Glucose transporter member 1 is involved in UVB‐induced epidermal hyperplasia by enhancing proliferation in epidermal keratinocytes. (20th January 2013)

• Record Type: Journal Article
• Authors: Tochio, Takumi; Tanaka, Hiroshi; Nakata, Satoru
• Is Part Of: International journal of dermatology. Volume 52:Number 3(2013:Mar.)
• Page Start: 300
• Page End: 308
• Publication Date: 2013-01-20
• Subjects: Dermatology -- Periodicals; 616.5
• DOI: 10.1111/j.1365-4632.2011.05299.x
• Languages: English
• ISSNs: 0011-9059

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p> <bold>Background </bold> Glucose transporter member 1 (GLUT‐1) is one of the major facilitated glucose transporters and contributes to the promotion of keratinocyte proliferation in psoriasis and carcinogenic lesions. In this study, we postulate that GLUT‐1 is involved in ultraviolet B (UVB)‐induced epidermal hyperplasia. The purpose of this study is to investigate the possible role of GLUT‐1 in UVB‐induced hyperplasia.</p> <p> <bold>Materials and methods </bold> The effects of UVB on GLUT‐1 expression levels were investigated in <italic>in vitro</italic> and <italic>in vivo</italic> studies. In addition, the involvement of epidermal growth factor (EGF) and hypoxia inducible factor‐1 alpha (HIF‐1α), transcriptional factors for GLUT‐1, in GLUT‐1‐related events were investigated.</p> <p> <bold>Results </bold> <italic>GLUT‐1</italic> mRNA and its protein levels were markedly increased by UVB irradiation in HaCaT cells. In <italic>in vivo</italic> studies, a strong immunofluorescence signal of GLUT‐1 was clearly observed around the basal layer of the epidermis, which proliferated excessively by UVB irradiation. In HaCaT cells, <italic>EGF</italic> mRNA and its protein levels were markedly increased by UVB irradiation, and then the <italic>GLUT‐1</italic> mRNA level was significantly increased by treatment with EGF. Additionally, the upregulation of <italic>GLUT‐1</italic> by both UVB irradiation and treatment with EGF was significantly suppressed by transfection with HIF‐1α siRNA.</p> <p> <bold>Conclusions </bold> We conclude that GLUT‐1 is involved in UVB‐induced epidermal hyperplasia by enhancing proliferation of epidermal basal cells, and the GLUT‐1‐related event might be regulated by an increase in HIF‐1α stimulated by EGF.</p> </abstract>