Susaki Y, Tanaka A, Honda E, Matsuda H
Department of Veterinary Clinic, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Japan.
J Vet Med Sci. 1998 Jan;60(1):87-91. doi: 10.1292/jvms.60.87.
We assessed the effect of nerve growth factor (NGF) on Fcgamma receptor (FcgammaR) expression on murine monocyte-macrophage J774A.1 cells. Flow cytometric analysis showed that treatment with various doses of NGF led to a rapid increase of FcgammaRI and FcgammaRII/III expression in a dose-dependent manner. Northern blot analysis with digoxigenin-labeled oligonucleotide probes demonstrated that NGF induced a marked increase in mRNA synthesis of FcgammaRI and FcgammaRII, but not FcgammaRIII. Since pretreatment with K-252a, a tyrosine kinase inhibitor, inhibited the stimulatory effect of NGF completely, the FcgammaR expression augmented by NGF may be mediated through p140trk with a tyrosine kinase domain. These results suggest that NGF may be a novel cytokine that is able to increase FcgammaRI and FcgammaRII expression on macrophages.
我们评估了神经生长因子（NGF）对小鼠单核巨噬细胞J774A.1细胞上Fcγ受体（FcγR）表达的影响。流式细胞术分析表明，用不同剂量的NGF处理会导致FcγRI和FcγRII/III表达以剂量依赖方式迅速增加。用地高辛标记的寡核苷酸探针进行的Northern印迹分析表明，NGF可诱导FcγRI和FcγRII的mRNA合成显著增加，但不能诱导FcγRIII的mRNA合成增加。由于用酪氨酸激酶抑制剂K-252a预处理可完全抑制NGF的刺激作用，因此NGF增强的FcγR表达可能是通过具有酪氨酸激酶结构域的p140trk介导的。这些结果表明，NGF可能是一种新型细胞因子，能够增加巨噬细胞上FcγRI和FcγRII的表达。
