Keratinocytes in human wounds express alpha v beta 6 integrin
Keratinocytes in human wounds express alpha v beta 6 integrin
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DOI：
10.1111/1523-1747.ep12327199
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发表时间：
1996-01-01
影响因子：
6.5
通讯作者：
Larjava, H
中科院分区：
文献类型：
--
作者：
Haapasalmi, K;Zhang, K;Larjava, H
整合素家族的细胞黏附受体在人体创面再上皮化过程中发挥着重要作用。我们以前已经证明，αv家族整合素的表达是在黏膜伤口的角质形成细胞中诱导的[1]。在目前的研究中，我们扩展了这些研究，以确定在人类伤口愈合过程中是否表达了αvβ6整合素。1-7天创面的粘膜和表皮组织切片用于整合素及其可能的配体的免疫定位。此外，利用新鲜分离的表皮角质形成细胞在体外研究整合素的表达。在黏膜和真皮伤口愈合过程中，整合素αvβ6的表达相对较晚。最大的表达出现在7天大的创面上皮片融合和肉芽组织存在。纤维连接蛋白和Tenascin是αvβ6整合素的可能配体，它们集中在表达该受体的基底上皮细胞的下方，且Tenascin的最大表达与αvβ6整合素的表达一致。新鲜分离的表皮角质形成细胞不表达αvβ6整合素，但传代培养后开始表达该整合素。我们的结果表明，在伤口愈合过程中，当上皮片融合时，角质形成细胞中诱导了αvβ6整合素的表达，这是一种可能与纤维连接蛋白和腱连接蛋白结合的整合素。
Cell adhesion receptors of the integrin family play a major role during re-epithelialization of human wounds. We have previously documented that the expression of alpha v family integrins is induced in keratinocytes of mucosal wounds [1]. In the present investigation, we extended these studies to determine whether alpha v beta 6 integrin is expressed during wound healing in humans. Mucosal and epidermal wound sections from 1- to 7-day-old wounds were used for immunolocalization of integrins and their putative ligands. In addition, freshly isolated epidermal keratinocytes were used to study integrin expression in vitro. Expression of alpha v beta 6 integrin appeared relatively late during mucosal and dermal wound healing. Maximal expression was seen in 7-day-old wounds in which epithelial sheets had fused and granulation tissue was present. Fibronectin and tenascin, both possible ligands for alpha v beta 6 integrin, were found concentrated underneath the basal epithelial cells expressing this receptor, and the maximal expression of tenascin coincided with that of alpha v beta 6 integrin. Freshly isolated epidermal keratinocytes did not stain for alpha v beta 6 integrin but began to express this integrin after subculturing. Our results suggest that the expression of alpha v beta 6 integrin, a putative binding integrin for fibronectin and tenascin, is induced in keratinocytes when epithelial sheets fuse during wound healing.