βig-h3 supports keratinocyte adhesion, migration, and proliferation through α3β1 integrin
βig-h3 supports keratinocyte adhesion, migration, and proliferation through α3β1 integrin
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DOI：
10.1016/s0006-291x(02)00576-4
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发表时间：
2002-06-28
影响因子：
3.1
通讯作者：
Kim, IS
中科院分区：
文献类型：
--
作者：
Bae, JS;Lee, SH;Kim, IS
β ig-h3是一种细胞外基质蛋白，其表达受TGF-β高度诱导，并且还被认为在皮肤伤口愈合中发挥重要作用。在本文中，我们证明了β ig-h3存在于真皮的乳头层中，并在体内在基底角质形成细胞中合成，并且其表达由正常人角质形成细胞（NHEK）和HaCaT细胞中的TGF-β诱导。β IG-H3不仅介导角质形成细胞的粘附和铺展，而且支持迁移和增殖。这些活性通过与α 3 β 1整联蛋白相互作用介导。先前鉴定的β ig-M的两个α 3 β 1整合素相互作用基序EPDIM和NKDIL负责这些活动。结果表明，betaig-h3可以调节正常皮肤中角质形成细胞的功能，并可能在伤口愈合过程中。(C)2002 Elsevier Science（美国）。All rights reserved.
betaig-h3 is an extracellular matrix protein and its expression is highly induced by TGF-beta and it has also been suggested to play important roles in skin wound healing. In this paper, we demonstrate that betaig-h3 is present in the papillary layer of dermis and synthesized in the basal keratinocytes in vivo and its expression is induced by TGF-beta in normal human keratinocytes (NHEK) and HaCaT cells. betaig-h3 mediates not only adhesion and spreading of keratinocytes but also supports migration and proliferation. These activities are mediated through interacting with alpha3beta1 integrin. Previously identified two alpha3beta1 integrin-interacting motifs of betaig-M, EPDIM, and NKDIL, are responsible for these activities. The results suggest that betaig-h3 may regulate keratinocyte functions in normal skin and potentially during wound-healing process. (C) 2002 Elsevier Science (USA). All rights reserved.