Changes in cell spreading and cytoskeletal organization are induced by adhesion to a fibronectin-fibrin matrix.
Changes in cell spreading and cytoskeletal organization are induced by adhesion to a fibronectin-fibrin matrix.
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DOI：
10.1182/blood.v88.1.158.bloodjournal881158
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发表时间：
1996-07
期刊：
影响因子：
20.3
通讯作者：
S. Corbett;C. Wilson;J. Schwarzbauer
中科院分区：
文献类型：
--
作者：
S. Corbett;C. Wilson;J. Schwarzbauer
在损伤反应期间与纤维蛋白交联的血浆纤连蛋白（pFN）提供细胞开始组织修复所需的临时基质。使用合成基质的pFN和纤维蛋白作为细胞粘附和扩散的基板，我们已经确定，pFN共价交联到纤维蛋白成一个复杂的多聚体是从固定到塑料表面上的pFN功能不同。在FN-纤维蛋白基质上的NIH-3 T3细胞达到在FN涂覆的塑料上铺展的细胞的最大细胞面积的50%。它们既不附着也不扩散在单独的交联纤维蛋白上。pFN-纤维蛋白基质上的细胞形成几个突出的应力纤维，并且当用罗丹明标记的鬼笔环肽染色时，在膜皱褶和丝状伪足延伸方面表现出明显的差异。有趣的是，这些差异通过蛋白激酶C的上调而增强。这些数据表明，细胞-FN相互作用可以通过细胞外基质内蛋白质的分子背景进行修饰，从而导致不同的细胞形态和细胞骨架组织。
Plasma fibronectin (pFN) cross-linked to fibrin during the injury response provides a provisional matrix required for cells to begin tissue repair. Using a synthetic matrix of pFN and fibrin as a substrate for cell adhesion and spreading, we have determined that pFN covalently cross-linked to fibrin into a complex multimer is functionally distinct from pFN immobilized onto a plastic surface. NIH-3T3 cells on a FN-fibrin matrix reach 50% of the maximal cell area of cells spread on FN-coated plastic. They neither attach nor spread on cross-linked fibrin alone. Cells on pFN-fibrin matrices form few prominent stress fibers and exhibit clear differences in membrane ruffling and filopodial extension when stained with rhodamine-labeled phalloidin. Interestingly, these differences are enhanced by upregulation of protein kinase C. These data suggest that cell-FN interactions can be modified by the molecular context of the protein within the extracellular matrix resulting in distinct cell morphology and cytoskeletal organization.