Liver is the major source of elevated serum lipocalin‐2 levels after bacterial infection or partial hepatectomy: A critical role for IL‐6/STAT3
Lipocalin‐2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase‐associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte‐specific Lcn2 knock...
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| Published in | Hepatology (Baltimore, Md.) Vol. 61; no. 2; pp. 692 - 702 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Wolters Kluwer Health, Inc
01.02.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Lipocalin‐2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase‐associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte‐specific Lcn2 knockout (Lcn2Hep–/–) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2Hep–/– mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (∼62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (∼6,000 ng/mL) postinfection and more than 60% post‐PHx (∼700 ng/mL). Interestingly, both Lcn2Hep–/– and global Lcn2 knockout (Lcn2–/–) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)‐6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte‐specific ablation of the IL‐6 receptor or Stat3, a major downstream effector of IL‐6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL‐6. Conclusion: Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL‐6 activation of the STAT3 signaling pathway. Thus, hepatocyte‐derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2015;61:692‐702) |
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| AbstractList | Lipocalin‐2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase‐associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte‐specific Lcn2 knockout (Lcn2Hep–/–) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2Hep–/– mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (∼62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (∼6,000 ng/mL) postinfection and more than 60% post‐PHx (∼700 ng/mL). Interestingly, both Lcn2Hep–/– and global Lcn2 knockout (Lcn2–/–) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)‐6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte‐specific ablation of the IL‐6 receptor or Stat3, a major downstream effector of IL‐6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL‐6. Conclusion: Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL‐6 activation of the STAT3 signaling pathway. Thus, hepatocyte‐derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2015;61:692‐702) Lipocalin‐2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase‐associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte‐specific Lcn2 knockout ( Lcn2 Hep–/– ) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2 Hep–/– mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (∼62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (∼6,000 ng/mL) postinfection and more than 60% post‐PHx (∼700 ng/mL). Interestingly, both Lcn2 Hep–/– and global Lcn2 knockout ( Lcn2 –/– ) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli . These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)‐6 stimulated hepatocytes to produce LCN2 in vitro and in vivo . Hepatocyte‐specific ablation of the IL‐6 receptor or Stat3 , a major downstream effector of IL‐6, markedly abrogated LCN2 elevation in vivo . Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL‐6. Conclusion : Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL‐6 activation of the STAT3 signaling pathway. Thus, hepatocyte‐derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (H epatology 2015;61:692‐702) Lipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2(Hep-/-)) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2(Hep-/-) mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (∼ 62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (∼ 6,000 ng/mL) postinfection and more than 60% post-PHx (∼ 700 ng/mL). Interestingly, both Lcn2(Hep-/-) and global Lcn2 knockout (Lcn2(-/-)) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6. Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. Lipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2Hep-/-) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2Hep-/- mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (6,000 ng/mL) postinfection and more than 60% post-PHx (700 ng/mL). Interestingly, both Lcn2Hep-/- and global Lcn2 knockout (Lcn2-/-) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6. Conclusion: Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2015;61:692-702) Lipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2(Hep-/-)) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2(Hep-/-) mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (∼ 62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (∼ 6,000 ng/mL) postinfection and more than 60% post-PHx (∼ 700 ng/mL). Interestingly, both Lcn2(Hep-/-) and global Lcn2 knockout (Lcn2(-/-)) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6.UNLABELLEDLipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2(Hep-/-)) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2(Hep-/-) mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (∼ 62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (∼ 6,000 ng/mL) postinfection and more than 60% post-PHx (∼ 700 ng/mL). Interestingly, both Lcn2(Hep-/-) and global Lcn2 knockout (Lcn2(-/-)) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6.Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration.CONCLUSIONHepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. Lipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2 super(Hep-/-)) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2 super(Hep-/-) mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (6,000 ng/mL) postinfection and more than 60% post-PHx (700 ng/mL). Interestingly, both Lcn2 super(Hep-/-) and global Lcn2 knockout (Lcn2 super(-/-)) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6. Conclusion: Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2015; 61:692-702) Lipocalin-2 (LCN2) was originally isolated from neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout ( Lcn2 Hep−/− ) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli ) or partial hepatectomy (PHx). Studies of Lcn2 Hep−/− mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (~62 ng/ml) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (~6,000 ng/ml) post-infection and more than 60% post-PHx (~700 ng/ml). Interestingly, both Lcn2 Hep−/− and global Lcn2 knockout ( Lcn2 −/− ) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli . These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with IL-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo . Hepatocyte-specific ablation of the IL-6 receptor or Stat3 , a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo . Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6. In conclusion, hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. |
| Author | Wu, Hailong Berger, Thorsten Porse, Bo Gao, Bin Feng, Dechun Kong, Xiaoni Chan, Yvonne Kolls, Jay Mak, Tak W. Cowland, Jack B. Wang, Hua Xu, Ming‐Jiang Borregaard, Niels |
| AuthorAffiliation | 2 Department of Physiology and Pathophysiology, School of Basic Medical Science, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China 1 Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA 3 State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China 4 Division of Pulmonary, Allergy and Critical Care Medicine, Dept. of Medicine, University of Pittsburgh, Pittsburgh, PA, USA 11 School of Biomedical Engineering & Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China 10 The Campbell Family Institute for Breast Cancer Research, University Health Network, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada 9 Danish Stem Cell Centre (DanStem) Faculty of Health Sciences, University of Copenhage |
| AuthorAffiliation_xml | – name: 1 Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA – name: 9 Danish Stem Cell Centre (DanStem) Faculty of Health Sciences, University of Copenhagen, Denmark – name: 11 School of Biomedical Engineering & Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China – name: 8 Biotech Research and Innovation Center (BRIC), University of Copenhagen, Denmark – name: 7 The Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark – name: 5 Richard King Mellon Foundation Institute for Pediatric Research, Children’s Hospital of Pittsburgh, Pittsburgh, PA, USA – name: 10 The Campbell Family Institute for Breast Cancer Research, University Health Network, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada – name: 3 State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China – name: 6 Granulocyte Research Laboratory, Rigshospitalet, Copenhagen, Denmark – name: 2 Department of Physiology and Pathophysiology, School of Basic Medical Science, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China – name: 4 Division of Pulmonary, Allergy and Critical Care Medicine, Dept. of Medicine, University of Pittsburgh, Pittsburgh, PA, USA |
| Author_xml | – sequence: 1 givenname: Ming‐Jiang surname: Xu fullname: Xu, Ming‐Jiang organization: Key Laboratory of Molecular Cardiovascular Science, Ministry of Education – sequence: 2 givenname: Dechun surname: Feng fullname: Feng, Dechun organization: National Institutes of Health – sequence: 3 givenname: Hailong surname: Wu fullname: Wu, Hailong organization: Shanghai Jiao Tong University – sequence: 4 givenname: Hua surname: Wang fullname: Wang, Hua organization: National Institutes of Health – sequence: 5 givenname: Yvonne surname: Chan fullname: Chan, Yvonne organization: University of Pittsburgh – sequence: 6 givenname: Jay surname: Kolls fullname: Kolls, Jay organization: Children's Hospital of Pittsburgh – sequence: 7 givenname: Niels surname: Borregaard fullname: Borregaard, Niels organization: Granulocyte Research Laboratory – sequence: 8 givenname: Bo surname: Porse fullname: Porse, Bo organization: University of Copenhagen – sequence: 9 givenname: Thorsten surname: Berger fullname: Berger, Thorsten organization: University Health Network – sequence: 10 givenname: Tak W. surname: Mak fullname: Mak, Tak W. organization: University Health Network – sequence: 11 givenname: Jack B. surname: Cowland fullname: Cowland, Jack B. organization: Granulocyte Research Laboratory – sequence: 12 givenname: Xiaoni surname: Kong fullname: Kong, Xiaoni organization: Shanghai Jiao Tong University – sequence: 13 givenname: Bin surname: Gao fullname: Gao, Bin organization: National Institutes of Health |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25234944$$D View this record in MEDLINE/PubMed |
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| Notes | Supported by the intramural program of NIAAA, NIH (B.G. and the State Key Laboratory of Oncogenes and Related Genes (90‐13‐02) (X.L.K.). Potential conflict of interest: Dr. Borregaard owns stock in Novo Nordisk and Novozymes. These authors contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 MJ.X, D.F, HL.W contributed equally to this work. |
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in mice publication-title: J Clin Invest doi: 10.1172/JCI59408 – volume: 58 start-page: 1349 year: 2013 ident: hep27447-bib-0016-20241017 article-title: Lipocalin‐2 negatively modulates the epithelial‐to‐mesenchymal transition in hepatocellular carcinoma through the epidermal growth factor (TGF‐beta1)/Lcn2/Twist1 pathway publication-title: Hepatology doi: 10.1002/hep.26467 – volume: 11 start-page: 314 year: 2013 ident: hep27447-bib-0022-20241017 article-title: Lipocalin‐2 gene expression during liver regeneration after partial hepatectomy in rats publication-title: Int J Surg doi: 10.1016/j.ijsu.2013.02.008 – volume: 134 start-page: 1148 year: 2008 ident: hep27447-bib-0024-20241017 article-title: Cell type‐dependent pro‐ and anti‐inflammatory role of signal transducer and activator of transcription 3 in alcoholic liver injury publication-title: Gastroenterology doi: 10.1053/j.gastro.2008.01.016 – volume: 154 start-page: 3525 year: 2013 ident: hep27447-bib-0019-20241017 article-title: 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publication-title: Hepatology doi: 10.1002/hep.22034 – volume: 60 start-page: 622 year: 2014 ident: hep27447-bib-0018-20241017 article-title: Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury publication-title: Hepatology doi: 10.1002/hep.26980 – volume: 143 start-page: 1609 year: 2012 ident: hep27447-bib-0035-20241017 article-title: Liver failure after extended hepatectomy in mice is mediated by a p21‐dependent barrier to liver regeneration publication-title: Gastroenterology doi: 10.1053/j.gastro.2012.08.043 – volume: 176 start-page: 5559 year: 2006 ident: hep27447-bib-0011-20241017 article-title: IL‐1beta‐specific up‐regulation of neutrophil gelatinase‐associated lipocalin is controlled by IkappaB‐zeta publication-title: J Immunol doi: 10.4049/jimmunol.176.9.5559 – volume: 7 start-page: 536 year: 2011 ident: hep27447-bib-0030-20241017 article-title: Signal transducer and activator of transcription 3 in liver diseases: a novel therapeutic target publication-title: Int J Biol Sci doi: 10.7150/ijbs.7.536 – volume: 1832 start-page: 660 year: 2013 ident: hep27447-bib-0031-20241017 article-title: Protective effects of lipocalin‐2 (LCN2) in acute liver injury suggest a novel function in liver homeostasis publication-title: Biochim Biophys Acta doi: 10.1016/j.bbadis.2013.01.014 – volume: 56 start-page: 435 year: 2011 ident: hep27447-bib-0007-20241017 article-title: Lipocalin 2 regulation and its complex role in inflammation and cancer publication-title: Cytokine doi: 10.1016/j.cyto.2011.07.021 – reference: 25865955 - Hepatology. 2016 Feb;63(2):674-5. doi: 10.1002/hep.27846. – reference: 26054053 - Hepatology. 2016 Feb;63(2):669-71. doi: 10.1002/hep.27930. – reference: 25865824 - Hepatology. 2016 Feb;63(2):673-4. doi: 10.1002/hep.27845. – reference: 26053944 - Hepatology. 2016 Feb;63(2):671-2. doi: 10.1002/hep.27928. |
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| Snippet | Lipocalin‐2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase‐associated lipocalin (NGAL). However, the functions of LCN2... Lipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2... Lipocalin-2 (LCN2) was originally isolated from neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and... |
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| SubjectTerms | Acute-Phase Proteins Animals Bacterial infections Bacterial Infections - blood Escherichia coli Hepatectomy Hepatocytes - metabolism Hepatology Infections Interleukin-6 - metabolism Klebsiella pneumoniae Lipocalin-2 Lipocalins - blood Liver Regeneration Mice, Inbred C57BL Oncogene Proteins - blood Receptors, Interleukin-6 - metabolism Rodents STAT3 Transcription Factor - metabolism |
| Title | Liver is the major source of elevated serum lipocalin‐2 levels after bacterial infection or partial hepatectomy: A critical role for IL‐6/STAT3 |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fhep.27447 https://www.ncbi.nlm.nih.gov/pubmed/25234944 https://www.proquest.com/docview/1646856520 https://www.proquest.com/docview/1652420820 https://www.proquest.com/docview/1654679871 https://pubmed.ncbi.nlm.nih.gov/PMC4303493 |
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