Cell and Tissue Research

, 331:283

Activation of stem cells in hepatic diseases

Authors

    • MRC/University of Edinburgh Centre for Inflammation Research, The Queen’s Medical Research InstituteUniversity of Edinburgh
  • S. Lorenzini
    • MRC/University of Edinburgh Centre for Inflammation Research, The Queen’s Medical Research InstituteUniversity of Edinburgh
  • S. J. Forbes
    • MRC/University of Edinburgh Centre for Inflammation Research, The Queen’s Medical Research InstituteUniversity of Edinburgh
Review

DOI: 10.1007/s00441-007-0542-z

Cite this article as:
Bird, T.G., Lorenzini, S. & Forbes, S.J. Cell Tissue Res (2008) 331: 283. doi:10.1007/s00441-007-0542-z

Abstract

The liver has enormous regenerative capacity. Following acute liver injury, hepatocyte division regenerates the parenchyma but, if this capacity is overwhelmed during massive or chronic liver injury, the intrinsic hepatic progenitor cells (HPCs) termed oval cells are activated. These HPCs are bipotential and can regenerate both biliary epithelia and hepatocytes. Multiple signalling pathways contribute to the complex mechanism controlling the behaviour of the HPCs. These signals are delivered primarily by the surrounding microenvironment. During liver disease, stem cells extrinsic to the liver are activated and bone-marrow-derived cells play a role in the generation of fibrosis during liver injury and its resolution. Here, we review our current understanding of the role of stem cells during liver disease and their mechanisms of activation.

Keywords

Liver regenerationLiver cirrhosisOval cellsStem cellsBone marrow

Abbreviations

αFP

Alpha-fetoprotein

AAF

2-N-acetylaminofluorene

BDL

Bile duct ligation

BM

Bone marrow

BMSC

Bone marrow stem cell

CCl4

Carbon tetrachloride

CDE

Choline-deficient ethionine-supplemented

CK

Cytokeratin

CTGF

Connective tissue growth factor

DDC

3,5-Diethoxycarbonlyl-1,4-dihydrocollidine-supplemented

DPPIV

Dipeptidyl peptidase IV

ECM

Extracellular matrix

ERK

Extracellular signal-regulated kinase

EGF

Epidermal growth factor

FAH −/−

Fumarylacetoacetate hydrolase knockout

FGF

Fibroblast growth factor

FGFR

FGF receptor

G-CSF

Granulocyte colony-stimulating factor

HGF

Hepatocyte growth factor

HCC

Hepatocellular carcinoma

HPC

Hepatic progenitor cell

IFN

Interferon

IL

Interleukin

JAK

Janus kinase

LIF

Leukaemia inhibitor factor

LIFR

LIF receptor

LT

Lymphotoxin

MMP

Metalloproteinase

OC

Oval cell

OSM

Oncostatin M

OSMR

OSM receptor

PH

Partial hepatectomy

PPAR

Peroxisome-proliferator-activated receptor

SCF

Stem cell factor

SDF-1

Stromal-cell-derived factor 1

SgIGSF

Spermatogenic immunoglobulin superfamily

STAT

Signal transductor and activator of transcription

TGF

Transforming growth factor

TNF

Tumour necrosis factor

TWEAK

TNF-like weak induction of apoptosis

uPA

Urokinase-type plasminogen activator

Copyright information

© Springer-Verlag 2007