Z Gastroenterol 2010; 48 - P1_04
DOI: 10.1055/s-0029-1246335

Lipocalin 2 (LCN2) in experimental liver injury

E Borkham-Kamphorst 1, F Drews 1, R Weiskirchen 2
  • 1Institute of Clinical Chemistry and Pathobiochemistry, University Hospital of The RWTH Aachen, Aachen
  • 2Institut für Klinische Chemie und Pathobiochemie, Universitätsklinikum der RWTH Aachen, Aachen

LCN2 is a member of the lipocalin super-family with a diverse functionality, including transport of fatty acids and apoptosis induction.

LCN2 expression is induced under pernicious conditions such as intoxication, infection, inflammation and other forms of cellular stress. The underlying reasons for activation however require further elucidation. Interestingly, our experimental liver injury models showed a rapid induction of well sustained LCN2 expression throughout our trials. Injured hepatocytes were identified as the main source of LCN2 production through primary liver cell isolation and immunohistochemistry.

Actuation of LCN2 was demonstrated in cultured HepG2 cells incubated with the p38-MAPK inhibitor (SB203580) accompanied by phosphorylated ERK1/2 MAPK and significantly increased the amounts of fat droplets.

Induction of LCN2 however was completely blocked by ERK MEK inhibitor (PD098059), confirming that LCN2 expression is regulated in part by MAPK pathways.

Amongst the known cytokines and growth factors involved in liver injury and tissue repair, IL-1beta stands out as the strongest activator of LCN2 production in vitro.

The in vivo liver injury models show a clear correlation of serum LCN2 with serum AST and ALT, the markers of liver damage. This finding implies a potential diagnostic value of LCN2.

LCN2