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Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway.

Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway.

Authors :
Lee, Byung-Cheol
Song, Jisun
Lee, Arim
Cho, Daeho
Kim, Tae Sung
Source :
International Journal of Molecular Sciences; Nov2018, Vol. 19 Issue 11, p3642, 1p
Publication Year :
2018

Abstract

Visfatin, a member of the adipokine family, plays an important role in many metabolic and stress responses. The mechanisms underlying the direct therapeutic effects of visfatin on wound healing have not been reported yet. In this study, we examined the effects of visfatin on wound healing in vitro and in vivo. Visfatin enhanced the proliferation and migration of human dermal fibroblasts (HDFs) and keratinocytes the expression of wound healing-related vascular endothelial growth factor (VEGF) in vitro and in vivo. Treatment of HDFs with visfatin induced activation of both extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinases 1 and 2 (JNK1/2) in a time-dependent manner. Inhibition of ERK1/2 and JNK1/2 led to a significant decrease in visfatin-induced proliferation and migration of HDFs. Importantly, blocking VEGF with its neutralizing antibodies suppressed the visfatin-induced proliferation and migration of HDFs and human keratinocytes, indicating that visfatin induces the proliferation and migration of HDFs and human keratinocytes via increased VEGF expression. Moreover, visfatin effectively improved wound repair in vivo, which was comparable to the wound healing activity of epidermal growth factor (EGF). Taken together, we demonstrate that visfatin promotes the proliferation and migration of HDFs and human keratinocytes by inducing VEGF expression and can be used as a potential novel therapeutic agent for wound healing. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
16616596
Volume :
19
Issue :
11
Database :
Complementary Index
Journal :
International Journal of Molecular Sciences
Publication Type :
Academic Journal
Accession number :
133157679
Full Text :
https://doi.org/10.3390/ijms19113642