Document Detail

Erratum to "Neutrophil-dominant psoriasis-like skin inflammation induced by epidermal-specific expression of Raf in mice" [J. Dermatol. Sci. 58 (2010) 28-35].
MedLine Citation:
PMID:  20578288     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Raf is one of the downstream effectors of Ras GTPases. The induction of Raf in the epidermis causes the proliferation of keratinocytes and epidermal hyperplasia. However, skin inflammation accompanying Ras-induced epidermal reactions has not been fully delineated.
OBJECTIVE: The aim of this study was to characterize inflammatory reactions induced by epidermal-specific Raf expression and to elucidate its role in skin inflammation.
METHODS: K14-Raf:ER transgenic mice, in which the 4-hydroxytamoxifen (4OHT)-responsive mutant estrogen receptor (ER) ligand binding domain-Raf fusion gene was expressed under control of the keratin 14 promoter, were used to characterize inflammatory reactions induced by Raf expression in the epidermis.
RESULTS: A single topical application of 4OHT induced the expression of phosphorylated extracellular signal-related kinase 1/2 and elicited neutrophil-dominant inflammatory infiltrates in the skin. The Raf expression also rapidly induced the production of several cytokines and chemokines, including VEGF and CXCL1, by keratinocytes and inmouse skin in vivo. Furthermore, CD4-positive cells from regional lymph nodes had the potential to differentiate into IFNg- and IL17-producing cells. Treatment with an anti-Gr-1 antibody diminished the Raf-induced cutaneous inflammation and partially reversed the epidermal hyperplasia and hyperkeratosis.
CONCLUSION: Activation of the Raf signaling pathway is involved in the epidermal hyperplasia and the neutrophil-dominant cutaneous inflammatory reactions which are characteristics of psoriasis.
Masahito Tartutani; Yasutomo Imai; Koubun Yasuda; Hiroko Tsutsui; Kenji Nakanishi; Kiyofumi Yamanishi
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Publication Detail:
Type:  Corrected and Republished Article; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of dermatological science     Volume:  59     ISSN:  1873-569X     ISO Abbreviation:  J. Dermatol. Sci.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-24     Completed Date:  2010-10-01     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  9011485     Medline TA:  J Dermatol Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  64-71     Citation Subset:  IM    
Department of Dermatology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
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MeSH Terms
Antigens, CD4 / analysis
Chemokine CXCL1 / analysis
Epidermis / pathology
Extracellular Signal-Regulated MAP Kinases / metabolism
Hyperplasia / pathology
Interferon-gamma / analysis
Interleukin-17 / analysis
Keratin-14 / genetics,  metabolism
Lymph Nodes / metabolism
Mice, Inbred C57BL
Mice, Transgenic
Neutrophils / pathology*
Promoter Regions, Genetic
Psoriasis / etiology*,  pathology*
Receptors, Estrogen / genetics,  metabolism
Tamoxifen / adverse effects,  analogs & derivatives
Vascular Endothelial Growth Factor A / analysis
raf Kinases / metabolism*
Reg. No./Substance:
0/Antigens, CD4; 0/Chemokine CXCL1; 0/Interleukin-17; 0/Keratin-14; 0/Krt1-14 protein, mouse; 0/Receptors, Estrogen; 0/Vascular Endothelial Growth Factor A; 10540-29-1/Tamoxifen; 17197F0KYM/afimoxifene; 82115-62-6/Interferon-gamma; EC Kinases; EC Signal-Regulated MAP Kinases
Erratum In:
J Dermatol Sci. 2010 Jul;59(1):63
Corrected and Republished From:
J Dermatol Sci. 2010 Apr;58(1):28-35   [PMID:  20188517 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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