Trabelsi N, Greffard A, Pairon J C, Kheuang L, Bignon J, Jaurand M C, Pilatte Y
INSERM Unité 139, Faculté de médecine,8 rue Géneral Sarrail, 94010 Créteil Cedex, France.
Biochem Biophys Res Commun. 1998 Apr 7;245(1):240-5. doi: 10.1006/bbrc.1998.8405.
In this report, we show that enhanced shedding of CD44 might contribute to the down-regulation of this receptor observed after phagocytosis of MnO2 particles by PMA-differentiated U-937. The apparent Mr of the soluble CD44 detected in culture supernatants was slightly lower than that of the membrane form suggesting that shedding resulted from proteolytic cleavage. Increased shedding of CD44 was also noted with other mineral particles (chrysotile and DQ12) but to a lower extent whereas some (TiO2 and amosite) had no effect on this process. These results indicate that shedding enhancement was particle-specific rather than a general consequence of phagocytosis. The ability of the particles to enhance CD44 shedding was not directly dependent on their cytotoxic potency. Different patterns of reactivity were noted with CD11b, suggesting that the underlying mechanisms are specific.
在本报告中，我们表明，CD44脱落增强可能导致在用佛波酯（PMA）分化的U - 937吞噬二氧化锰颗粒后观察到的该受体下调。在培养上清液中检测到的可溶性CD44的表观分子量略低于膜形式，这表明脱落是由蛋白水解切割引起的。在用其他矿物颗粒（温石棉和DQ12）处理时也观察到CD44脱落增加，但程度较低，而一些颗粒（二氧化钛和铁石棉）对这一过程没有影响。这些结果表明，脱落增强是颗粒特异性的，而不是吞噬作用的普遍结果。颗粒增强CD44脱落的能力并不直接取决于它们的细胞毒性效力。用CD11b观察到不同的反应模式，表明潜在机制具有特异性。
