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Review
. 2015 Jul:269:169-87.
doi: 10.1016/j.expneurol.2015.04.006. Epub 2015 Apr 18.

Chondroitin sulfate proteoglycans: Key modulators in the developing and pathologic central nervous system

Scott M Dyck  1 , Soheila Karimi-Abdolrezaee  2
Affiliations
Review

Chondroitin sulfate proteoglycans: Key modulators in the developing and pathologic central nervous system

Scott M Dyck et al. Exp Neurol. 2015 Jul.

Abstract

Chondroitin Sulfate Proteoglycans (CSPGs) are a major component of the extracellular matrix in the central nervous system (CNS) and play critical role in the development and pathophysiology of the brain and spinal cord. Developmentally, CSPGs provide guidance cues for growth cones and contribute to the formation of neuronal boundaries in the developing CNS. Their presence in perineuronal nets plays a crucial role in the maturation of synapses and closure of critical periods by limiting synaptic plasticity. Following injury to the CNS, CSPGs are dramatically upregulated by reactive glia which form a glial scar around the lesion site. Increased level of CSPGs is a hallmark of all CNS injuries and has been shown to limit axonal plasticity, regeneration, remyelination, and conduction after injury. Additionally, CSPGs create a non-permissive milieu for cell replacement activities by limiting cell migration, survival and differentiation. Mounting evidence is currently shedding light on the potential benefits of manipulating CSPGs in combination with other therapeutic strategies to promote spinal cord repair and regeneration. Moreover, the recent discovery of multiple receptors for CSPGs provides new therapeutic targets for targeted interventions in blocking the inhibitory properties of CSPGs following injury. Here, we will provide an in depth discussion on the impact of CSPGs in normal and pathological CNS. We will also review the recent preclinical therapies that have been developed to target CSPGs in the injured CNS.

Keywords: Axonal regeneration; Central; Chondroitin sulfate proteoglycans; Development; Extracellular matrix; Glial scar; Intacellular mechanisms; LAR; Multiple sclerosis; Nervous system; PTPσ; Plasticity; Spinal cord injury.

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