Suppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein
- Authors
- Lee, Sun Hwa; Kim, Dae Won; Eom, Seon Ae; Jun, Se-Young; Park, Meeyoung; Kim, Duk-Soo; Kwon, Hyung Joo; Kwon, Hyeok Yil; Han, Kyu Hyung; Park, Jinseu; Hwang, Hyun Sook; Eum, Won Sik; Choi, Soo Young
- Issue Date
- 30-Jun-2012
- Publisher
- 생화학분자생물학회
- Keywords
- Cytokine; Inflammation; MAPK; Tat-ANX1; TPA
- Citation
- BMB Reports, v.45, no.6, pp 354 - 359
- Pages
- 6
- Journal Title
- BMB Reports
- Volume
- 45
- Number
- 6
- Start Page
- 354
- End Page
- 359
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/15053
- DOI
- 10.5483/BMBRep.2012.45.6.036
- ISSN
- 1976-6696
1976-670X
- Abstract
- We examined that the protective effects of ANX1 on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in animal models using a Tat-ANX1 protein. Topical application of the Tat-ANX1 protein markedly inhibited TPA-induced ear edema and expression levels of cyclooxygenase-2 (COX-2) as well as pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha). Also, application of Tat-ANX1 protein significantly inhibited nuclear translocation of nuclear factor-kappa B (NF-kappa B) and phosphorylation of p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) in TPA-treated mice ears. The results indicate that Tat-ANX1 protein inhibits the inflammatory response by blocking NF-kappa B and MAPK activation in TPA-induced mice ears. Therefore, the Tat-ANX1 protein may be useful as a therapeutic agent against inflammatory skin diseases. [BMB Reports 2012; 45(6): 354-359]
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Collections - College of Medicine > Department of Anatomy > 1. Journal Articles
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