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Activin B Promotes BMSC-Mediated Cutaneous Wound Healing by Regulating Cell Migration Via the JNK‐ERK Signaling Pathway

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Bone marrow-derived mesenchymal stem cells (BMSCs) are able to differentiate into various types of skin cells and participate in skin regeneration and repair. Activin signaling can regulate wound healing and reepithelialization. The present study assessed the impact of activin B on BMSC-mediated cutaneous wound healing in rats and explored the possible mechanism involved. We found that CFSE-labeled BMSCs participated in wound healing in vivo, and compared to administration with PBS, activin B, or BMSCs, activin B plus BMSCs significantly promoted wound healing and hair follicle regeneration. Activin B induced actin stress fiber formation and cell migration in BMSCs in vitro. Activation of JNK and ERK, but not p38, was required for activin B-induced actin stress fiber formation and BMSC migration. These results show that activin B may promote BMSC-mediated wound healing by inducing actin stress fiber formation and BMSC migration via the ERK and JNK signal pathways. Combined administration of BMSCs and cytokines may be a promising therapeutic strategy for the management of skin wounds.
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Keywords: Activin B; Bone marrow-derived mesenchymal stem cells (BMSCs); Extracellular signal regulated kinase (ERK); Skin; Wound healing; c-JUN NH2-terminal protein kinase (JNK)

Document Type: Research Article

Affiliations: Department of Histology and Embryology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China

Publication date: 15 September 2014

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