McAbee D D, Grinnell F
J Cell Physiol. 1985 Aug;124(2):240-6. doi: 10.1002/jcp.1041240211.
Studies on the receptor specificity and dynamics involved in fibroblast phagocytosis of latex beads revealed the following: 1) Ligands other than fibronectin such as concanavalin A (ConA) and serum spreading factor, when coated on latex beads, were found to promote phagocytosis of the beads. This indicates that fibroblast phagocytosis, like spreading, is a ligand-receptor mediated phenomenon not specifically requiring fibronectin (pFN); 2) Anti-pFN antibodies were found to inhibit the ability of cells to ingest pFN-coated beads that previously were bound on the cell surfaces. Consequently, binding of beads to the cell surfaces per se is not a sufficient signal to promote ingestion of the beads; 3) Finally, divalent cations protected receptor function necessary for phagocytosis of pFN-coated beads from proteolysis by trypsin, as previously was found for receptors involved in cell attachment and spreading on pFN-coated culture dishes. Recovery experiments carried out with cells whose surface receptors had been destroyed indicated that there was an internal (or cryptic cell surface) pool of receptors that amounted to at least 50% of the receptors normally found on the cell surface. After complete destruction of the cell surface and cryptic pools of receptors, reappearance of receptors required for bead binding and phagocytosis required several hours and did not occur in the absence of new protein synthesis.
1)发现除纤连蛋白外的其他配体,如伴刀豆球蛋白A(ConA)和血清铺展因子,包被在乳胶珠上时可促进珠子的吞噬作用。这表明成纤维细胞吞噬作用,如同铺展一样,是一种配体 - 受体介导的现象,并非特别需要纤连蛋白(pFN);2)发现抗pFN抗体可抑制细胞摄取先前结合在细胞表面的pFN包被珠子的能力。因此,珠子与细胞表面的结合本身并非促进珠子摄取的充分信号;3)最后,二价阳离子可保护pFN包被珠子吞噬作用所需的受体功能免受胰蛋白酶的蛋白水解作用,正如先前在参与细胞在pFN包被培养皿上附着和铺展的受体中所发现的那样。对表面受体已被破坏的细胞进行的恢复实验表明,存在一个内部(或隐蔽细胞表面)受体池,其数量至少占细胞表面正常发现的受体的50%。在细胞表面和隐蔽受体池完全被破坏后,珠子结合和吞噬所需受体的重新出现需要数小时,并且在没有新蛋白质合成的情况下不会发生。