Chandrasekhar S, Millis A J
J Cell Physiol. 1980 Apr;103(1):47-54. doi: 10.1002/jcp.1041030108.
Late passage fibroblasts show decreased cell-substrate adhesion. We provide evidence that the reduced adhesion is due to a defect in the adhesive glycoprotein fibronectin. Late passage cells become more adhesive in culture media that has been conditioned by the growth of early passage cells. Analysis of fibronectins purifed from early and late passage cell conditioned media indicates that there are striking differences in their abilities to promote cell adhesion. Young cell fibronectin supports the maximal adhesion of both young and old cells. However, old cells require quantitatively more fibronectin. In contrast, old cell fibronectin is less effective in supporting the adhesion of either cell type. In addition, neither cell type achieves a normal morphology in the presence of old cell fibronectin. The results support the conclusion that the fibronectin released by late passage cells i defective and does not support normal cell-substrate interactions.
传代后期的成纤维细胞显示出细胞与底物的粘附力下降。我们提供的证据表明，粘附力降低是由于粘附糖蛋白纤连蛋白存在缺陷所致。传代后期的细胞在由传代早期细胞生长所调节的培养基中会变得更具粘附性。对从传代早期和传代后期细胞条件培养基中纯化的纤连蛋白进行分析表明，它们促进细胞粘附的能力存在显著差异。年轻细胞的纤连蛋白支持年轻细胞和年老细胞的最大粘附。然而，年老细胞需要定量更多的纤连蛋白。相比之下，年老细胞的纤连蛋白在支持任何一种细胞类型的粘附方面效果较差。此外，在存在年老细胞纤连蛋白的情况下，两种细胞类型均无法实现正常形态。这些结果支持以下结论：传代后期细胞释放的纤连蛋白存在缺陷，无法支持正常的细胞与底物相互作用。
