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Internalization of modified lipids by CD36 and SR-A leads to hepatic inflammation and lysosomal cholesterol storage in Kupffer cells.

BACKGROUND & AIMSNon-alcoholic steatohepatitis (NASH) is characterized by steatosis and inflammation, which can further progress into fibrosis and cirrhosis. Recently, we demonstrated that combined deletion of the two main scavenger receptors, CD36 and macrophage scavenger receptor 1 (MSR1), which a... Full description

Journal Title: PloS one 2012, Vol.7(3), p.e34378
Main Author: Bieghs, Veerle
Other Authors: Verheyen, Fons , van Gorp, Patrick J , Hendrikx, Tim , Wouters, Kristiaan , Lütjohann, Dieter , Gijbels, Marion J J , Febbraio, Maria , Binder, Christoph J , Hofker, Marten H , Shiri-Sverdlov, Ronit
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0034378
Link: http://search.proquest.com/docview/964192083/?pq-origsite=primo
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title: Internalization of modified lipids by CD36 and SR-A leads to hepatic inflammation and lysosomal cholesterol storage in Kupffer cells.
format: Article
creator:
  • Bieghs, Veerle
  • Verheyen, Fons
  • van Gorp, Patrick J
  • Hendrikx, Tim
  • Wouters, Kristiaan
  • Lütjohann, Dieter
  • Gijbels, Marion J J
  • Febbraio, Maria
  • Binder, Christoph J
  • Hofker, Marten H
  • Shiri-Sverdlov, Ronit
subjects:
  • Animals–Deficiency
  • Bone Marrow Transplantation–Genetics
  • Cd36 Antigens–Metabolism
  • Cholesterol–Metabolism
  • Fatty Liver–Metabolism
  • Female–Pathology
  • Inflammation–Pathology
  • Kupffer Cells–Metabolism
  • Lipid Metabolism–Pathology
  • Lipids–Chemistry
  • Liver–Metabolism
  • Lysosomes–Pathology
  • Mice–Metabolism
  • Mice, Knockout–Deficiency
  • Non-Alcoholic Fatty Liver Disease–Genetics
  • Receptors, LDL–Metabolism
  • Scavenger Receptors, Class A–Deficiency
  • Scavenger Receptors, Class A–Genetics
  • Scavenger Receptors, Class A–Metabolism
  • Cd36 Antigens
  • Lipids
  • Msr1 Protein, Mouse
  • Receptors, LDL
  • Scavenger Receptors, Class A
  • Cholesterol
ispartof: PloS one, 2012, Vol.7(3), p.e34378
description: BACKGROUND & AIMSNon-alcoholic steatohepatitis (NASH) is characterized by steatosis and inflammation, which can further progress into fibrosis and cirrhosis. Recently, we demonstrated that combined deletion of the two main scavenger receptors, CD36 and macrophage scavenger receptor 1 (MSR1), which are important for modified cholesterol-rich lipoprotein uptake, reduced NASH. The individual contributions of these receptors to NASH and the intracellular mechanisms by which they contribute to inflammation have not been established. We hypothesize that CD36 and MSR1 contribute independently to the onset of inflammation in NASH, by affecting intracellular cholesterol distribution inside Kupffer cells (KCs). METHODS & RESULTSLdlr(-/-) mice were transplanted with wild-type (Wt), Cd36(-/-) or Msr1(-/-) bone marrow and fed a Western diet for 3 months. Cd36(-/-)- and Msr1(-/-)- transplanted (tp) mice showed a similar reduction in hepatic inflammation compared to Wt-tp mice. While the total amount of cholesterol inside KCs was similar in all groups, KCs of Cd36(-/-)- and Msr1(-/-)-tp mice showed increased cytoplasmic cholesterol accumulation, while Wt-tp mice showed increased lysosomal cholesterol accumulation. CONCLUSIONCD36 and MSR1 contribute similarly and independently to the progression of inflammation in NASH. One possible explanation for the inflammatory response related to expression of these receptors could be abnormal cholesterol trafficking in KCs. These data provide a new basis for prevention and treatment of NASH.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0034378
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleInternalization of modified lipids by CD36 and SR-A leads to hepatic inflammation and lysosomal cholesterol storage in Kupffer cells.
creatorBieghs, Veerle ; Verheyen, Fons ; van Gorp, Patrick J ; Hendrikx, Tim ; Wouters, Kristiaan ; Lütjohann, Dieter ; Gijbels, Marion J J ; Febbraio, Maria ; Binder, Christoph J ; Hofker, Marten H ; Shiri-Sverdlov, Ronit
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ispartofPloS one, 2012, Vol.7(3), p.e34378
identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0034378
subjectAnimals–Deficiency ; Bone Marrow Transplantation–Genetics ; Cd36 Antigens–Metabolism ; Cholesterol–Metabolism ; Fatty Liver–Metabolism ; Female–Pathology ; Inflammation–Pathology ; Kupffer Cells–Metabolism ; Lipid Metabolism–Pathology ; Lipids–Chemistry ; Liver–Metabolism ; Lysosomes–Pathology ; Mice–Metabolism ; Mice, Knockout–Deficiency ; Non-Alcoholic Fatty Liver Disease–Genetics ; Receptors, LDL–Metabolism ; Scavenger Receptors, Class A–Deficiency ; Scavenger Receptors, Class A–Genetics ; Scavenger Receptors, Class A–Metabolism ; Cd36 Antigens ; Lipids ; Msr1 Protein, Mouse ; Receptors, LDL ; Scavenger Receptors, Class A ; Cholesterol
descriptionBACKGROUND & AIMSNon-alcoholic steatohepatitis (NASH) is characterized by steatosis and inflammation, which can further progress into fibrosis and cirrhosis. Recently, we demonstrated that combined deletion of the two main scavenger receptors, CD36 and macrophage scavenger receptor 1 (MSR1), which are important for modified cholesterol-rich lipoprotein uptake, reduced NASH. The individual contributions of these receptors to NASH and the intracellular mechanisms by which they contribute to inflammation have not been established. We hypothesize that CD36 and MSR1 contribute independently to the onset of inflammation in NASH, by affecting intracellular cholesterol distribution inside Kupffer cells (KCs). METHODS & RESULTSLdlr(-/-) mice were transplanted with wild-type (Wt), Cd36(-/-) or Msr1(-/-) bone marrow and fed a Western diet for 3 months. Cd36(-/-)- and Msr1(-/-)- transplanted (tp) mice showed a similar reduction in hepatic inflammation compared to Wt-tp mice. While the total amount of cholesterol inside KCs was similar in all groups, KCs of Cd36(-/-)- and Msr1(-/-)-tp mice showed increased cytoplasmic cholesterol accumulation, while Wt-tp mice showed increased lysosomal cholesterol accumulation. CONCLUSIONCD36 and MSR1 contribute similarly and independently to the progression of inflammation in NASH. One possible explanation for the inflammatory response related to expression of these receptors could be abnormal cholesterol trafficking in KCs. These data provide a new basis for prevention and treatment of NASH.
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9Hofker, Marten H
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titleInternalization of modified lipids by CD36 and SR-A leads to hepatic inflammation and lysosomal cholesterol storage in Kupffer cells.
descriptionBACKGROUND & AIMSNon-alcoholic steatohepatitis (NASH) is characterized by steatosis and inflammation, which can further progress into fibrosis and cirrhosis. Recently, we demonstrated that combined deletion of the two main scavenger receptors, CD36 and macrophage scavenger receptor 1 (MSR1), which are important for modified cholesterol-rich lipoprotein uptake, reduced NASH. The individual contributions of these receptors to NASH and the intracellular mechanisms by which they contribute to inflammation have not been established. We hypothesize that CD36 and MSR1 contribute independently to the onset of inflammation in NASH, by affecting intracellular cholesterol distribution inside Kupffer cells (KCs). METHODS & RESULTSLdlr(-/-) mice were transplanted with wild-type (Wt), Cd36(-/-) or Msr1(-/-) bone marrow and fed a Western diet for 3 months. Cd36(-/-)- and Msr1(-/-)- transplanted (tp) mice showed a similar reduction in hepatic inflammation compared to Wt-tp mice. While the total amount of cholesterol inside KCs was similar in all groups, KCs of Cd36(-/-)- and Msr1(-/-)-tp mice showed increased cytoplasmic cholesterol accumulation, while Wt-tp mice showed increased lysosomal cholesterol accumulation. CONCLUSIONCD36 and MSR1 contribute similarly and independently to the progression of inflammation in NASH. One possible explanation for the inflammatory response related to expression of these receptors could be abnormal cholesterol trafficking in KCs. These data provide a new basis for prevention and treatment of NASH.
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15Receptors, LDL–Metabolism
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titleInternalization of modified lipids by CD36 and SR-A leads to hepatic inflammation and lysosomal cholesterol storage in Kupffer cells.
authorBieghs, Veerle ; Verheyen, Fons ; van Gorp, Patrick J ; Hendrikx, Tim ; Wouters, Kristiaan ; Lütjohann, Dieter ; Gijbels, Marion J J ; Febbraio, Maria ; Binder, Christoph J ; Hofker, Marten H ; Shiri-Sverdlov, Ronit
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4Fatty Liver–Metabolism
5Female–Pathology
6Inflammation–Pathology
7Kupffer Cells–Metabolism
8Lipid Metabolism–Pathology
9Lipids–Chemistry
10Liver–Metabolism
11Lysosomes–Pathology
12Mice–Metabolism
13Mice, Knockout–Deficiency
14Non-Alcoholic Fatty Liver Disease–Genetics
15Receptors, LDL–Metabolism
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17Scavenger Receptors, Class A–Genetics
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20Lipids
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abstractBACKGROUND & AIMSNon-alcoholic steatohepatitis (NASH) is characterized by steatosis and inflammation, which can further progress into fibrosis and cirrhosis. Recently, we demonstrated that combined deletion of the two main scavenger receptors, CD36 and macrophage scavenger receptor 1 (MSR1), which are important for modified cholesterol-rich lipoprotein uptake, reduced NASH. The individual contributions of these receptors to NASH and the intracellular mechanisms by which they contribute to inflammation have not been established. We hypothesize that CD36 and MSR1 contribute independently to the onset of inflammation in NASH, by affecting intracellular cholesterol distribution inside Kupffer cells (KCs). METHODS & RESULTSLdlr(-/-) mice were transplanted with wild-type (Wt), Cd36(-/-) or Msr1(-/-) bone marrow and fed a Western diet for 3 months. Cd36(-/-)- and Msr1(-/-)- transplanted (tp) mice showed a similar reduction in hepatic inflammation compared to Wt-tp mice. While the total amount of cholesterol inside KCs was similar in all groups, KCs of Cd36(-/-)- and Msr1(-/-)-tp mice showed increased cytoplasmic cholesterol accumulation, while Wt-tp mice showed increased lysosomal cholesterol accumulation. CONCLUSIONCD36 and MSR1 contribute similarly and independently to the progression of inflammation in NASH. One possible explanation for the inflammatory response related to expression of these receptors could be abnormal cholesterol trafficking in KCs. These data provide a new basis for prevention and treatment of NASH.
doi10.1371/journal.pone.0034378
urlhttp://search.proquest.com/docview/964192083/
date2012-01-01