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Macrophage-specific deletion of BACE1 does not enhance macrophage recruitment to the injured peripheral nerve
Journal of Neuroimmunology ( IF 2.9 ) Pub Date : 2020-12-01 , DOI: 10.1016/j.jneuroim.2020.577423
John Fissel , Mohamed H. Farah

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.

中文翻译:

BACE1 的巨噬细胞特异性缺失不会增强巨噬细胞向受损周围神经的募集

周围神经损伤后,巨噬细胞从循环中被募集到损伤部位以清除细胞碎片。受伤的 β-分泌酶 1 (BACE1) 敲除小鼠的巨噬细胞募集和碎片清除增强,这可能是由于巨噬细胞中的 BACE1 活性或在 BACE1 敲除小鼠中观察到的髓鞘形成不足所致。为了评估巨噬细胞的 BACE1 表达是否介导了增强的巨噬细胞募集,我们使用了巨噬细胞特异性 BACE1 缺失的小鼠,并且在损伤后没有发现巨噬细胞募集的增加。这项研究表明,巨噬细胞对 BACE1 的表达可能不是先前在全球 BACE1 KO 小鼠中观察到的募集增加所必需的。
更新日期:2020-12-01
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