作者: Ira Wong , Hong Liao , Xianshu Bai , Antony Zaknic , Jinhua Zhong
DOI: 10.1016/J.BBI.2010.01.001
关键词: Central nervous system 、 Cord 、 Cell biology 、 Inflammation 、 Integrin alpha M 、 Spinal cord 、 Wallerian degeneration 、 Spinal cord injury 、 Immunology 、 Medicine 、 Myelin
摘要: The central nervous system (CNS) does not regenerate partly due to the slow clearance of debris from degenerated myelin sheath by Wallerian degeneration. mechanism underlying inefficiency in is clear. Here we showed that endogenous proBDNF may inhibit infiltration ED1+ inflammatory cells after spinal cord injury. After injury, and its receptors sortilin p75NTR are expressed as determined Western blots immunocytochemistry. ProBDNF mature BDNF were released macrophages vitro. Macrophages vivo (ED1+) isolated vitro (CD11b+) express moderate levels proBDNF, p75NTR. suppressed migration antibody enhanced migration. Suppression administering antiserum prodomain injury (SCI) increased number neurons injured cord. BBB tests treatment improved functional recovery Our data suggest a suppressing factor for macrophage play detrimental role SCI.