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Thymosin β 4 has a major role in dermal burn wound healing that involves actin cytoskeletal remodelling via heat‐shock protein 70
Author(s) -
Kim Sokho,
Kwon Jungkee
Publication year - 2017
Publication title -
journal of tissue engineering and regenerative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.835
H-Index - 72
eISSN - 1932-7005
pISSN - 1932-6254
DOI - 10.1002/term.2028
Subject(s) - wound healing , microbiology and biotechnology , angiogenesis , hsp70 , heat shock protein , actin cytoskeleton , cytoskeleton , actin , chemistry , neovascularization , biology , immunology , cancer research , cell , biochemistry , gene
Abstract Rapid vascular remodelling of damaged dermal tissue is required to heal burn wounds. Thymosin β 4 (T β 4) is a growth factor that has been shown to promote angiogenesis and dermal wound repair. However, the underlying mechanisms based on T β 4 function have not yet been fully investigated. In the present study, we investigated how T β 4 improves dermal burn wound healing via actin cytoskeletal remodelling and the action of heat‐shock proteins (HSPs), which are a vital set of chaperone proteins that respond to heat shock. Our in vitro results achieved with the use of human umbilical vein endothelial cells (HUVECs) revealed a possible signal between T β 4 and HSP70. Moreover, we confirmed that remodelling of filamentous actin (F‐actin) was regulated by T β 4‐induced HSP70 in HUVECs. Based on these in vitro results, we confirmed the healing effects of T β 4 in an adapted dermal burn wound in vivo model. T β 4 improved wound‐healing markers, such as wound closure and vascularization. Moreover, T β 4 maintained the long‐term expression of HSP70, which is associated with F‐actin regulation during the wound‐healing period. These results suggest that an association between T β 4 and HSP70 is responsible for the healing of burn wounds, and that this association may regulate F‐actin remodelling. Copyright © 2015 John Wiley & Sons, Ltd.