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首页> 外文期刊>Cell motility and the cytoskeleton >Keratinocyte motility induced by TGF-beta1 is accompanied by dramatic changes in cellular interactions with laminin 5.
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Keratinocyte motility induced by TGF-beta1 is accompanied by dramatic changes in cellular interactions with laminin 5.

机译：TGF-β1诱导的角质形成细胞运动伴随着层粘连蛋白5细胞相互作用的剧烈变化。

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Transforming growth factor-beta1 (TGF-beta1) has the ability to induce epithelial cell migration while stopping proliferation. In this study, we show that, concomitant to promoting migration of normal human keratinocytes in vitro, TGF-beta1 induced a marked decrease in their adhesion capacity to processed alpha3-containing laminin 5-coated surfaces. Indeed, the expression levels of alpha3 and alpha6 integrin subunit mRNA and protein, as well as the cell surface alpha3beta1 and alpha6beta4 integrins, were down-regulated. Recent studies showed that keratinocytes over express and deposit laminin 5 during migration and we have shown that laminin 5 found in the matrix of TGF-beta1 induced migrating keratinocytes is present in its unprocessed form [Decline and Rousselle, 2001: J. Cell Sci. 114:811-823]. We show here that TGF-beta1 treatment of the cells promoted a significant increase in their adhesion to the alpha3 chain carboxy-terminal LG4/5 subdomain and that this interaction is likely to be mediated by a heparan sulfate proteoglycan type of receptor. Our results indicate that alpha6beta4 and alpha3beta1 integrin interactions with laminin 5 are diminished during migration while a specific interaction occurs between an additional cellular receptor and the alpha3 LG4/5 module present on unprocessed laminin 5.
机译：转化生长因子-beta1（TGF-beta1）具有诱导上皮细胞迁移同时停止增殖的能力。在这项研究中，我们表明，伴随促进体外正常人角质形成细胞的迁移，TGF-β1诱导了它们对已加工的含alpha3层粘连蛋白5涂层表面的粘附能力显着降低。实际上，α3和α6整联蛋白亚基mRNA和蛋白的表达水平以及细胞表面α3beta1和α6beta4整联蛋白的表达水平均被下调。最近的研究表明，角质形成细胞在迁移过程中过度表达和沉积层粘连蛋白5，并且我们已经发现，在TGF-β1诱导的迁移角质形成细胞的基质中发现的层粘连蛋白5以其未加工的形式存在[Decline and Rousselle，2001：J. 114：811-823]。我们在这里显示细胞的TGF-β1处理促进了它们对α3链羧基末端LG4 / 5子结构域的粘附力的显着增加，并且这种相互作用很可能是由硫酸乙酰肝素蛋白聚糖类型的受体介导的。我们的结果表明，在迁移过程中，与层粘连蛋白5的alpha6beta4和alpha3beta1整联蛋白的相互作用被减少，而在未处理的层粘连蛋白5上存在的其他细胞受体和alpha3 LG4 / 5模块之间发生了特定的相互作用。

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