title: Lipocalin 2 Upregulation Protects Hepatocytes from IL1-β-Induced Stress.
abstract: BACKGROUND
  Lipocalin 2 (LCN2), a protein primarily produced by hepatocytes, is highly upregulated under various conditions that induce cellular stress, such as intoxication, infection or inflammation. However, the precise biological functions and underlying mechanisms of LCN2 in hepatocytes remains unknown.
  
  
  METHODS
  Hepatocyte stress was successfully induced by treating Huh7 cells with interleukin-1β (IL-1β). Interleukin-6 (IL-6), Tumor Necrosis Factor-α (TNF-α) and LCN2 levels were measured in IL-1β treated Huh7 cells and supernatant. Additionally, microarray analysis was conducted to identify genes differentially expressed in LCN2-silenced and control Huh7 cells.
  
  
  RESULTS
  TNF-α, IL-6 and LCN2 were significantly elevated in Huh7 cells after IL-1β) treatment. In LCN2-silenced Huh7 cells, expression of IL-6 and TNF-α was significantly increased when compared with the expression levels of control Huh7 cells. Furthermore, differentially expressed genes were observed between the LCN2-silenced and control cells. Microarray analysis indicated that LCN2 acted by influencing genes involved in protein metabolism, stress response, cell cycle and proliferation.
  
  
  CONCLUSIONS
  Our results suggest that LCN2 upregulation protects hepatocytes from IL-1β-induced stress. Additionally, our microarray analysis of LCN2-silenced and control cells provides a better understanding of the mechanisms that may be influenced by LCN2 induction.
authors.affiliation: State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Hu
authors.forename: Jihua
authors.initials: J
authors.lastname: Xue
authors.forename: Ying
authors.initials: Y
authors.lastname: Yang
authors.forename: Xiaotang
authors.initials: X
authors.lastname: Zhou
authors.forename: Chaochao
authors.initials: C
authors.lastname: Qin
authors.forename: Min
authors.initials: M
authors.lastname: Zheng
authors.forename: Haihong
authors.initials: H
authors.lastname: Zhu
authors.forename: Yanning
authors.initials: Y
authors.lastname: Liu
authors.forename: Weixia
authors.initials: W
authors.lastname: Liu
authors.forename: Guohua
authors.initials: G
authors.lastname: Lou
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Shanshan
authors.initials: S
authors.lastname: Wu
authors.forename: Zhi
authors.initials: Z
authors.lastname: Chen
authors.forename: Feng
authors.initials: F
authors.lastname: Chen
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics* / Q000276:immunology; D002460:Cell Line; D005786:Gene Expression Regulation; D022781:Hepatocytes / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology*; D015850:Interleukin-6 / Q000235:genetics; D000071068:Lipocalin-2; D054834:Lipocalins / Q000235:genetics* / Q000276:immunology; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000276:immunology; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D015854:Up-Regulation
chemical_list: D000209:Acute-Phase Proteins; C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha