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

• DOI: 10.1042/cs20140735
• Publication Date: 2015-05-22T14:04:09Z
• Authors: Minjuan Wu; Shizhao Ji; Shichu Xiao; Zhengdong Kong; He Fang; Yunqing Zhang; Kaihong Ji; Yongjun Zheng; Houqi Liu; Zhaofan Xia
• Keywords: 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

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.