• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>PLoS Clinical Trials >Fibroin and Sericin from Bombyx mori Silk Stimulate Cell Migration through Upregulation and Phosphorylation of c-Jun
【2h】

Fibroin and Sericin from Bombyx mori Silk Stimulate Cell Migration through Upregulation and Phosphorylation of c-Jun

机译：家蚕丝素中的丝素和丝胶蛋白通过c-Jun的上调和磷酸化刺激细胞迁移

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Wound healing is a biological process directed to the restoration of tissue that has suffered an injury. An important phase of wound healing is the generation of a basal epithelium able to wholly replace the epidermis of the wound. A broad range of products derived from fibroin and sericin from Bombyx mori silk are used to stimulate wound healing. However, so far the molecular mechanism underlying this phenomenon has not been elucidated. The aim of this work was to determine the molecular basis underlying wound healing properties of silk proteins using a cell model. For this purpose, we assayed fibroin and sericin in a wound healing scratch assay using MDA-MB-231 and Mv1Lu cells. Both proteins stimulated cell migration. Furthermore, treatment with sericin and fibroin involved key factors of the wound healing process such as upregulation of c-Jun and c-Jun protein phosphorylation. Moreover, fibroin and sericin stimulated the phosphorylation of ERK 1/2 and JNK 1/2 kinases. All these experiments were done in the presence of specific inhibitors for some of the cell signalling pathways referred above. The obtained results revealed that MEK, JNK and PI3K pathways are involved in fibroin and sericin stimulated cells migration. Inhibition of these three kinases prevented c-Jun upregulation and phosphorylation by fibroin or sericin. Fibroin and sericin were tested in the human keratinocyte cell line, HaCaT, with similar results. Altogether, our results showed that fibroin and sericin initiate cell migration by activating the MEK, JNK and PI3K signalling pathways ending in c-Jun activation.
机译：伤口愈合是针对遭受损伤的组织进行恢复的生物学过程。伤口愈合的重要阶段是基底上皮的产生，该基底上皮能够完全替代伤口的表皮。广泛使用家蚕丝素和丝胶蛋白衍生的产品来刺激伤口愈合。但是，到目前为止，尚未阐明这种现象的分子机制。这项工作的目的是使用细胞模型确定丝蛋白伤口愈合特性的分子基础。为此，我们使用MDA-MB-231和Mv1Lu细胞在伤口愈合刮擦试验中测定了纤维蛋白和丝胶蛋白。两种蛋白质均刺激细胞迁移。此外，使用丝胶和丝蛋白治疗涉及伤口愈合过程的关键因素，例如c-Jun和c-Jun蛋白磷酸化的上调。此外，纤维蛋白和丝胶蛋白刺激ERK 1/2和JNK 1/2激酶的磷酸化。所有这些实验均在针对上述某些细胞信号通路的特异性抑制剂存在下完成。获得的结果表明，MEK，JNK和PI3K途径与丝心蛋白和丝胶蛋白刺激的细胞迁移有关。对这三种激酶的抑制作用可阻止c-Jun上调和丝蛋白或丝胶蛋白的磷酸化。在人角质形成细胞HaCaT中测试了丝蛋白和丝胶蛋白，结果相似。总而言之，我们的结果表明纤维蛋白和丝胶蛋白通过激活以c-Jun激活终止的MEK，JNK和PI3K信号通路来启动细胞迁移。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号