

    Abstract The role of Fas-mediated apoptosis and its effect on proinflammatory cytokine production in early alcoholic liver disease has not been addressed. Wild-type mice (C57Bl/6) or mice with a functional mutation in the Fas ligand (B6.gld) were given either high-fat control diet or ethanol diet by intragastric cannulation for 2 or 4 weeks. Liver injury, hepatic lipid accumulation, and proinflammatory cytokine production associated with chronic ethanol consumption were largely prevented in B6.gld mice compared with wild-type mice. Conversely, B6.gld mice given ethanol exhibited increases in collagen deposition, hepatic collagen gene expression, and profibrogenic cytokines (eg, transforming growth factor-β and IL-13) and alterations in matrix remodeling proteins (eg, matrix metalloproteinases and tissue inhibitor of metalloproteinases) compared with wild-type mice. Hepatic F4/80(+) macrophage populations were increased significantly in B6.gld mice compared with wild-type mice; hepatic CD3(+) cell populations were not significantly different. Importantly, a shift toward the expression of M2/Th2 cytokines (eg, IL-4 and IL-13) after ethanol exposure was observed in B6.gld mice compared with classical M1 cytokine expression in wild-type mice under similar conditions. In isolated macrophages, stimulation of Fas receptor minimally enhances lipopolysaccharide-induced M1 cytokine production and significantly limits M2 cytokine production. These data support the hypothesis that Fas-mediated signaling is important for an early ethanol-induced proinflammatory response but limits the profibrogenic response, regulating collagen production in response to chronic ethanol.
    MeSH term(s) Animals ; Apoptosis/physiology ; Blotting, Western ; Disease Models, Animal ; Fas Ligand Protein/metabolism ; Immunohistochemistry ; In Situ Nick-End Labeling ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; Macrophages/cytology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Phenotype ; Real-Time Polymerase Chain Reaction ; fas Receptor/metabolism
    Chemical Substances Fas Ligand Protein ; Fas protein, mouse ; fas Receptor
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2016.02.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Fatty acid-binding protein 5 limits the anti-inflammatory response in murine macrophages.

    Moore, Sherri M / Holt, Vivian V / Malpass, Lillie R / Hines, Ian N / Wheeler, Michael D

    Molecular immunology

    2015  Volume 67, Issue 2 Pt B, Page(s) 265–275

    Abstract: The beginning stages of liver damage induced by various etiologies (i.e. high fat diet, alcohol consumption, toxin exposure) are characterized by abnormal accumulation of lipid in liver. Alterations in intracellular lipid transport, storage, and ... ...

    Abstract The beginning stages of liver damage induced by various etiologies (i.e. high fat diet, alcohol consumption, toxin exposure) are characterized by abnormal accumulation of lipid in liver. Alterations in intracellular lipid transport, storage, and metabolism accompanied by cellular insult within the liver play an important role in the pathogenesis of liver disease, often involving a sustained inflammatory response. The intracellular lipid transporter, fatty acid binding protein 5 (FABP5), is highly expressed in macrophages and may play an important role in the hepatic inflammatory response after endotoxin exposure in mice. This study tested the hypothesis that FABP5 regulates macrophage response to LPS in male C57bl/6 (wild type) and FABP5 knockout mice, both in vitro and in vivo. Treatment with LPS revealed that loss of FABP5 enhances the number of hepatic F4/80(+) macrophages in the liver despite limited liver injury. Conversely, FABP5 knock out mice display higher mRNA levels of anti-inflammatory cytokines IL-10, arginase, YM-1, and Fizz-1 in liver compared to wild type mice. Bone marrow derived macrophages stimulated with inflammatory (LPS and IFN-γ) or anti-inflammatory (IL-4) mediators also showed significantly higher expression of anti-inflammatory/regulatory factors. These findings reveal a regulatory role of FABP5 in the acute inflammatory response to LPS-induced liver injury, which is consistent with the principle finding that FABP5 is a regulator of macrophage phenotype. Specifically, these findings demonstrate that loss of FABP5 promotes a more anti-inflammatory response.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Biomarkers/metabolism ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/metabolism ; Cell Polarity/drug effects ; Cell Separation ; Fatty Acid-Binding Proteins/genetics ; Fatty Acid-Binding Proteins/metabolism ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Inflammation/metabolism ; Inflammation/pathology ; Lipopolysaccharides/pharmacology ; Liver/injuries ; Liver/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neutrophil Infiltration/drug effects ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Time Factors
    Chemical Substances Anti-Inflammatory Agents ; Biomarkers ; Fabp5 protein, mouse ; Fatty Acid-Binding Proteins ; Lipopolysaccharides ; Neoplasm Proteins ; RNA, Messenger
    Language English
    Publishing date 2015-10
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 424427-8
    ISSN 1872-9142 ; 0161-5890
    ISSN (online) 1872-9142
    ISSN 0161-5890
    DOI 10.1016/j.molimm.2015.06.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 166: Show issues Location:
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  4. Article: Fatty acid-binding protein 5 limits the anti-inflammatory response in murine macrophages

    Moore, Sherri M / Ian N. Hines / Lillie R. Malpass / Michael D. Wheeler / Vivian V. Holt

    Molecular Immunology. 2015 Oct., v. 67

    2015  

    Abstract: The beginning stages of liver damage induced by various etiologies (i.e. high fat diet, alcohol consumption, toxin exposure) are characterized by abnormal accumulation of lipid in liver. Alterations in intracellular lipid transport, storage, and ... ...

    Abstract The beginning stages of liver damage induced by various etiologies (i.e. high fat diet, alcohol consumption, toxin exposure) are characterized by abnormal accumulation of lipid in liver. Alterations in intracellular lipid transport, storage, and metabolism accompanied by cellular insult within the liver play an important role in the pathogenesis of liver disease, often involving a sustained inflammatory response. The intracellular lipid transporter, fatty acid binding protein 5 (FABP5), is highly expressed in macrophages and may play an important role in the hepatic inflammatory response after endotoxin exposure in mice. This study tested the hypothesis that FABP5 regulates macrophage response to LPS in male C57bl/6 (wild type) and FABP5 knockout mice, both in vitro and in vivo. Treatment with LPS revealed that loss of FABP5 enhances the number of hepatic F4/80+ macrophages in the liver despite limited liver injury. Conversely, FABP5 knock out mice display higher mRNA levels of anti-inflammatory cytokines IL-10, arginase, YM-1, and Fizz-1 in liver compared to wild type mice. Bone marrow derived macrophages stimulated with inflammatory (LPS and IFN-γ) or anti-inflammatory (IL-4) mediators also showed significantly higher expression of anti-inflammatory/regulatory factors. These findings reveal a regulatory role of FABP5 in the acute inflammatory response to LPS-induced liver injury, which is consistent with the principle finding that FABP5 is a regulator of macrophage phenotype. Specifically, these findings demonstrate that loss of FABP5 promotes a more anti-inflammatory response.
    Keywords alcohol drinking ; arginase ; bone marrow ; endotoxins ; fatty acid-binding proteins ; high fat diet ; inflammation ; interferon-gamma ; interleukin-10 ; interleukin-4 ; knockout mutants ; lipids ; liver ; liver diseases ; macrophages ; males ; messenger RNA ; metabolism ; mice ; pathogenesis ; phenotype
    Language English
    Dates of publication 2015-10
    Size p. 265-275.
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 424427-8
    ISSN 1872-9142 ; 0161-5890
    ISSN (online) 1872-9142
    ISSN 0161-5890
    DOI 10.1016/j.molimm.2015.06.001
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Smad3 signaling in the regenerating liver: implications for the regulation of IL-6 expression.

    Kremer, Michael / Son, Gakuhei / Zhang, Kun / Moore, Sherri M / Norris, Amber / Manzini, Giulia / Wheeler, Michael D / Hines, Ian N

    Transplant international : official journal of the European Society for Organ Transplantation

    2014  Volume 27, Issue 7, Page(s) 748–758

    Abstract: Liver regeneration is vital for graft survival and adequate organ function. Smad activation regulates hepatocyte proliferation and macrophage function. The aim of the current study was to evaluate the impact of Smad3 signaling during liver regeneration ... ...

    Abstract Liver regeneration is vital for graft survival and adequate organ function. Smad activation regulates hepatocyte proliferation and macrophage function. The aim of the current study was to evaluate the impact of Smad3 signaling during liver regeneration in the mouse. Male C57Bl/6 wild-type (wt) mice or mice deficient in Smad3 (Smad3(-/-) ) were subjected to a 70% partial hepatectomy (pHx) or sham surgery and sacrificed 24, 42, or 48 h later. Tissue was analyzed for TGF-β signaling, the mitogenic cytokine response [i.e., tumor necrosis factor alpha, TNF-α; interleukin (IL)-6], and liver regeneration. Partial hepatectomy stimulated a strong regenerative response measured by proliferating cell nuclear antigen-positive hepatocytes 42 and 48 h post-pHx in conjunction with an increased expression of IL-6, TNF-α, and Smad2/3 phosphorylation 24 h post-pHx in both hepatocytes and nonparenchymal cells. Surprisingly, Smad3 deficiency led to reduced hepatocyte proliferation 42 h post-pHx which recovered by 48 h, a process that correlated with and was preceded by significant reductions in IL-6 expression and signal transducer and activator of transcription 3 phosphorylation, and cyclin D1 induction 24 h post-pHx. Loss of Smad3 signaling suppresses the expression of key mitogenic cytokines and delays hepatocellular regeneration. Therapies directed at finely regulating Smad3 activation early within the regenerating liver may prove useful in promoting liver cell proliferation and restoration of liver mass.
    MeSH term(s) Animals ; Hepatectomy ; Interleukin-6/biosynthesis ; Liver Regeneration/physiology ; Male ; Mice, Inbred C57BL ; Protein Inhibitors of Activated STAT/physiology ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Smad3 Protein/physiology
    Chemical Substances Interleukin-6 ; Pias3 protein, mouse ; Protein Inhibitors of Activated STAT ; STAT3 Transcription Factor ; Smad3 Protein ; Smad3 protein, mouse ; Stat3 protein, mouse
    Language English
    Publishing date 2014-05-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639435-8
    ISSN 1432-2277 ; 0934-0874
    ISSN (online) 1432-2277
    ISSN 0934-0874
    DOI 10.1111/tri.12322
    Database MEDical Literature Analysis and Retrieval System OnLINE

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