JAM-A promotes wound healing by enhancing both homing and secretory activities of mesenchymal stem cells

Male 0301 basic medicine 2. Zero hunger Mice, Inbred BALB C 0303 health sciences Chemotaxis Lentivirus Mice, Nude Cell Differentiation Mesenchymal Stem Cells Receptors, Cell Surface Coculture Techniques 3. Good health Platelet Endothelial Cell Adhesion Molecule-1 Mice 03 medical and health sciences Cell Movement Cell Adhesion Leukocytes, Mononuclear Animals Humans Epidermis Promoter Regions, Genetic Cell Adhesion Molecules Transcription Factors
DOI: 10.1042/cs20140735 Publication Date: 2015-05-22T14:04:09Z
ABSTRACT
The homing ability and secretory function of mesenchymal stem cells (MSCs) are key factors that influence cell involvement in wound repair. These factors are controlled by multilayer regulatory circuitry, including adhesion molecules, core transcription factors (TFs) and certain other regulators. However, the role of adhesion molecules in this regulatory circuitry and their underlying mechanism remain undefined. In the present paper, we demonstrate that an adhesion molecule, junction adhesion molecule A (JAM-A), may function as a key promoter molecule to regulate skin wound healing by MSCs. In in vivo experiments, we show that JAM-A up-regulation promoted both MSC homing to full-thickness skin wounds and wound healing-related cytokine secretion by MSCs. In vitro experiments also showed that JAM-A promoted MSC proliferation and migration by activating T-cell lymphoma invasion and metastasis 1 (Tiam1). We suggest that JAM-A up-regulation can increase the proliferation, cytokine secretion and wound-homing ability of MSCs, thus accelerating the repair rate of full-thickness skin defects. These results may provide insights into a novel and potentially effective approach to improve the efficacy of MSC treatment.
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