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
AUTHORS (10)
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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