Asami Toshio, Ito Takuya, Fukumitsu Hidefumi, Nomoto Hiroshi, Furukawa Yoshiko, Furukawa Shoei
Laboratory of Molecular Biology, Gifu Pharmaceutical University, 5-6-1, Mitahora-Higashi, Gifu 502-8585, Japan.
Biochem Biophys Res Commun. 2006 Jun 9;344(3):941-7. doi: 10.1016/j.bbrc.2006.03.228. Epub 2006 Apr 19.
To elucidate a significance of the expression of brain-derived neurotrophic factor (BDNF) in the activated microglia/macrophages of the injured central nervous system, we examined BDNF actions on or BDNF synthesis by macrophages cultured from the mouse peritoneal cavity. They synthesized BDNF and neurotrophin-3 (NT-3) in addition to expressing high-affinity neurotrophin receptors, full-length TrkB (FL), truncated TrkB (TK(-)), and TrkC, thus suggesting an autocrine influence of BDNF and NT-3. BDNF, but not NT-3, enhanced phagocytic activity and stimulated synthesis/secretion of interleukin-1beta in the same manner as lipopolysaccharide (LPS). Furthermore, there was a significant correlation of the phagocytic activity with the expression of BDNF or TrkB (FL). These results imply that the phagocytic activity of macrophages depends on BDNF synthesis and/or TrkB (FL) expression, suggesting that BDNF participates in the activation processes of macrophages by acting in an autocrine manner.
为阐明脑源性神经营养因子(BDNF)在损伤的中枢神经系统激活的小胶质细胞/巨噬细胞中表达的意义,我们检测了BDNF对从小鼠腹腔培养的巨噬细胞的作用或BDNF的合成。它们除了表达高亲和力神经营养因子受体、全长TrkB(FL)、截短型TrkB(TK(-))和TrkC外,还合成BDNF和神经营养因子-3(NT-3),因此提示BDNF和NT-3的自分泌影响。BDNF而非NT-3,以与脂多糖(LPS)相同的方式增强吞噬活性并刺激白细胞介素-1β的合成/分泌。此外,吞噬活性与BDNF或TrkB(FL)的表达存在显著相关性。这些结果表明巨噬细胞的吞噬活性取决于BDNF合成和/或TrkB(FL)表达,提示BDNF通过自分泌作用参与巨噬细胞的激活过程。