Targeted migration of mesenchymal stem cells modified with CXCR4 to acute failing liver improves liver regeneration

World J Gastroenterol. 2014 Oct 28;20(40):14884-94. doi: 10.3748/wjg.v20.i40.14884.

Abstract

Aim: To improve the colonization rate of transplanted mesenchymal stem cells (MSCs) in the liver and effect of MSC transplantation for acute liver failure (ALF).

Methods: MSC was modified with the chemokine CXC receptor 4 (CXCR4) gene (CXCR4-MSC) or not (Null-MSC) through lentiviral transduction. The characteristics of CXCR4-MSCs and Null-MSCs were determined by real-time quantitative polymerase chain reaction, Western blotting and flow cytometry. CXCR4-MSCs and Null-MSCs were infused intravenously 24 h after administration of CCl4 in nude mice. The distribution of the MSCs, survival rates, liver function, hepatocyte regeneration and growth factors of the recipient mice were analyzed.

Results: In vitro, CXCR4-MSCs showed better migration capability toward stromal cell-derived factor-1α and a protective effect against thioacetamide in hepatocytes. In vivo imaging showed that CXCR4-MSCs migrated to the liver in larger numbers than Null-MSCs 1 and 5 d after ALF. Higher colonization led to a longer lifetime and better liver function. Either CXCR4-MSCs or Null-MSCs exhibited a paracrine effect through secreting hepatocyte growth factor and vascular endothelial growth factor. Immunohistochemical analysis of Ki-67 showed increased cell proliferation in the damaged liver of CXCR4-MSC-treated animals.

Conclusion: Genetically modified MSCs expressing CXCR4 showed greater colonization and conferred better functional recovery in damaged liver.

Keywords: Acute liver failure; Cell mobilization; Cell transplantation; Chemokine CXC receptor 4; Mesenchymal stem cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Movement*
  • Cell Proliferation
  • Cell Survival
  • Cell Tracking / methods
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / genetics
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / pathology
  • Chemical and Drug Induced Liver Injury / therapy*
  • Disease Models, Animal
  • Genetic Therapy / methods*
  • Green Fluorescent Proteins / biosynthesis
  • Green Fluorescent Proteins / genetics
  • Hepatocyte Growth Factor / metabolism
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Liver / metabolism*
  • Liver / pathology
  • Liver Failure, Acute / chemically induced
  • Liver Failure, Acute / genetics
  • Liver Failure, Acute / metabolism
  • Liver Failure, Acute / pathology
  • Liver Failure, Acute / therapy*
  • Liver Regeneration
  • Male
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / metabolism*
  • Mice, Nude
  • Paracrine Communication
  • Receptors, CXCR4 / biosynthesis*
  • Receptors, CXCR4 / genetics
  • Thioacetamide
  • Time Factors
  • Transfection
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • CXCR4 protein, human
  • HGF protein, human
  • Receptors, CXCR4
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • enhanced green fluorescent protein
  • Thioacetamide
  • Green Fluorescent Proteins
  • Hepatocyte Growth Factor