Department of Neurology at Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Neurology at Johns Hopkins University School of Medicine, Baltimore, MD, USA.
J Neuroimmunol. 2020 Dec 15;349:577423. doi: 10.1016/j.jneuroim.2020.577423. Epub 2020 Oct 6.
Following peripheral nerve injury, macrophages are recruited to the injury site from circulation to clear cellular debris. Injured β-secretase 1 (BACE1) knockout mice have enhanced macrophage recruitment and debris clearance, which may be due to BACE1 activity in macrophages or the hypomyelination observed in BACE1 knockout mice. To assess if BACE1 expression by macrophages mediates enhanced macrophage recruitment we utilized mice with macrophage specific deletion of BACE1 and saw no increase in macrophage recruitment following injury. This study suggests that expression of BACE1 by macrophages may not be essential for increased recruitment observed previously in global BACE1 KO mice.
在外周神经损伤后，巨噬细胞从循环中募集到损伤部位，以清除细胞碎片。受伤的β-分泌酶 1（BACE1）基因敲除小鼠有增强的巨噬细胞募集和碎片清除，这可能是由于巨噬细胞中的 BACE1 活性或 BACE1 基因敲除小鼠中观察到的少突胶质细胞形成不良。为了评估巨噬细胞中的 BACE1 表达是否介导了增强的巨噬细胞募集，我们利用巨噬细胞特异性敲除 BACE1 的小鼠，在损伤后没有观察到巨噬细胞募集的增加。这项研究表明，巨噬细胞中 BACE1 的表达对于先前在全局 BACE1 KO 小鼠中观察到的增强的募集可能不是必需的。
