| First Author | Chen J | Year | 2016 |
| Journal | Cell Physiol Biochem | Volume | 39 |
| Issue | 6 | Pages | 2262-2274 |
| PubMed ID | 27832634 | Mgi Jnum | J:323174 |
| Mgi Id | MGI:6856069 | Doi | 10.1159/000447919 |
| Citation | Chen J, et al. (2016) Epidermal CFTR Suppresses MAPK/NF-kappaB to Promote Cutaneous Wound Healing. Cell Physiol Biochem 39(6):2262-2274 |
| abstractText | 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-kappaB signaling. We undertook the present study to explore a possible role of CFTR in regulating MAPK/NF-kappaB 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-kappaB signaling were examined. Inhibitors of MAPK/NF-kappaB 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 IkappaBalpha. The disturbance of inflammation, proliferation and differentiation in HaCaT cells were reversed by CFTR overexpression or inhibition of MAPK or NF-kappaB. CONCLUSION: CFTR plays a role in suppressing MAPK/NF-kappaB to relieve inflammation, reduce proliferation and promote differentiation of keratinocytes, and thus promotes cutaneous wound healing. |
