Abstract
BackgroundActivin B has been reported to promote the proliferation and migration of keratinocytes in vitro via the RhoA-JNK signaling pathway, whereas its in vivo role and mechanism in wound healing process has not yet been elucidated.Principal FindingsIn this study, we explored the potential mechanism by which activin B induces epithelial wound healing in mice. Recombinant lentiviral plasmids, with RhoA (N19) and RhoA (L63) were used to infect wounded KM mice. The wound healing process was monitored after different treatments. Activin B-induced cell proliferation on the wounded skin was visualized by electron microscopy and analyzed by 5′-bromodeoxyuridine (BrdU) incorporation assay. Protein expression of p-JNK or p-cJun was determined by immunohistochemical staining and immunoblotting analysis. Activin B efficiently stimulated the proliferation of keratinocytes and hair follicle cells at the wound area and promoted wound closure. RhoA positively regulated activin B-induced wound healing by up-regulating the expression of p-JNK and p-cJun. Moreover, suppression of RhoA activation delayed activin B-induced wound healing, while JNK inhibition recapitulated phenotypes of RhoA inhibition on wound healing.ConclusionThese results demonstrate that activin B promotes epithelial wound closure in vivo through the RhoA-Rock-JNK-cJun signaling pathway, providing novel insight into the essential role of activin B in the therapy of wound repair.
Highlights
Cutaneous wound repair is a complex process, which involves a series of biological events involving inflammation, new tissue formation and tissue remodeling [1]
These results demonstrate that activin B promotes epithelial wound closure in vivo through the RhoA-RockJNK-cJun signaling pathway, providing novel insight into the essential role of activin B in the therapy of wound repair
scanning electron microscopy (SEM) analysis further confirmed newly formed epithelial tissue and epithelial cells distributed along collagen on the surface of the healed wound area after activin B treatment (Fig. 1D)
Summary
Cutaneous wound repair is a complex process, which involves a series of biological events involving inflammation, new tissue formation and tissue remodeling [1]. During the process of new tissue formation, the proliferation and migration of keratinocytes is required for wound re-epithelialization and healing [2]. Various growth factors and cytokines have been found to play a critical role in wound healing [3]. Among these factors, activins, which are members of the transforming growth factor b (TGF-b) superfamily, play an important role in regulating normal function of epithelial cells, skin development and wound healing [4,5]. Activin B has been reported to promote the proliferation and migration of keratinocytes in vitro via the RhoAJNK signaling pathway, whereas its in vivo role and mechanism in wound healing process has not yet been elucidated
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