Both authors contributed equally to this study.
Liver Failure and Growth
The role of lipocalin-2 in liver regeneration
Version of Record online: 25 JUL 2014
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 35, Issue 4, pages 1195–1202, April 2015
How to Cite
Liver Int. 2015; 35: 1195–1202
- Issue online: 11 MAR 2015
- Version of Record online: 25 JUL 2014
- Accepted manuscript online: 10 JUL 2014 09:57AM EST
- Manuscript Accepted: 1 JUL 2014
- Manuscript Received: 13 NOV 2013
- hepatic proliferation;
- liver regeneration;
- partial hepatectomy
Background & Aims
Various immune mediators such as interleukin-6 (IL-6) have been implicated in the process of liver regeneration. Lipocalin-2 (LCN2) has been recently characterized as a prototypic immune mediator produced by various cell types being involved mainly in host defence. In addition, numerous studies have demonstrated its clinical value as a biomarker. This study aimed at defining the role of LCN2 in liver regeneration.
We studied LCN2 expression in wild-type mice in a model of partial hepatectomy (PH). Furthermore, we evaluated liver regeneration after PH in LCN-deficient mice compared to littermate controls. Serum levels of LCN2 were assessed in a small group of patients undergoing hepatic resection.
LCN2 is dramatically induced in livers and sera of wild-type mice after PH, whereas liver LCN2-receptor expression was decreased. Sham operations did not affect hepatic and serum LCN2 expression. Although LCN2-deficient mice exhibited increased baseline liver expression indices, LCN2-deficient mice did not differ from wild-type mice with respect to hepatic proliferation suggesting that this molecule is not involved in hepatic repair. Only serum IL-1β levels were slightly lower in LCN−/− mice, whereas IL-6 serum levels did not differ between various tested animal groups. In humans undergoing hepatic resection, LCN2 levels increased significantly within 24 h following surgery.
LCN2, although massively induced in mice after PH, is not relevant in murine hepatic regeneration. Further, human studies have to define whether LCN2 could evolve as biomarker after liver surgery.