ProBDNF inhibits infiltration of ED1+macrophages after spinal cord injury

Ira Wong; Hong Liao; Xianshu Bai; Antony Zaknic; Jin Hua Zhong; Y Guan; Hong-Yun Li; Yan Jiang Wang; Xin-Fu Zhou

doi:10.1016/j.bbi.2010.01.001

ProBDNF inhibits infiltration of ED1+macrophages after spinal cord injury

Ira Wong, Hong Liao, Xianshu Bai, Antony Zaknic, Jin Hua Zhong, Y Guan, Hong-Yun Li, Yan Jiang Wang, Xin-Fu Zhou

Research output: Contribution to journal › Article › peer-review

46 Citations (Scopus)

Abstract

The central nervous system (CNS) does not regenerate partly due to the slow clearance of debris from the degenerated myelin sheath by Wallerian degeneration. The mechanism underlying the inefficiency in myelin clearance is not clear. Here we showed that endogenous proBDNF may inhibit the infiltration of ED1+ inflammatory cells after spinal cord injury. After injury, proBDNF and its receptors sortilin and p75NTR are expressed in the spinal cord as determined by Western blots and immunocytochemistry. ProBDNF and mature BDNF were released from macrophages in vitro. Macrophages in vivo (ED1+) and isolated in vitro (CD11b+) express moderate levels of proBDNF, sortilin and p75NTR. ProBDNF suppressed the migration of isolated macrophages in vitro and the antibody to proBDNF enhanced the migration. Suppression of proBDNF in vivo by administering the antiserum to the prodomain of BDNF after spinal cord injury (SCI) increased the infiltration of macrophages and increased number of neurons in the injured cord. BBB tests showed that the treatment of the antibody to proBDNF improved the functional recovery after spinal cord injury. Our data suggest that proBDNF is a suppressing factor for macrophage migration and infiltration and may play a detrimental role after SCI.

Original language	English
Pages (from-to)	585-597
Number of pages	13
Journal	Brain, Behavior, and Immunity
Volume	24
Issue number	4
DOIs	https://doi.org/10.1016/j.bbi.2010.01.001
Publication status	Published - May 2010

Keywords

Infiltration
Inflammation
Macrophages
ProBDNF
Spinal cord injury

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10.1016/j.bbi.2010.01.001

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title = "ProBDNF inhibits infiltration of ED1+macrophages after spinal cord injury",

abstract = "The central nervous system (CNS) does not regenerate partly due to the slow clearance of debris from the degenerated myelin sheath by Wallerian degeneration. The mechanism underlying the inefficiency in myelin clearance is not clear. Here we showed that endogenous proBDNF may inhibit the infiltration of ED1+ inflammatory cells after spinal cord injury. After injury, proBDNF and its receptors sortilin and p75NTR are expressed in the spinal cord as determined by Western blots and immunocytochemistry. ProBDNF and mature BDNF were released from macrophages in vitro. Macrophages in vivo (ED1+) and isolated in vitro (CD11b+) express moderate levels of proBDNF, sortilin and p75NTR. ProBDNF suppressed the migration of isolated macrophages in vitro and the antibody to proBDNF enhanced the migration. Suppression of proBDNF in vivo by administering the antiserum to the prodomain of BDNF after spinal cord injury (SCI) increased the infiltration of macrophages and increased number of neurons in the injured cord. BBB tests showed that the treatment of the antibody to proBDNF improved the functional recovery after spinal cord injury. Our data suggest that proBDNF is a suppressing factor for macrophage migration and infiltration and may play a detrimental role after SCI.",

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author = "Ira Wong and Hong Liao and Xianshu Bai and Antony Zaknic and Zhong, {Jin Hua} and Y Guan and Hong-Yun Li and Wang, {Yan Jiang} and Xin-Fu Zhou",

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AU - Wong, Ira

AU - Liao, Hong

AU - Bai, Xianshu

AU - Zaknic, Antony

AU - Zhong, Jin Hua

AU - Guan, Y

AU - Li, Hong-Yun

AU - Wang, Yan Jiang

AU - Zhou, Xin-Fu

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N2 - The central nervous system (CNS) does not regenerate partly due to the slow clearance of debris from the degenerated myelin sheath by Wallerian degeneration. The mechanism underlying the inefficiency in myelin clearance is not clear. Here we showed that endogenous proBDNF may inhibit the infiltration of ED1+ inflammatory cells after spinal cord injury. After injury, proBDNF and its receptors sortilin and p75NTR are expressed in the spinal cord as determined by Western blots and immunocytochemistry. ProBDNF and mature BDNF were released from macrophages in vitro. Macrophages in vivo (ED1+) and isolated in vitro (CD11b+) express moderate levels of proBDNF, sortilin and p75NTR. ProBDNF suppressed the migration of isolated macrophages in vitro and the antibody to proBDNF enhanced the migration. Suppression of proBDNF in vivo by administering the antiserum to the prodomain of BDNF after spinal cord injury (SCI) increased the infiltration of macrophages and increased number of neurons in the injured cord. BBB tests showed that the treatment of the antibody to proBDNF improved the functional recovery after spinal cord injury. Our data suggest that proBDNF is a suppressing factor for macrophage migration and infiltration and may play a detrimental role after SCI.

AB - The central nervous system (CNS) does not regenerate partly due to the slow clearance of debris from the degenerated myelin sheath by Wallerian degeneration. The mechanism underlying the inefficiency in myelin clearance is not clear. Here we showed that endogenous proBDNF may inhibit the infiltration of ED1+ inflammatory cells after spinal cord injury. After injury, proBDNF and its receptors sortilin and p75NTR are expressed in the spinal cord as determined by Western blots and immunocytochemistry. ProBDNF and mature BDNF were released from macrophages in vitro. Macrophages in vivo (ED1+) and isolated in vitro (CD11b+) express moderate levels of proBDNF, sortilin and p75NTR. ProBDNF suppressed the migration of isolated macrophages in vitro and the antibody to proBDNF enhanced the migration. Suppression of proBDNF in vivo by administering the antiserum to the prodomain of BDNF after spinal cord injury (SCI) increased the infiltration of macrophages and increased number of neurons in the injured cord. BBB tests showed that the treatment of the antibody to proBDNF improved the functional recovery after spinal cord injury. Our data suggest that proBDNF is a suppressing factor for macrophage migration and infiltration and may play a detrimental role after SCI.

KW - Infiltration

KW - Inflammation

KW - Macrophages

KW - ProBDNF

KW - Spinal cord injury

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ProBDNF inhibits infiltration of ED1+macrophages after spinal cord injury

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Keywords

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