Fukasawa M, Sekine F, Miura M, Nishijima M, Hanada K
Department of Biochemistry and Cell Biology, National Institute of Health, Shinjuku-ku, Tokyo, Japan.
Exp Cell Res. 1997 Jan 10;230(1):154-62. doi: 10.1006/excr.1996.3403.
Chinese hamster ovary (CHO) K1 cells, typical nonprofessional phagocytes, exhibited intense phagocytosis of latex beads when incubated under serum-free conditions. Under the serum-free conditions, the recognition mechanism of latex beads by cells was investigated. Exogenous heparin and heparan sulfate but not chondroitin sulfate effectively inhibited the binding of latex beads to cells. The binding of latex beads to cells was also inhibited by treatment of cells with heparitinase more effectively than by treatment of cells with chondroitinase. Furthermore, CHO mutant cells defective in biosyntheses of both heparan sulfate and chondroitin sulfate proteoglycans almost completely lacked binding activity of latex beads. Another mutant, which is deficient in heparan sulfate proteoglycans but rather overproduces chondroitin sulfate proteoglycans, also showed lower binding activity, compared with wild-type cells. Coculture of these proteoglycan-less mutants and the wild-type cells did not restore the binding activity of the mutant cells, suggesting that membrane-bound rather than secretory proteoglycans were responsible for the binding of latex beads. These results indicated that heparan sulfate proteoglycans at the cell surface were involved in the binding step for phagocytosis of latex beads by CHO cells.
中国仓鼠卵巢（CHO）K1细胞是典型的非专职吞噬细胞，在无血清条件下孵育时，对乳胶珠表现出强烈的吞噬作用。在无血清条件下，研究了细胞对乳胶珠的识别机制。外源性肝素和硫酸乙酰肝素而非硫酸软骨素能有效抑制乳胶珠与细胞的结合。用肝素酶处理细胞比用软骨素酶处理细胞更有效地抑制乳胶珠与细胞的结合。此外，硫酸乙酰肝素和硫酸软骨素蛋白聚糖生物合成均有缺陷的CHO突变细胞几乎完全缺乏乳胶珠的结合活性。另一种突变体缺乏硫酸乙酰肝素蛋白聚糖，但硫酸软骨素蛋白聚糖产生过多，与野生型细胞相比，其结合活性也较低。这些蛋白聚糖缺失突变体与野生型细胞共培养并不能恢复突变体细胞的结合活性，这表明膜结合而非分泌型蛋白聚糖负责乳胶珠的结合。这些结果表明，细胞表面的硫酸乙酰肝素蛋白聚糖参与了CHO细胞吞噬乳胶珠的结合步骤。
