• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Rat glomerular mesangial cells require laminin-9 to migrate in response to insulin-like growth factor binding protein-5.
【24h】

Rat glomerular mesangial cells require laminin-9 to migrate in response to insulin-like growth factor binding protein-5.

机译：大鼠肾小球系膜细胞需要层粘连蛋白9才能响应胰岛素样生长因子结合蛋白5迁移。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Temporal and spatial differences in extracellular matrix play critical roles in cell proliferation, differentiation and migration. Different migratory stimuli use different substrates and receptors to achieve cell migration. To understand the mechanism of insulin-like growth factor binding protein-5 (IGFBP-5)-induced migration in mesangial cells, the roles of integrins and substrates were examined. IGFBP-5 induced an increase in mRNA expression for laminin (LN) chains lama4, lamb2, and lamc1, suggesting that LN-9 might be required for migration. Antibodies to the LNalpha(4) and LNbeta(2) chains, but not LNbeta(1), blocked IGFBP-5-induced migration. Anti-sense morpholino oligonucleotide inhibition of expression of LNalpha(4) substantially reduced expression of LN-8/9 (alpha(4)beta(1)gamma(1)/alpha(4)beta(2)gamma(1), 411/421) and prevented IGFBP-5-induced migration. Anti-sense inhibition of lamb2 reduced expression of LN-9. Absence of LN-9 prevented IGFBP-5-induced migration, which was not preserved by continued expression of LN-8. The requirement for LN-9 was further supported by studies of T98G cells, which express predominantly LN-8. IGFBP-5 had little effect on migration in these cells, but increased migration when T98G cells were plated on LN-8/9. IGFBP-5-mediated mesangial cell migration was inhibited by antibodies that block attachment to alpha(6)beta(1)-integrins but was unaffected by antibodies and disintegrins that block binding to other integrins. Furthermore, in cells with anti-sense inhibited expression of LN-9, integrin alpha(6)beta(1) was no longer detected on the cell surface. These studies suggest the specificity of mechanisms of migration induced by specific stimuli and for the first time demonstrate a unique function for LN-9 in mediating IGFBP-5-induced migration.
机译：细胞外基质中的时空差异在细胞增殖，分化和迁移中起关键作用。不同的迁移刺激使用不同的底物和受体来实现细胞迁移。为了了解胰岛素样生长因子结合蛋白5（IGFBP-5）诱导的肾小球系膜细胞迁移的机制，检查了整合素和底物的作用。 IGFBP-5诱导层粘连蛋白（LN）链lama4，lamb2和lamc1的mRNA表达增加，这表明可能需要LN-9进行迁移。 LNalpha（4）和LNbeta（2）链，但不是LNbeta（1）的抗体阻止了IGFBP-5诱导的迁移。反义吗啉代寡核苷酸抑制LNalpha（4）的表达大大降低了LN-8 / 9的表达（alpha（4）beta（1）gamma（1）/ alpha（4）beta（2）gamma（1），411 / 421）并阻止了IGFBP-5诱导的迁移。反义抑制lamb2会降低LN-9的表达。 LN-9的缺乏阻止了IGFBP-5诱导的迁移，而LN-8的持续表达并不能保留这一迁移。对T98G细胞的研究进一步支持了对LN-9的需求，这些细胞主要表达LN-8。 IGFBP-5对这些细胞的迁移几乎没有影响，但是当将T98G细胞接种在LN-8 / 9上时迁移增加。 IGFBP-5介导的肾小球系膜细胞迁移受阻断与alpha（6）beta（1）-整联蛋白结合的抗体抑制，但不受阻断与其他整联蛋白结合的抗体和解整蛋白的影响。此外，在具有反义抑制LN-9表达的细胞中，在细胞表面不再检测到整联蛋白alpha（6）beta（1）。这些研究表明由特定刺激诱导的迁移机制的特异性，并首次证明LN-9在介导IGFBP-5诱导的迁移中具有独特的功能。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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