Epidermal CFTR Suppresses MAPK/NF-κB to Promote Cutaneous Wound Healing

Jing Chen, Yu Chen, Yajie Chen, Zicheng Yang, Bo You, Yechun Ruan, Yizhi Peng

Research output: Journal article publicationJournal articleAcademic researchpeer-review

31 Citations (Scopus)

Abstract

Karger AG, Basel. Background: CFTR is implicated in cutaneous wound healing although the underlying mechanisms are not fully understood. In other cell types, CFTR is reported to regulate MAPK/ NF-κB signaling. We undertook the present study to explore a possible role of CFTR in regulating MAPK/NF-κB during cutaneous wound healing. Methods & Results: The splint-excisional and incisional wound healing models were used in CFTR mutant (DF508) mice. The cell-scratch model was used in a human keratinocyte line, HaCaT, in conjunction with CFTR knockdown or overexpression. The epidermal inflammation, keratinocyte proliferation and differentiation, as well as MAPK/NF-κB signaling were examined. Inhibitors of MAPK/NF-κB were also used. Results: Both DF508 mice and HaCaT cells with CFTR knockdown exhibited delayed cutaneous wound healing with exuberant inflammation, increased proliferation and aberrant differentiation. Knockdown of CFTR in HaCaT cells resulted in phosphorylation of ERK, p38 and IκBα. The disturbance of inflammation, proliferation and differentiation in HaCaT cells were reversed by CFTR overexpression or inhibition of MAPK or NF-κB. Conclusion: CFTR plays a role in suppressing MAPK/NF-κB to relieve inflammation, reduce proliferation and promote differentiation of keratinocytes, and thus promotes cutaneous wound healing.
Original languageEnglish
Pages (from-to)2262-2274
Number of pages13
JournalCellular Physiology and Biochemistry
Volume39
Issue number6
DOIs
Publication statusPublished - 1 Nov 2016
Externally publishedYes

Keywords

  • CFTR
  • Cutaneous wound healing
  • MAPK
  • NF-κB

ASJC Scopus subject areas

  • Physiology

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