Edashige K, Watanabe Y, Sato E F, Takehara Y, Utsumi K
Institute for Laboratory Animals, Kochi Medical School, Japan.
Arch Biochem Biophys. 1993 May;302(2):343-7. doi: 10.1006/abbi.1993.1221.
Hypotonic shock enhanced both formyl-methionyl-leucyl-phenylalanine (FMLP)-induced superoxide (O2-.) generation and tyrosyl phosphorylation of cellular proteins including 120-, 115-, 83-, 63-, and 54-kDa proteins of human peripheral neutrophils. The time course of the enhancement correlated with that of tyrosyl phosphorylation of the 115-kDa protein. The "primed state" was reversed to the nonprimed resting state by changing the conditions from hypotonic to isotonic, with a concomitant decrease in tyrosyl phosphorylation. Genistein inhibited the increase in both O2-. generation and tyrosyl phosphorylation of the 120-, 115-, 63-, and 54-kDa proteins. These results suggest the involvement of tyrosyl phosphorylation of a cellular protein(s) in hypotonic shock-induced priming of neutrophils.
低渗休克增强了甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）诱导的超氧阴离子（O2-.）生成以及包括人外周血中性粒细胞120、115、83、63和54 kDa蛋白质在内的细胞蛋白质的酪氨酸磷酸化。增强的时间进程与115 kDa蛋白质的酪氨酸磷酸化时间进程相关。通过将条件从低渗变为等渗，“预激状态”恢复到未预激的静息状态，同时酪氨酸磷酸化减少。染料木黄酮抑制了120、115、63和54 kDa蛋白质的O2-.生成增加以及酪氨酸磷酸化。这些结果表明细胞蛋白质的酪氨酸磷酸化参与了低渗休克诱导的中性粒细胞预激。
