1. Academic Validation
  2. TWEAK/Fn14 Signals Mediate Burn Wound Repair

TWEAK/Fn14 Signals Mediate Burn Wound Repair

  • J Invest Dermatol. 2019 Jan;139(1):224-234. doi: 10.1016/j.jid.2018.05.036.
Jing Liu 1 Yale Liu 1 Lingling Peng 1 Juxue Li 2 Kunyi Wu 3 Linlin Xia 3 Jiawen Wu 1 Sijia Wang 1 Xuening Wang 1 Qilu Liu 1 Weihui Zeng 4 Yumin Xia 5
Affiliations

Affiliations

  • 1 Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
  • 2 Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, China.
  • 3 Core Research Laboratory, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
  • 4 Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China. Electronic address: zengwh88@126.com.
  • 5 Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China. Electronic address: xiayumin1202@163.com.
Abstract

TWEAK acts by engaging with Fn14 to regulate inflammatory responses, fibrosis, and tissue remodeling, which are central in the repair processes of wounds. This study aims to explore the potential role of the TWEAK/Fn14 pathway in the healing of cutaneous burn wounds. Third-degree burns were introduced in wild-type and Fn14-deficient BALB/c mice, followed by evaluation of wound areas and histological changes. The downstream cytokines including growth factors were also examined in lesional skin. Moreover, human dermal microvascular endothelial cells and dermal fibroblasts were analyzed in vitro upon TWEAK stimulation. The healing of burn wounds was delayed in Fn14-deficient mice and was accompanied by the suppression of inflammatory responses, growth factor production, and extracellular matrix synthesis. Moreover, TWEAK/Fn14 activation enhanced the migration and cytokine production of both dermal microvascular endothelial cells and dermal fibroblasts. TWEAK also facilitates the expression of α-SMA and palladin in dermal fibroblasts. Furthermore, transfection of Fn14 small interfering RNA abrogated such promotion effect of TWEAK on these cells. In conclusion, TWEAK/Fn14 signals mediate the healing of burn wounds, possibly involving TWEAK regulation of the function of resident cells.

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