Lipocalin-2 gene expression during liver regeneration after partial hepatectomy in rats

Lai, Hung-Wen; Wu, Yao‐Ming; Lai, Siu‐Wai; Lin, Wen-Hsi

doi:10.1016/j.ijsu.2013.02.008

Cited by 14 publications

(14 citation statements)

References 31 publications

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“…Moreover, in another investigation we confirmed the dramatic upregulation of LCN2 in inflammatory responses underpinning the essential role of LCN2 in restoring liver homeostasis after appropriate insult [50]. This assumption was further confirmed in experiments in which the expression of LCN2 was measured during liver regeneration using a partial hepatectomy model [72]. In this study, the expression of LCN2 was markedly enhanced one day after the surgery, more in hepatocytes than in nonparenchymal cell subpopulations.…”

Section: Lipocalin 2 and Its Receptorssupporting

confidence: 78%

Lipocalin 2 in the pathogenesis of fatty liver disease and nonalcoholic steatohepatitis

Asimakopoulou

Weiskirchen

2015

Clinical Lipidology

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Section: Lipocalin 2 and Its Receptorssupporting

confidence: 78%

Lipocalin 2 in the pathogenesis of fatty liver disease and nonalcoholic steatohepatitis

Asimakopoulou

Weiskirchen

2015

Clinical Lipidology

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“…In addition, the serum and hepatic LCN2 protein levels are markedly elevated in various models of liver injury, and LCN2 appears to play a protective role in ameliorating liver damage induced by concanavalin A, carbon tetrachloride, and endotoxin . The serum and hepatic LCN2 levels are also elevated after PHx . A very recent article reported that the number of proliferating cell nuclear antigen (PCNA)‐positive or bromodeoxyuridine (BrdU)‐positive nuclei/per field after PHx was comparable in Lcn2 –/– mice and WT mice .…”

Section: Discussionmentioning

confidence: 99%

Liver is the major source of elevated serum lipocalin‐2 levels after bacterial infection or partial hepatectomy: A critical role for IL‐6/STAT3

et al. 2015

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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 (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) post-infection 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 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.

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“…Instead, IFN-γ production is attributed to activated lymphocytes, such as NK cells, T lymphocytes, and NKT cells, which either reside in the liver or are recruited to the liver in response to inflammation and injury [5]. During liver injury and inflammation, hepatocytes increase expression of the transmembrane IFN-γ receptor [6], which presumably increases their sensitivity to IFN-γ stimulation [7]. In the liver, IFN-γ also activates the IFN-γ receptor expressed on nonparenchymal cells, which include resident macrophages called Kupffer cells, the activation of which is important for mediating both innate and adaptive immune responses [8].…”

Section: Hepatic Sources and Targets Of Ifn-γmentioning

confidence: 99%

Regulation of hepatocyte fate by interferon-γ

Horras

Lamb

Mitchell

2011

Cytokine & Growth Factor Reviews

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Interferon (IFN)-γ is a cytokine known for its immunomodulatory and anti-proliferative action. In the liver, IFN-γ can induce hepatocyte apoptosis or inhibit hepatocyte cell cycle progression. This article reviews recent mechanistic reports that describe how IFN-γ may direct the fate of hepatocytes either towards apoptosis or a cell cycle arrest. This review also describes a probable role for IFN-γ in modulating hepatocyte fate during liver regeneration, transplantation, hepatitis, fibrosis and hepatocellular carcinoma, and highlights promising areas of research that may lead to the development of IFN-γ as a therapy to enhance recovery from liver disease.

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Lipocalin-2 gene expression during liver regeneration after partial hepatectomy in rats

Abstract: The expressions of Lcn2 gene and mRNA, and its related protein increased markedly after PH. Lcn2 might be important in the genetic regulation of liver regeneration after PH.

Cited by 14 publications

References 31 publications

Lipocalin 2 in the pathogenesis of fatty liver disease and nonalcoholic steatohepatitis

Lipocalin 2 in the pathogenesis of fatty liver disease and nonalcoholic steatohepatitis

Liver is the major source of elevated serum lipocalin‐2 levels after bacterial infection or partial hepatectomy: A critical role for IL‐6/STAT3

Regulation of hepatocyte fate by interferon-γ

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