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ID 22189341
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タイトル Podoplanin expression in wound and hyperproliferative psoriatic epidermis: Regulation by TGF-β and STAT-3 activating cytokines, IFN-γ, IL-6, and IL-22
著者
本間, 大 (Honma, Masaru)
Minami-Hori, Masako
Takahashi, Hidetoshi
Iizuka, Hajime
上位タイトル
Journal of Dermatological Science Vol.65, No.2  (2012. 02) ,p.134- 140
識別番号
ISSN
0923-1811
DOI 10.1016/j.jdermsci.2011.11.011
URI http://www.sciencedirect.com/science/article/pii/S0923181111003276
抄録 Background: Podoplanin (PDPN)/T1a/aggrus/PA2.26 antigen, a transmembranous glycoprotein, is a
well-known lymphatic endothelial marker. Recent evidence indicates that PDPN is also expressed in
keratinocytes especially of sebaceous glands.
Objective: To verify expression-pattern and the regulatory mechanism of PDPN in human epidermal
keratinocytes.
Methods: PDPN-expression pattern was analyzed in normal and psoriatic epidermis by immunostaining.
The regulatory mechanism of PDPN-expression of keratinocytes by cytokines was analyzed using
specific inhibitors, siRNA, and adenoviral shRNA of signaling pathways.
Results: In normal skin, PDPN was expressed on the basal cell layer of sebaceous glands and on the outer
root sheath of hair follicles. While no expression was detected in the normal interfollicular epidermis,
PDPN was detected in the basal cell layer of wound and hyperproliferative psoriatic epidermis, where the
granular layer is lacking. TGF-b1 and IFN-g independently upregulated PDPN-expression of
keratinocytes via TGF-b receptor-Smad pathway and JAK-STAT pathway, respectively. IL-6 and IL-22
also stimulated PDPN-expression of keratinocytes accompanied by STAT-3 phosphorylation. siRNA of
STAT-1, inhibitors of STAT-3 signaling, AG490, STAT-3 inhibitor VI, and si/shRNA of STAT-3 inhibited the
PDPN-expression of keratinocytes induced by IFN-g, IL-6 and IL-22 but not by TGF-b1.
Conclusion: These results indicate that TGF-b1, IFN-g, IL-6, and IL-22 induce PDPN-expression of
keratinocytes, which might be significantly involved in the wound healing process as well as in the
pathomechanism of hyperproliferative psoriatic epidermis.
キーワード
Proriasis
Wound healing
Cytokines
STAT
SMAD
注記 Author
言語
eng
資源タイプ text
ジャンル Journal Article
著者版フラグ author
Index
/ Public
/ Public / 国外雑誌論文
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