期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 117, 期 6, 页码 1538-1545出版社
BLACKWELL PUBLISHING INC
DOI: 10.1046/j.0022-202x.2001.01535.x
关键词
focal adhesion kinase; integrin; keratinocytes; psoriasis
类别
资金
- NIAMS NIH HHS [AR41707, KO8AR02063] Funding Source: Medline
We previously proposed that the keratinocyte hyperproliferative state in psoriatic skin results from a combination of T cell cytokine interaction with basal keratinocytes that exist in a primed state. We now provide evidence that basal keratinocytes from psoriatic uninvolved skin are in a preactivated state with regard to their interaction with fibronectin. Freshly isolated basal keratinocytes (K-1/K-10(-)) from nonlesional psoriatic skin demonstrated a significantly higher percentage of spreading cells 1 h after plating on fibronectin-coated plates than keratinocytes isolated from normal skin (p = 0.0002). No differences were observed on collagen-laminin-coated plates, however. The keratinocyte spreading on fibronectin-coated plates involved alpha5 beta1 and alphaV beta1 integrins. To address the potential signaling cascades that may respond to integrin changes in psoriatic keratinocytes, focal adhesion kinase changes were assessed. The percentage of keratinocytes from psoriatic uninvolved skin that exhibit positive focal adhesion kinase staining was significantly greater than the percentage from healthy volunteers after 1 h incubation on fibronectin (p = 0.006). Additionally, focal adhesion kinase isolated from uninvolved psoriatic keratinocytes had a greater degree of tyrosine phosphorylation. Thus, the proliferative effect of fibronectin in combination with T cell lymphokines on psoriatic uninvolved basal keratinocyte progenitors may be due to abnormal in vivo integrin-driven focal adhesion kinase activity and downstream signaling.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据