16 results on '"Jeurissen, Mike L J"'
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2. Exogenously Added Oxyphytosterols Do Not Affect Macrophage‐Mediated Inflammatory Responses
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Oligschlaeger, Yvonne, primary, Houben, Tom, additional, Jeurissen, Mike L. J., additional, Bitorina, Albert V., additional, Konings, Maurice, additional, Baumgartner, Sabine, additional, Plat, Jogchum, additional, and Shiri‐Sverdlov, Ronit, additional
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- 2018
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3. Plasma cathepsin D correlates with histological classifications of fatty liver disease in adults and responds to intervention
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Walenbergh, Sofie M. A., primary, Houben, Tom, additional, Rensen, Sander S., additional, Bieghs, Veerle, additional, Hendrikx, Tim, additional, van Gorp, Patrick J., additional, Oligschlaeger, Yvonne, additional, Jeurissen, Mike L. J., additional, Gijbels, Marion J. J., additional, Buurman, Wim A., additional, Vreugdenhil, Anita C. E., additional, Greve, Jan Willem M., additional, Plat, Jogchum, additional, Hofker, Marten H., additional, Kalhan, Satish, additional, Pihlajamäki, Jussi, additional, Lindsey, Patrick, additional, Koek, Ger H., additional, and Shiri-Sverdlov, Ronit, additional
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- 2016
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4. Myeloid DLL4 Does Not Contribute to the Pathogenesis of Non-Alcoholic Steatohepatitis in Ldlr-/- Mice
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Jeurissen, Mike L. J., primary, Walenbergh, Sofie M. A., additional, Houben, Tom, additional, Hendrikx, Tim, additional, Li, Jieyi, additional, Oligschlaeger, Yvonne, additional, van Gorp, Patrick J., additional, Gijbels, Marion J. J., additional, Bitorina, Albert, additional, Nessel, Isabell, additional, Radtke, Freddy, additional, Vooijs, Marc, additional, Theys, Jan, additional, and Shiri-Sverdlov, Ronit, additional
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- 2016
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5. Macrophage Stimulating Protein Enhances Hepatic Inflammation in a NASH Model
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Li, Jieyi, primary, Chanda, Dipanjan, additional, van Gorp, Patrick J., additional, Jeurissen, Mike L. J., additional, Houben, Tom, additional, Walenbergh, Sofie M. A., additional, Debets, Jacques, additional, Oligschlaeger, Yvonne, additional, Gijbels, Marion J. J., additional, Neumann, Dietbert, additional, and Shiri-Sverdlov, Ronit, additional
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- 2016
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6. MSP is a negative regulator of inflammation and lipogenesis in ex vivo models of non-alcoholic steatohepatitis
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Chanda, Dipanjan, primary, Li, Jieyi, additional, Oligschlaeger, Yvonne, additional, Jeurissen, Mike L J, additional, Houben, Tom, additional, Walenbergh, Sofie M A, additional, Shiri-Sverdlov, Ronit, additional, and Neumann, Dietbert, additional
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- 2016
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7. Plasma Cathepsin D Levels: A Novel Tool to Predict Pediatric Hepatic Inflammation
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Walenbergh, Sofie M A, primary, Houben, Tom, additional, Hendrikx, Tim, additional, Jeurissen, Mike L J, additional, van Gorp, Patrick J, additional, Vreugdenhil, Anita C E, additional, Adriaanse, Marlou P, additional, Buurman, Wim A, additional, Hofker, Marten H, additional, Mosca, Antonella, additional, Lindsey, Patrick J, additional, Alisi, Anna, additional, Liccardo, Daniela, additional, Panera, Nadia, additional, Koek, Ger H, additional, Nobili, Valerio, additional, and Shiri-Sverdlov, Ronit, additional
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- 2015
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8. Protective Role of Plant Sterol and Stanol Esters in Liver Inflammation: Insights from Mice and Humans
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Plat, Jogchum, primary, Hendrikx, Tim, additional, Bieghs, Veerle, additional, Jeurissen, Mike L. J., additional, Walenbergh, Sofie M. A., additional, van Gorp, Patrick J., additional, De Smet, Els, additional, Konings, Maurice, additional, Vreugdenhil, Anita C. E., additional, Guichot, Yasmin Dias, additional, Rensen, Sander S., additional, Buurman, Wim A., additional, Greve, Jan Willem M., additional, Lütjohann, Dieter, additional, Mensink, Ronald P., additional, and Shiri-Sverdlov, Ronit, additional
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- 2014
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9. Myeloid DLL4 Does Not Contribute to the Pathogenesis of Non-Alcoholic Steatohepatitis in Ldlr-/- Mice.
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Jeurissen, Mike L. J., Walenbergh, Sofie M. A., Houben, Tom, Hendrikx, Tim, Li, Jieyi, Oligschlaeger, Yvonne, van Gorp, Patrick J., Gijbels, Marion J. J., Bitorina, Albert, Nessel, Isabell, Radtke, Freddy, Vooijs, Marc, Theys, Jan, and Shiri-Sverdlov, Ronit
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FATTY liver , *LIGAND binding (Biochemistry) , *NOTCH signaling pathway , *DISEASE progression , *MURIDAE - Abstract
Non-alcoholic steatohepatitis (NASH) is characterized by liver steatosis and inflammation. Currently, the underlying mechanisms leading to hepatic inflammation are not fully understood and consequently, therapeutic options are poor. Non-alcoholic steatohepatitis (NASH) and atherosclerosis share the same etiology whereby macrophages play a key role in disease progression. Macrophage function can be modulated via activation of receptor-ligand binding of Notch signaling. Relevantly, global inhibition of Notch ligand Delta-Like Ligand-4 (DLL4) attenuates atherosclerosis by altering the macrophage-mediated inflammatory response. However, the specific contribution of macrophage DLL4 to hepatic inflammation is currently unknown. We hypothesized that myeloid DLL4 deficiency in low-density lipoprotein receptor knock-out (Ldlr-/-) mice reduces hepatic inflammation. Irradiated Ldlr-/- mice were transplanted (tp) with bone marrow from wild type (Wt) or DLL4f/fLysMCre+/0 (DLL4del) mice and fed either chow or high fat, high cholesterol (HFC) diet for 11 weeks. Additionally, gene expression was assessed in bone marrow-derived macrophages (BMDM) of DLL4f/fLysMCreWT and DLL4f/fLysMCre+/0 mice. In contrast to our hypothesis, inflammation was not decreased in HFC-fed DLL4del-transplanted mice. In line, in vitro, there was no difference in the expression of inflammatory genes between DLL4-deficient and wildtype bone marrow-derived macrophages. These results suggest that myeloid DLL4 deficiency does not contribute to hepatic inflammation in vivo. Since, macrophage-DLL4 expression in our model was not completely suppressed, it can’t be totally excluded that complete DLL4 deletion in macrophages might lead to different results. Nevertheless, the contribution of non-myeloid Kupffer cells to notch signaling with regard to the pathogenesis of steatohepatitis is unknown and as such it is possible that, DLL4 on Kupffer cells promote the pathogenesis of steatohepatitis. [ABSTRACT FROM AUTHOR]
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- 2016
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10. Macrophage Specific Caspase-1/11 Deficiency Protects against Cholesterol Crystallization and Hepatic Inflammation in Hyperlipidemic Mice
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Hendrikx, Tim, primary, Bieghs, Veerle, additional, Walenbergh, Sofie M. A., additional, van Gorp, Patrick J., additional, Verheyen, Fons, additional, Jeurissen, Mike L. J., additional, Steinbusch, Mandy M. F., additional, Vaes, Nathalie, additional, Binder, Christoph J., additional, Koek, Ger H., additional, Stienstra, Rinke, additional, Netea, Mihai G., additional, Hofker, Marten H., additional, and Shiri-Sverdlov, Ronit, additional
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- 2013
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11. Weekly Treatment of 2-Hydroxypropyl-β-cyclodextrin Improves Intracellular Cholesterol Levels in LDL Receptor Knockout Mice.
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Walenbergh, Sofie M. A., Houben, Tom, Hendrikx, Tim, Jeurissen, Mike L. J., van Gorp, Patrick J., Vaes, Nathalie, Olde Damink, Steven W. M., Verheyen, Fons, Koek, Ger H., Lütjohann, Dieter, Grebe, Alena, Latz, Eicke, and Shiri-Sverdlov, Ronit
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CYCLODEXTRINS ,CHOLESTEROL metabolism ,FAMILIAL hypercholesterolemia ,MICE as carriers of disease ,METABOLIC syndrome treatment ,ELECTRON microscopy ,LYSOSOMES ,THERAPEUTICS - Abstract
Recently, the importance of lysosomes in the context of the metabolic syndrome has received increased attention. Increased lysosomal cholesterol storage and cholesterol crystallization inside macrophages have been linked to several metabolic diseases, such as atherosclerosis and non-alcoholic fatty liver disease (NAFLD). Two-hydroxypropyl-β-cyclodextrin (HP-B-CD) is able to redirect lysosomal cholesterol to the cytoplasm in Niemann-Pick type C1 disease, a lysosomal storage disorder. We hypothesize that HP-B-CD ameliorates liver cholesterol and intracellular cholesterol levels inside Kupffer cells (KCs). Hyperlipidemic low-density lipoprotein receptor knockout (Ldlr
-/- ) mice were given weekly, subcutaneous injections with HP-B-CD or control PBS. In contrast to control injections, hyperlipidemic mice treated with HP-B-CD demonstrated a shift in intracellular cholesterol distribution towards cytoplasmic cholesteryl ester (CE) storage and a decrease in cholesterol crystallization inside KCs. Compared to untreated hyperlipidemic mice, the foamy KC appearance and liver cholesterol remained similar upon HP-B-CD administration, while hepatic campesterol and 7α-hydroxycholesterol levels were back increased. Thus, HP-B-CD could be a useful tool to improve intracellular cholesterol levels in the context of the metabolic syndrome, possibly through modulation of phyto- and oxysterols, and should be tested in the future. Additionally, these data underline the existence of a shared etiology between lysosomal storage diseases and NAFLD. [ABSTRACT FROM AUTHOR]- Published
- 2015
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12. Bone marrow-specific caspase-1/11 deficiency inhibits atherosclerosis development in Ldlr −/− mice.
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Hendrikx, Tim, Jeurissen, Mike L. J., Gorp, Patrick J., Gijbels, Marion J., Walenbergh, Sofie M. A., Houben, Tom, Gorp, Rick, Pöttgens, Chantal C., Stienstra, Rinke, Netea, Mihai G., Hofker, Marten H., Donners, Marjo M. P. C., and Shiri‐Sverdlov, Ronit
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BONE marrow , *CASPASES , *ENZYME deficiency , *ATHEROSCLEROSIS , *CYTOKINES , *LABORATORY mice - Abstract
Recent investigations have suggested that inflammasome activation plays an important role during atherosclerosis. Upon activation, the inflammasome induces processing and release of pro-inflammatory cytokines interleukin 1β ( IL-1β) and interleukin 18 ( IL-18) via activation of caspase-1/11. Previously, it was shown that complete caspase-1 deficiency is protective against atherosclerosis development. However, while macrophages are the main inflammatory cells involved in atherosclerosis, the exact role of macrophage-specific caspase-1/11 activation during development of cardiovascular disease has never been investigated. We hypothesized that hematopoietic caspase-1/11 deficiency leads to reduced atherosclerosis development. To investigate the specific contribution of hematopoietic caspase-1/11 activation to atherosclerosis development, Ldlr −/− mice received a transplant (tp) of wild-type ( WT) or caspase-1/11−/− bone marrow, to create WT-tp mice and caspase-1/11−/−-tp mice, and fed a high-fat, high-cholesterol diet for 12 weeks. Our results showed an increase in anti-inflammatory blood leukocytes in caspase-1/11−/−-tp mice compared with WT-tp mice, as indicated by a decreased level of Ly6Chigh monocytes and an increased level of Ly6Clow monocytes. In line with our hypothesis, hematopoietic deletion of caspase-1/11 resulted in a strong reduction in atherosclerotic plaque size. Furthermore, necrotic core content was dramatically decreased in caspase-1/11−/−-tp mice. Our data indicate that hematopoietic caspase-1/11 activation is involved in vascular inflammation and atherosclerosis, and plays an important role in cardiovascular disease progression. [ABSTRACT FROM AUTHOR]
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- 2015
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13. Prevention of oxLDL uptake leads to decreased atherosclerosis in hematopoietic NPC1-deficient Ldlr -/- mice.
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Jeurissen MLJ, Walenbergh SMA, Houben T, Gijbels MJJ, Li J, Hendrikx T, Oligschlaeger Y, van Gorp PJ, Binder CJ, Donners MMPC, and Shiri-Sverdlov R
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- Animals, Atherosclerosis genetics, Atherosclerosis immunology, Atherosclerosis metabolism, Biological Transport, Bone Marrow Transplantation, Cholesterol metabolism, Disease Models, Animal, Genetic Predisposition to Disease, Intracellular Signaling Peptides and Proteins, Lysosomes metabolism, Macrophages immunology, Mice, Inbred C57BL, Mice, Knockout, Niemann-Pick C1 Protein, Phenotype, Plaque, Atherosclerotic, Pneumococcal Vaccines administration & dosage, Pneumococcal Vaccines immunology, Proteins genetics, Receptors, LDL genetics, Streptococcus pneumoniae immunology, Whole-Body Irradiation, Atherosclerosis prevention & control, Lipoproteins, LDL metabolism, Macrophages metabolism, Proteins metabolism, Receptors, LDL deficiency
- Abstract
Background and Aims: Atherosclerosis is a chronic inflammatory disease of medium and large vessels and is typically characterized by the predominant accumulation of low-density lipoprotein (LDL)-cholesterol inside macrophages that reside in the vessel walls. Previous studies clearly demonstrated an association specifically between the oxidized type of LDL (oxLDL) and atherosclerotic lesion formation. Further observations revealed that these atherosclerotic lesions displayed enlarged, lipid-loaded lysosomes. By increasing natural antibodies against oxLDL, pneumococcal vaccination has been shown to reduce atherosclerosis in LDL receptor knockout (Ldlr
-/- ) mice. Relevantly, loss of the lysosomal membrane protein Niemann-Pick Type C1 (NPC1) led to lysosomal accumulation of various lipids and promoted atherosclerosis. Yet, the importance of lysosomal oxLDL accumulation inside macrophages, compared to non-modified LDL, in atherosclerosis has never been established., Methods: By transplanting NPC1 bone marrow into lethally irradiated Ldlr-/- mice, a hematopoietic mouse model for lysosomal cholesterol accumulation was created. Through injections with heat-inactivated pneumococci, we aimed to demonstrate the specific contribution of lysosomal oxLDL accumulation inside macrophages in atherosclerosis development., Results: While there were no differences in plaque morphology, a reduction in plaque size and plaque inflammation was found in immunized NPC1mut -transplanted mice, compared to non-immunized NPC1mut -transplanted mice., Conclusions: Lysosomal oxLDL accumulation within macrophages contributes to murine atherosclerosis. Future intervention strategies should focus specifically on preventing oxLDL, unlike non-modified LDL, from being internalized into lysosomes. Such an intervention can have an additive effect to current existing treatments against atherosclerosis., (Copyright © 2016 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.)- Published
- 2016
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14. Hematopoietic overexpression of Cyp27a1 reduces hepatic inflammation independently of 27-hydroxycholesterol levels in Ldlr(-/-) mice.
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Hendrikx T, Jeurissen ML, Bieghs V, Walenbergh SM, van Gorp PJ, Verheyen F, Houben T, Guichot YD, Gijbels MJ, Leitersdorf E, Hofker MH, Lütjohann D, and Shiri-Sverdlov R
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- Animals, Bone Marrow Transplantation, Cholestanetriol 26-Monooxygenase biosynthesis, Disease Models, Animal, Kupffer Cells metabolism, Kupffer Cells pathology, Lipoproteins, LDL metabolism, Male, Mice, Mice, Inbred C57BL, Non-alcoholic Fatty Liver Disease metabolism, Non-alcoholic Fatty Liver Disease pathology, Cholestanetriol 26-Monooxygenase genetics, DNA genetics, Gene Expression Regulation, Hydroxycholesterols metabolism, Non-alcoholic Fatty Liver Disease genetics
- Abstract
Background & Aims: Non-alcoholic steatohepatitis (NASH) is characterized by hepatic lipid accumulation and inflammation. Currently, the underlying mechanisms, leading to hepatic inflammation, are still unknown. The breakdown of free cholesterol inside Kupffer cells (KCs) by the mitochondrial enzyme CYP27A1 produces 27-hydroxycholesterol (27HC). We recently demonstrated that administration of 27HC to hyperlipidemic mice reduced hepatic inflammation. In line, hematopoietic deletion of Cyp27a1 resulted in increased hepatic inflammation. In the current manuscript, the effect of hematopoietic overexpression of Cyp27a1 on the development of NASH and cholesterol trafficking was investigated. We hypothesized that Cyp27a1 overexpression in KCs will lead to reduced hepatic inflammation., Methods: Irradiated Ldlr(-/-) mice were transplanted (tp) with bone marrow from mice overexpressing Cyp27a1 (Cyp27a1(over)) and wild type (Wt) mice and fed either chow or a high-fat, high-cholesterol (HFC) diet for 3 months. Additionally, gene expression was assessed in bone marrow-derived macrophages (BMDM) from Cyp27a1(over) and Wt mice., Results: In line with our hypothesis, hepatic inflammation in HFC-fed Cyp27a1(over)-tp mice was reduced and KCs were less foamy compared to Wt-tp mice. Remarkably, these changes occurred even though plasma and liver levels of 27HC did not differ between both groups. BMDM from Cyp27a1(over) mice revealed reduced inflammatory gene expression and increased expression of cholesterol transporters compared to Wt BMDM after lipopolysaccharide (LPS) stimulation., Conclusions: Our data suggest that overexpression of Cyp27a1 in KCs reduces hepatic inflammation independently of 27HC levels in plasma and liver, further pointing towards KCs as specific target for improving the therapy of NASH., (Copyright © 2014 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)
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- 2015
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15. Plasma IL-1 receptor antagonist levels correlate with the development of non-alcoholic steatohepatitis.
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Hendrikx T, Walenbergh SM, Jeurissen ML, Houben T, van Gorp PJ, Lindsey PJ, Koek GH, Kalhan S, Pihlajamaki J, Hofker MH, and Shiri-Sverdlov R
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- Adult, Case-Control Studies, Female, Humans, Inflammation blood, Inflammation complications, Liver pathology, Male, Middle Aged, Non-alcoholic Fatty Liver Disease complications, Non-alcoholic Fatty Liver Disease diagnosis, Obesity blood, Obesity complications, ROC Curve, Interleukin 1 Receptor Antagonist Protein blood, Non-alcoholic Fatty Liver Disease blood, Non-alcoholic Fatty Liver Disease pathology
- Abstract
Aim: Nonalcoholic steatohepatitis (NASH) is a liver disease characterized by lipid accumulation and inflammation. Here, we aimed to evaluate plasma IL-1Ra as a marker for NASH and to determine whether diagnosis of NASH can be further improved by adding IL-1Ra measurements., Materials & Methods: Therefore, plasma concentrations of IL-1Ra were measured from 146 subjects of a biopsy-proven NASH cohort with matched controls., Results: NASH patients had higher levels of plasma IL-1Ra compared with patients with steatosis or healthy controls., Conclusion: Our data confirm that IL-1Ra can be a useful tool in the diagnosis of hepatic inflammation and suggest that measuring plasma IL-1Ra levels in addition to ALT will improve the diagnosis for NASH at all stages of the disease.
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- 2015
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16. The cholesterol derivative 27-hydroxycholesterol reduces steatohepatitis in mice.
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Bieghs V, Hendrikx T, van Gorp PJ, Verheyen F, Guichot YD, Walenbergh SM, Jeurissen ML, Gijbels M, Rensen SS, Bast A, Plat J, Kalhan SC, Koek GH, Leitersdorf E, Hofker MH, Lütjohann D, and Shiri-Sverdlov R
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- ATP Binding Cassette Transporter 1, ATP Binding Cassette Transporter, Subfamily G, Member 1, ATP-Binding Cassette Transporters metabolism, Alanine Transaminase blood, Animals, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Bone Marrow Transplantation, Cholestanetriol 26-Monooxygenase deficiency, Cholestanetriol 26-Monooxygenase genetics, Cholesterol, Dietary administration & dosage, Dietary Fats administration & dosage, Fatty Liver complications, Female, Foam Cells drug effects, Foam Cells metabolism, Gene Expression, Hepatitis pathology, Hepatitis prevention & control, Humans, Hydroxycholesterols blood, Kupffer Cells drug effects, Lipids blood, Lipoproteins metabolism, Liver metabolism, Liver pathology, Liver X Receptors, Lysosomes drug effects, Male, Mice, Mice, Knockout, Non-alcoholic Fatty Liver Disease, Orphan Nuclear Receptors genetics, Receptors, LDL genetics, Sterol Regulatory Element Binding Protein 1 metabolism, Triglycerides metabolism, Cholestanetriol 26-Monooxygenase metabolism, Cholesterol, Dietary metabolism, Hepatitis etiology, Hepatitis metabolism, Hydroxycholesterols pharmacology, Kupffer Cells metabolism, Lysosomes metabolism, Receptors, LDL deficiency
- Abstract
Background & Aims: Non-alcoholic steatohepatitis is characterized by hepatic steatosis with inflammation. Although steatosis is benign and reversible, inflammation can increase liver damage. Hepatic inflammation has been associated with accumulation of cholesterol in lysosomes of Kupffer cells. 27-Hydroxycholesterol (27HC), a derivative of cholesterol formed by CYP27A1, can mobilize cholesterol from the lysosomes to the cytoplasm. We investigated whether 27HC can change the intracellular distribution cholesterol and reduce hepatic inflammation in mice., Methods: We transplanted bone marrow from irradiated wild-type or Cyp27a1(-/-) mice to mice that do not express the low density lipoprotein receptor (Ldlr(-/-)), which are hyperlipidemic; 9 weeks later, mice were fed either regular chow or a high-fat, high-cholesterol (HFC) diet for 3 months. In a separate experiment, Ldlr(-/-) mice were given subcutaneous injections of 27HC and placed on regular chow or HFC diets for 3 weeks. Blood and liver tissues samples were collected and analyzed for intracellular cholesterol distribution and inflammation., Results: In Ldlr(-/-) mice that received bone marrow transplants from Cyp27a1(-/-) mice, lysosomes of Kupfer cells had a greater accumulation of cholesterol than those of mice that received bone marrow from wild-type mice, after the HFC diet. Liver histology and gene expression analyses showed increased inflammation and liver damage in mice given bone marrow transplants from Cyp27a1(-/-) mice and placed on the HFC diet. Administration of 27HC to Ldlr(-/-) mice, following the HFC diet, reduced the accumulation of lysosomal cholesterol and hepatic inflammation, compared with mice that were not given 27HC., Conclusions: Accumulation of cholesterol in lysosomes of Kupfer cells promotes hepatic inflammation in mice. The cholesterol derivative 27HC reduces accumulation of cholesterol in lysosomes and might be used to treat non-alcoholic steatohepatitis., (Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
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