Myofibroblast phenotype and apoptosis in keloid and palmar fibroblasts in vitro

被引:51
作者
Chipev, CC [1 ]
Simman, R
Hatch, G
Katz, AE
Siegel, DM
Simon, M
机构
[1] SUNY Stony Brook, Living Skin Bank, Stony Brook, NY 11794 USA
[2] SUNY Stony Brook, Hlth Sci Ctr, Dept Surg, Stony Brook, NY 11794 USA
[3] SUNY Stony Brook, Hlth Sci Ctr, Dept Otolaryngol, Stony Brook, NY 11794 USA
[4] SUNY Stony Brook, Hlth Sci Ctr, Dept Dermatol, Stony Brook, NY 11794 USA
[5] SUNY Stony Brook, Hlth Sci Ctr, Dept Oral Biol & Pathol, Stony Brook, NY 11794 USA
关键词
alpha smooth muscle actin; collagen I; thrombospondin-1; serum starvation;
D O I
10.1038/sj.cdd.4400605
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Keloid formation is a wound healing response, which fails to resolve and leads to formation of a raised collagen mass extending beyond the original wound margins, Keloids are typically excluded from palms and soles. Therefore we compared keloid and palmar fibroblasts in vitro using fibroblasts from nonaffected individuals as controls. Collagen I, alpha-smooth muscle actin and thrombospondin-1 were found at higher levels in keloid than in palmar fibroblasts. These differences were ameliorated by addition of TGF beta 1. The potential for resolution of the wound healing response was estimated analyzing apoptosis during serum starvation. Annexin V and TUNEL assays showed that palmar fibroblasts underwent faster apoptosis, than did the keloid fibroblasts, and started detaching. Addition of TGF beta 1 counteracted this effect. The weak expression of the myofibroblast phenotype and the advanced apoptosis of palmar fibroblasts suggest mechanisms for the exclusion of keloids from palmer sites.
引用
收藏
页码:166 / 176
页数:11
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