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In Vitro Cell Dev Biol Anim ; 50(7): 648-55, 2014 Aug.
Article in English | MEDLINE | ID: mdl-24652046

ABSTRACT

A better understanding of the organ specific factors that regulate the migration of mesenchymal stem cells (MSCs) into the target organ is essential for optimization of strategies to improve the repair after injury. In the present study, we showed that the kidney injury molecule-1 (KIM-1), a well-known kidney-specific biomarker, enhanced the in vitro migration capacity of MSCs as a potent kidney-specific chemo-attractant or an inducer. The in vitro roles were verified by migration assay using KIM1-PK1 cell lines, the mouse proximal tubular epithelial cells (mPTEs) and recombinant human KIM-1 proteins (rhKIM-1). Immunofluorescence staining displayed specific ectodomain binding of KIM-1 on the surface of MSCs. Upregulation of chemokine receptor type 4 (CXCR4) protein when treated with tumor necrosis factor alpha (TNF-α) was shown. The effect of KIM-1 on migration of MSCs was augmented by TNF-α pretreatment in a dose-dependent manner, and reduced by AMD3100, an antagonist of CXCR4. These results suggest that KIM-1 is a potential chemo-ligand of CXCR4 and may play an important role in kidney-specific migration of MSCs via interaction between KIM-1 and CXCR4.


Subject(s)
Cell Movement/physiology , Chemotaxis/physiology , Membrane Glycoproteins/metabolism , Mesenchymal Stem Cells/physiology , Receptors, Virus/metabolism , Analysis of Variance , Animals , Benzylamines , Blotting, Western , Cyclams , Dose-Response Relationship, Drug , Flow Cytometry , Fluorescent Antibody Technique , Hepatitis A Virus Cellular Receptor 1 , Heterocyclic Compounds , Humans , Mesenchymal Stem Cells/metabolism , Mice , Receptors, CXCR4/antagonists & inhibitors , Receptors, CXCR4/metabolism , Tumor Necrosis Factor-alpha/pharmacology
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