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

Jing Chen | Zendy; Yu Chen | Zendy; Yajie Chen | Zendy; Zicheng Yang | Zendy; Bo You | Zendy; Ye Chun Ruan | Zendy; Yizhi Peng | Zendy

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

Author(s) -

Jing Chen,

Yu Chen,

Yajie Chen,

Zicheng Yang,

Bo You,

Ye Chun Ruan,

Yizhi Peng

Publication year - 2016

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000447919

Subject(s) - hacat , wound healing , mapk/erk pathway , keratinocyte , gene knockdown , inflammation , cancer research , microbiology and biotechnology , p38 mitogen activated protein kinases , cell growth , nf κb , chemistry , kinase , medicine , immunology , biology , cell culture , biochemistry , genetics

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.

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