Transcription Factor SOX10 Improves Migration and Homing of MSCs After Myocardial Infarction by Upregulating CXCR4

<b>Background:</b> CXCR4 enhances the homing of mesenchymal stem cells (MSCs), thereby potentially improving outcomes in myocardial infarction (MI). However, the molecular mechanisms underlying MSC homing remain poorly understood. <b>Methods:</b> The identity of MSCs was confirmed through flow cytometry, utilizing their cluster of differentiation (CD) marker profile. Migration and invasion were assessed using wound healing and transwell assays. In a rat MI model, myocardial function, hemodynamic parameters, and the degree of myocardial fiber damage were evaluated post-MSC treatment, along with the observation of MSC homing. Luciferase assays identified binding sites between SOX10 and the CXCR4 promoter, and the effects of SOX10 on MSC migration, invasion, and homing were explored both <i>in vitro</i> and <i>in vivo</i>. <b>Results:</b> Overexpression of CXCR4 significantly enhanced MSC migration, invasion, and homing. MSCs overexpressing CXCR4 improved cardiac function and reduced infarct size in the rat MI model. A direct interaction between SOX10 and CXCR4 was confirmed, with SOX10 acting as a transcription factor to upregulate CXCR4 expression, thereby enhancing MSC homing and ameliorating MI in rats. Knockdown of SOX10 reversed the beneficial effects of CXCR4-overexpressing MSCs on MI therapy, as well as the functional impact of CXCR4 on MSCs. <b>Conclusion:</b> In conclusion, SOX10 facilitates MSC homing by upregulating CXCR4 expression, offering a potential therapeutic approach for MI treatment.