Sulfated glycosaminoglycans and non-classically secreted proteins, basic FGF and epimorphin, coordinately regulate TGF-β-induced cell behaviors of human scar dermal fibroblasts

Highlights • TGF-β induces the αSMA expression in HSF, which is hampered by heparinoid. • Leaderless proteins bFGF and epimorphin can oppositely regulate the TGF-β signaling. • Highly sulfated CS or its substitute heparinoid binds to TGF-β, bFGF and epimorphin. • Heparinoid controls the activities o...

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Veröffentlicht in:	Journal of dermatological science 2017-05, Vol.86 (2), p.132-141
Hauptverfasser:	Horigome, Tomoatsu, Takumi, Shinya, Shirai, Kota, Kido, Takumi, Hagiwara-Chatani, Natsumi, Nakashima, Ayumi, Adachi, Naoki, Yano, Hiroko, Hirai, Yohei
Format:	Artikel
Sprache:	eng
Schlagworte:	Actins - metabolism Alpha smooth muscle actin Animals bFGF Cell Membrane - metabolism Cercopithecus aethiops Chondroitin Sulfates - chemistry Cicatrix - metabolism COS Cells Dermatology Epimorphin Fibroblast Growth Factor 2 - pharmacology Fibroblasts - metabolism Glycosaminoglycan Glycosaminoglycans - chemistry Heparinoid Heparinoids - metabolism Humans Proteoglycans - metabolism Recombinant Proteins - pharmacology Scar Signal Transduction Swine Syntaxin 1 - metabolism Transforming Growth Factor beta - pharmacology
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Zusammenfassung:	Highlights • TGF-β induces the αSMA expression in HSF, which is hampered by heparinoid. • Leaderless proteins bFGF and epimorphin can oppositely regulate the TGF-β signaling. • Highly sulfated CS or its substitute heparinoid binds to TGF-β, bFGF and epimorphin. • Heparinoid controls the activities of bFGF and epimorphin in a different manner.
ISSN:	0923-1811 1873-569X
DOI:	10.1016/j.jdermsci.2017.01.014