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  1. Article ; Online: Membrane lipid interactions in intestinal ischemia/reperfusion-induced Injury.

    Slone, Emily Archer / Fleming, Sherry D

    Clinical immunology (Orlando, Fla.)

    2014  Volume 153, Issue 1, Page(s) 228–240

    Abstract: Ischemia, lack of blood flow, and reperfusion, return of blood flow, are a common phenomenon affecting millions of Americans each year. Roughly 30,000 Americans per year experience intestinal ischemia-reperfusion (IR), which is associated with a high ... ...

    Abstract Ischemia, lack of blood flow, and reperfusion, return of blood flow, are a common phenomenon affecting millions of Americans each year. Roughly 30,000 Americans per year experience intestinal ischemia-reperfusion (IR), which is associated with a high mortality rate. Previous studies of the intestine established a role for neutrophils, eicosanoids, the complement system and naturally occurring antibodies in IR-induced pathology. Furthermore, data indicate involvement of a lipid or lipid-like moiety in mediating IR-induced damage. It has been proposed that antibodies recognize exposure of neo-antigens, triggering action of the complement cascade. While it is evident that the pathophysiology of IR-induced injury is complex and multi-factorial, we focus this review on the involvement of eicosanoids, phospholipids and neo-antigens in the early pathogenesis. Lipid changes occurring in response to IR, neo-antigens exposed and the role of a phospholipid transporter, phospholipid scramblase 1 will be discussed.
    MeSH term(s) Animals ; Antibodies/immunology ; Antigens/immunology ; Humans ; Hypoxia/metabolism ; Intestinal Mucosa/metabolism ; Intestines/blood supply ; Intestines/immunology ; Intestines/pathology ; Membrane Lipids/metabolism ; Phospholipid Transfer Proteins/metabolism ; Reperfusion Injury/immunology ; Reperfusion Injury/metabolism ; Signal Transduction
    Chemical Substances Antibodies ; Antigens ; Membrane Lipids ; Phospholipid Transfer Proteins
    Language English
    Publishing date 2014-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2014.04.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Phospholipid scramblase 1 is required for β2-glycoprotein I binding in hypoxia and reoxygenation-induced endothelial inflammation.

    Slone, Emily Archer / Pope, Michael R / Fleming, Sherry D

    Journal of leukocyte biology

    2015  Volume 98, Issue 5, Page(s) 791–804

    Abstract: Multiple pathologic conditions, including hemorrhage, tumor angiogenesis, and ischemia-reperfusion events, will result in hypoxia and subsequent reperfusion. Previous studies have analyzed the lipid changes within whole tissues and indicated that ... ...

    Abstract Multiple pathologic conditions, including hemorrhage, tumor angiogenesis, and ischemia-reperfusion events, will result in hypoxia and subsequent reperfusion. Previous studies have analyzed the lipid changes within whole tissues and indicated that ischemia-reperfusion altered tissue and cellular phospholipids. Using an in vitro cell culture model of hypoxia and reoxygenation, we examined the endothelial lipid changes. We hypothesized that phospholipid scramblase 1, a protein that regulates bilayer asymmetry, is involved in altering the phospholipids of endothelial cells during hypoxia, a component of ischemia, leading to β2-glycoprotein I and IgM binding and subsequent lipid-mediated, inflammatory responses. We have completed the first comprehensive study of steady-state phospholipid scramblase 1 mRNA levels, protein expression, and activity under conditions of hypoxia and reoxygenation. Phospholipid scramblase 1 regulates phosphatidylserine exposure in response to oxygen stress, leading to β2-glycoprotein I and IgM binding and lipid-mediated, inflammatory responses.
    MeSH term(s) Animals ; Cell Hypoxia ; Cell Line ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Immunoglobulin M/genetics ; Immunoglobulin M/metabolism ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Mice ; Phospholipid Transfer Proteins/genetics ; Phospholipid Transfer Proteins/metabolism ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Vasculitis/genetics ; Vasculitis/metabolism ; Vasculitis/pathology ; beta 2-Glycoprotein I/genetics ; beta 2-Glycoprotein I/metabolism
    Chemical Substances Immunoglobulin M ; Phospholipid Transfer Proteins ; Plscr1 protein, mouse ; beta 2-Glycoprotein I
    Language English
    Publishing date 2015-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.3A1014-480R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: TLR9 is dispensable for intestinal ischemia/reperfusion-induced tissue damage.

    Slone, Emily Archer / Pope, Michael R / Roth, Mary / Welti, Ruth / Fleming, Sherry D

    American journal of clinical and experimental immunology

    2012  Volume 1, Issue 2, Page(s) 124–135

    Abstract: The mortality rate due to intestinal ischemia/reperfusion (IR) remains at 60-80%. As toll-like receptor (TLR) 4 has been shown to be critical for IR injury in several organs, including the intestine, and TLR9 is necessary for IR-induced damage of the ... ...

    Abstract The mortality rate due to intestinal ischemia/reperfusion (IR) remains at 60-80%. As toll-like receptor (TLR) 4 has been shown to be critical for IR injury in several organs, including the intestine, and TLR9 is necessary for IR-induced damage of the liver, we investigated the hypothesis that TLR9 is involved in intestinal IR-induced damage. Wildtype (C57Bl/6) and TLR9(-/-) mice were subjected to intestinal IR or Sham treatment. Several markers of damage and inflammation were assessed, including mucosal injury, eicosanoid production, cytokine secretion and complement deposition. Although IR-induced injury was not altered, PGE(2) production was decreased in TLR9(-/-) mice. Attenuated PGE(2) production was not due to differences in percentage of lipids or COX-2 transcription. The data indicate that TLR9 is not required for IR-induced injury or inflammation of the intestine.
    Language English
    Publishing date 2012-10-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2695562-3
    ISSN 2164-7712
    ISSN 2164-7712
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Intestinal lipid alterations occur prior to antibody-induced prostaglandin E2 production in a mouse model of ischemia/reperfusion.

    Sparkes, Byron L / Slone, Emily E Archer / Roth, Mary / Welti, Ruth / Fleming, Sherry D

    Biochimica et biophysica acta

    2010  Volume 1801, Issue 4, Page(s) 517–525

    Abstract: Ischemia/reperfusion (IR) induced injury results in significant tissue damage in wild-type, but not antibody-deficient, Rag-1(-/-) mice. However, Rag-1(-/-) mice sustain intestinal damage after administration of wild-type antibodies or naturally ... ...

    Abstract Ischemia/reperfusion (IR) induced injury results in significant tissue damage in wild-type, but not antibody-deficient, Rag-1(-/-) mice. However, Rag-1(-/-) mice sustain intestinal damage after administration of wild-type antibodies or naturally occurring, specific anti-phospholipid related monoclonal antibodies, suggesting involvement of a lipid antigen. We hypothesized that IR initiates metabolism of cellular lipids, resulting in production of an antigen recognized by anti-phospholipid antibodies. At multiple time points after Sham or IR treatment, lipids extracted from mouse jejunal sections were analyzed by electrospray ionization triple quadrupole mass spectrometry. Within 15min of reperfusion, IR induced significantly more lysophosphatidylcholine (lysoPC), lysophosphatidylglycerol (lysoPG) and free arachidonic acid (AA) production than Sham treatment. While lysoPC, lysoPG, and free AA levels were similar in C57Bl/6 (wild-type) and Rag-1(-/-) mice, IR led to Cox-2 activation and prostaglandin E(2) (PGE(2)) production in wild-type, but not in the antibody-deficient, Rag-1(-/-) mice. Administration of wild-type antibodies to Rag-1(-/-) mice restored PGE(2) production and intestinal damage. These data indicate that IR-induced intestinal damage requires antibodies for Cox-2 stimulated PGE(2) production but not for production of lysoPC and free AA.
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Homeodomain Proteins/physiology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Ischemia/immunology ; Ischemia/metabolism ; Ischemia/pathology ; Jejunum/injuries ; Jejunum/metabolism ; Lysophosphatidylcholines/metabolism ; Lysophospholipids/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phospholipids/immunology ; Phospholipids/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Reperfusion Injury/immunology ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Spectrometry, Mass, Electrospray Ionization ; Sphingomyelins/metabolism
    Chemical Substances Antibodies, Monoclonal ; Homeodomain Proteins ; Lysophosphatidylcholines ; Lysophospholipids ; Phospholipids ; RNA, Messenger ; Sphingomyelins ; lysophosphatidylglycerol ; RAG-1 protein (128559-51-3) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2010-01-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbalip.2010.01.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Overexpression of eIF5 or its protein mimic 5MP perturbs eIF2 function and induces ATF4 translation through delayed re-initiation.

    Kozel, Caitlin / Thompson, Brytteny / Hustak, Samantha / Moore, Chelsea / Nakashima, Akio / Singh, Chingakham Ranjit / Reid, Megan / Cox, Christian / Papadopoulos, Evangelos / Luna, Rafael E / Anderson, Abbey / Tagami, Hideaki / Hiraishi, Hiroyuki / Slone, Emily Archer / Yoshino, Ken-Ichi / Asano, Masayo / Gillaspie, Sarah / Nietfeld, Jerome / Perchellet, Jean-Pierre /
    Rothenburg, Stefan / Masai, Hisao / Wagner, Gerhard / Beeser, Alexander / Kikkawa, Ushio / Fleming, Sherry D / Asano, Katsura

    Nucleic acids research

    2016  Volume 44, Issue 18, Page(s) 8704–8713

    Abstract: ATF4 is a pro-oncogenic transcription factor whose translation is activated by eIF2 phosphorylation through delayed re-initiation involving two uORFs in the mRNA leader. However, in yeast, the effect of eIF2 phosphorylation can be mimicked by eIF5 ... ...

    Abstract ATF4 is a pro-oncogenic transcription factor whose translation is activated by eIF2 phosphorylation through delayed re-initiation involving two uORFs in the mRNA leader. However, in yeast, the effect of eIF2 phosphorylation can be mimicked by eIF5 overexpression, which turns eIF5 into translational inhibitor, thereby promoting translation of GCN4, the yeast ATF4 equivalent. Furthermore, regulatory protein termed eIF5-mimic protein (5MP) can bind eIF2 and inhibit general translation. Here, we show that 5MP1 overexpression in human cells leads to strong formation of 5MP1:eIF2 complex, nearly comparable to that of eIF5:eIF2 complex produced by eIF5 overexpression. Overexpression of eIF5, 5MP1 and 5MP2, the second human paralog, promotes ATF4 expression in certain types of human cells including fibrosarcoma. 5MP overexpression also induces ATF4 expression in Drosophila The knockdown of 5MP1 in fibrosarcoma attenuates ATF4 expression and its tumor formation on nude mice. Since 5MP2 is overproduced in salivary mucoepidermoid carcinoma, we propose that overexpression of eIF5 and 5MP induces translation of ATF4 and potentially other genes with uORFs in their mRNA leaders through delayed re-initiation, thereby enhancing the survival of normal and cancer cells under stress conditions.
    MeSH term(s) Activating Transcription Factor 4/metabolism ; Animals ; Carcinogenesis/pathology ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Drosophila melanogaster/metabolism ; Eukaryotic Initiation Factor-2/metabolism ; Eukaryotic Initiation Factor-3 ; Eukaryotic Initiation Factor-5/metabolism ; Fibrosarcoma/pathology ; Gene Knockdown Techniques ; HEK293 Cells ; HeLa Cells ; Humans ; Male ; Mass Spectrometry ; Mice, Nude ; Peptide Chain Initiation, Translational
    Chemical Substances BZW2 protein, human ; DNA-Binding Proteins ; Eukaryotic Initiation Factor-2 ; Eukaryotic Initiation Factor-3 ; Eukaryotic Initiation Factor-5 ; Activating Transcription Factor 4 (145891-90-3)
    Language English
    Publishing date 2016-06-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkw559
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1067: Show issues Location:
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