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

The homing ability and secretory function of mesenchymal stem cells (MSCs) are key factors that influence the cells’ involvement in wound repair. These factors are controlled by a 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. Here, we demonstrate that an adhesion molecule, junction adhesion molecule A (JAM-A), may function as a key promoter molecule that regulates 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 rate of repair of full-thickness skin defects. These results may provide insights into a novel and potentially effective approach to improve the efficacy of MSC treatment.
Source: Clinical Science - Category: Biomedical Science Authors: Source Type: research