PirB is a novel potential therapeutic target for enhancing axonal regeneration and synaptic plasticity following CNS injury in mammals. (June 2014)

• Record Type: Journal Article
• Authors: Gou, Zhaoyu; Mi, Yajing; Jiang, Fengliang; Deng, Bin; Yang, Jun; Gou, Xingchun
• Is Part Of: Journal of drug targeting. Volume 22:Number 5(2014)
• Page Start: 365
• Page End: 371
• Publication Date: 2014-06
• Subjects: Drug delivery systems -- Periodicals; Drug Delivery Systems; Vehicles; Drug Administration Routes; Drug Evaluation; 615.7
• DOI: 10.3109/1061186X.2013.878939
• Languages: English
• ISSNs: 1061-186X

Abstract

<abstract> <title>Abstract</title> <p>A major barrier to axonal regeneration in mammals is the unfavorable extracellular environment that develops following injury to the central nervous system (CNS). In particular, three myelin-associated inhibitory proteins (MAIs) – Nogo, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp) – are known to inhibit axonal regeneration and functional recovery. These MAIs share a common receptor, glycosylphosphatidylinositol-anchored Nogo receptor (NgR). However, paired immunoglobulin-like receptor B (PirB) – which was originally identified as a receptor for class I major histocompatibility complex (MHCI) in the immune system – is also expressed in neurones and plays a similarly inhibitory role in axonal regeneration and synaptic plasticity following CNS injury through its association with MAIs. Importantly, suppression of PirB activity through antibody antagonism or genetic means can partially relieve the inhibition of neurite outgrowth <italic>in vitro</italic> and <italic>in vivo</italic>. In this review, we present the molecular features, expression patterns and known signaling pathways of PirB, and we specifically focus on putative roles for PirB in the CNS and its potential as a target of molecular therapies for enhancing axonal regeneration and synaptic plasticity following CNS injury.</p> </abstract>