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Suppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein.

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 TPAinduced ear edema and expression levels of cyclooxygenase-2 (COX-2) as... Full description

Journal Title: BMB reports June 2012, Vol.45(6), pp.354-359
Main Author: Lee, Sun Hwa
Other Authors: 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
Format: Electronic Article Electronic Article
Language: English
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ID: E-ISSN: 1976-670X
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title: Suppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein.
format: Article
creator:
  • 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
subjects:
  • Animals–Therapeutic Use
  • Annexins–Metabolism
  • Cyclooxygenase 2–Chemically Induced
  • Edema–Drug Therapy
  • Extracellular Signal-Regulated MAP Kinases–Metabolism
  • Gene Products, Tat–Metabolism
  • Interleukin-1beta–Therapeutic Use
  • Interleukin-6–Metabolism
  • Male–Metabolism
  • Mice–Metabolism
  • Mice, Inbred Icr–Therapeutic Use
  • Nf-Kappa B–Chemically Induced
  • Phosphorylation–Drug Therapy
  • Recombinant Fusion Proteins–Metabolism
  • Skin Diseases–Metabolism
  • Tetradecanoylphorbol Acetate–Metabolism
  • Tumor Necrosis Factor-Alpha–Metabolism
  • P38 Mitogen-Activated Protein Kinases–Metabolism
  • Annexins
  • Gene Products, Tat
  • Interleukin-1beta
  • Interleukin-6
  • Nf-Kappa B
  • Recombinant Fusion Proteins
  • Tat-Anx1 Fusion Protein
  • Tumor Necrosis Factor-Alpha
  • Cyclooxygenase 2
  • Extracellular Signal-Regulated MAP Kinases
  • P38 Mitogen-Activated Protein Kinases
  • Tetradecanoylphorbol Acetate
ispartof: BMB reports, June 2012, Vol.45(6), pp.354-359
description: 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 TPAinduced ear edema and expression levels of cyclooxygenase-2 (COX-2) as well as pro-inflammatory cytokines such as interleukin- 1 beta (IL-1 β), IL-6, and tumor necrosis factor-alpha (TNF-α). Also, application of Tat-ANX1 protein significantly inhibited nuclear translocation of nuclear factor-kappa B (NF-κ B) and phosphorylation of p38 and extracellular signalregulated 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-κ 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.
language: eng
source:
identifier: E-ISSN: 1976-670X
fulltext: fulltext
issn:
  • 1976670X
  • 1976-670X
url: Link


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titleSuppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein.
creatorLee, 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
contributorLee, Sun Hwa (correspondence author) ; Lee, Sun Hwa (record owner)
ispartofBMB reports, June 2012, Vol.45(6), pp.354-359
identifierE-ISSN: 1976-670X
subjectAnimals–Therapeutic Use ; Annexins–Metabolism ; Cyclooxygenase 2–Chemically Induced ; Edema–Drug Therapy ; Extracellular Signal-Regulated MAP Kinases–Metabolism ; Gene Products, Tat–Metabolism ; Interleukin-1beta–Therapeutic Use ; Interleukin-6–Metabolism ; Male–Metabolism ; Mice–Metabolism ; Mice, Inbred Icr–Therapeutic Use ; Nf-Kappa B–Chemically Induced ; Phosphorylation–Drug Therapy ; Recombinant Fusion Proteins–Metabolism ; Skin Diseases–Metabolism ; Tetradecanoylphorbol Acetate–Metabolism ; Tumor Necrosis Factor-Alpha–Metabolism ; P38 Mitogen-Activated Protein Kinases–Metabolism ; Annexins ; Gene Products, Tat ; Interleukin-1beta ; Interleukin-6 ; Nf-Kappa B ; Recombinant Fusion Proteins ; Tat-Anx1 Fusion Protein ; Tumor Necrosis Factor-Alpha ; Cyclooxygenase 2 ; Extracellular Signal-Regulated MAP Kinases ; P38 Mitogen-Activated Protein Kinases ; Tetradecanoylphorbol Acetate
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descriptionWe 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 TPAinduced ear edema and expression levels of cyclooxygenase-2 (COX-2) as well as pro-inflammatory cytokines such as interleukin- 1 beta (IL-1 β), IL-6, and tumor necrosis factor-alpha (TNF-α). Also, application of Tat-ANX1 protein significantly inhibited nuclear translocation of nuclear factor-kappa B (NF-κ B) and phosphorylation of p38 and extracellular signalregulated 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-κ 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.
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titleSuppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein.
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titleSuppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein.
authorLee, 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
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5Gene Products, Tat–Metabolism
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