Crosstalk between glia, extracellular matrix and neurons.

Abstract:

:Extracellular matrix (ECM) molecules in the central nervous system form highly organized ECM structures around cell somata, axon initial segments, and synapses and play prominent roles in early development by guiding cell migration, neurite outgrowth and synaptogenesis, and by regulating closure of the critical period of development, synaptic plasticity and stability, cognitive flexibility, and axonal regeneration in adults. Major components of neural ECM, including chondroitin sulfate proteoglycans (CSPGs), tenascin-R and hyaluronic acid, are synthesized by both neurons and glial cells. The expression of these molecules is dynamically regulated during brain development in physiological conditions, shaping both neuronal and glial functions through multitude of molecular mechanisms. Upregulation of particular CSPGs and other ECM molecules, in particular by reactive astrocytes, after CNS injuries, during aging, neuroinflammation, and neurodegeneration on the one hand results in formation of growth-impermissive environment and impaired synaptic plasticity. On the other hand, ECM appeared to have a neuroprotective effect, at least in the form of perineuronal nets. CSPGs-degrading matrix metalloproteinases (MMPs) and several members of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family of proteases are secreted by neurons and glia and may drive neural ECM remodeling in physiological conditions as well as after brain injury and other brain disorders. Thus, targeting expression of specific ECM molecules, associated glycans and degrading enzymes may lead to development of new therapeutic strategies promoting regeneration and synaptic plasticity.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Song I,Dityatev A

doi

10.1016/j.brainresbull.2017.03.003

subject

Has Abstract

pub_date

2018-01-01 00:00:00

pages

101-108

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(17)30135-1

journal_volume

136

pub_type

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