2026-03-08T23:20:29Z https://hirosaki.repo.nii.ac.jp/oai

oai:hirosaki.repo.nii.ac.jp:00003600 2023-05-15T09:59:49Z 557:1754615242943:561:641

230-kD類天疱瘡抗原発現に対するTGF-βの抑制効果 230-kDルイ テンホウソウ コウゲン ハッソウ ニ タイスル TGF-β ノ ヨクセイ コウカ Inhibitory Effect of TGF-β on Expression of 230KD Bullous Pemphigoid Antigen Harada, Ken Tamai, Katsuto Nakano, Hajime Sasaki, Chiaki Hanada, Katsumi Hashimoto, Isao Sawamura, Daisuke 494.8 外科系臨床医学 Keratinocyte BPAG1 TGF-β IFN-γ 表皮細胞 application/pdf 230-kD bullous pemphigoid antigen (BPAG1) is known as an autoantigen in bullous pemphigoid and is expressed exclusively in proliferating basal keratinocytes. TGF-β is a growth factor that has pleiotropic effects on a wide range of target cells and induces differentiation of basal keratinocytes. Therefore. TGF-β is postulated to inhibit BPAG1 expression. However. previous report conversely demonstrated an increase of BPAG1 expression by TGF-β. In this study. to understand regulatory role of TGF-β on BPAG1 functions. we examined the effect of TGF-β on BPAG1 gene expression using cultured keratinocytes. This study showed that BPAG1 mRNA expression was inhibited by TGF-β1 in concentration higher than 1.0 ng/ml. Furthermore. incubation of the cells with TGF-β1 in the presence of cycloheximide demonstrated that newly synthesized protein was required for BPAG1 regulation. To understand the detailed mechanisms of BPAGI modulation by TGF-β, we preformed transient transfection assay with a BPAGI promoter-CAT construct to know the detailed mechanisms of BPAG1 modulation by TGF-β. The results revealed that calcium and IFN-γ inhibited BPAG1 expression at transcriptional level, but TGF-β1 is not responsible for that transcriptional inhibition, suggesting that TGF-β may have differential molecular mechanism for down-regulation of BPAG1 gene expression from the events induced by IFN-γ. 弘前医学. 59, 2007, p.7-14 departmental bulletin paper 弘前大学大学院医学研究科・弘前医学会 2007-11-15 VoR application/pdf 弘前医学 1 59 7 14 AN00211444 0439-1713 https://hirosaki.repo.nii.ac.jp/record/3600/files/AN00211444_59_7.pdf http://hdl.handle.net/10129/689 https://hirosaki.repo.nii.ac.jp/records/3600 eng