期刊
EXPERIMENTAL NEUROLOGY
卷 220, 期 2, 页码 320-327出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2009.09.007
关键词
DRG; Mouse; L-14.5; Macrophage; Rhizotomy
资金
- Michael Smith Foundation for Health Research (MSFHR)
- Natural Sciences and Engineering Research Council of Canada (NSERC)
Galectin-1 (Gal1) is a multi-functional protein that has key roles in organismal growth and survival. In the adult nervous system, Gal1 promotes axonal regeneration following peripheral nerve injury. Although the mechanism by which Gal1 promotes regeneration is unclear, previous reports suggested that Gal1 acts indirectly by activating macrophages. An appropriate response of macrophages is crucial for repair of injured nerves: these immune cells remove obstructive axon and myelin debris in the distal nerve. Here we establish a role for Gal1 in the accumulation of immune cells following peripheral axotomy. We used immunohistochemistry to visualize macrophages (F4/80) in wild-type (Lgals1(+/+)) and knockout (Lgals1(-/-)) mouse sciatic nerves following injury and/or manipulation of Gal1 levels. Density of F4/80 immunoreactivity, which peaks around 3 days post-injury, was decreased in Lgals1(+/+) nerves injected with Gal1 antibody. The typical injury-induced peak of macrophage/microglial density was delayed in the sciatic nerves and fifth lumbar dorsal root ganglia of Lgals1(-/-) mice relative to control mice. Injection of oxidized Gal1 into uninjured sciatic nerve promoted the accumulation of macrophages in Lgals1(+/+) nerves. Finally, we used transplants of sciatic nerve to uncover a compensatory mechanism in Lgals1(-/-) mice that allows for macrophage accumulation (albeit delayed and diminished) following axotomy. We conclude that Gal1 is necessary to direct the typical accumulation of macrophages in the injured peripheral nerve, and that Gal1 is sufficient to promote macrophage accumulation in the uninjured nerve of wild-type mice. (C) 2009 Published by Elsevier Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据