Neural ECM proteases in learning and synaptic plasticity

Tsilibary, Effie C.; Τzinia, Athina K.; Radenović, Lidija; Stamenković, Vera; Lebitko, Tomasz; Mucha, Mariusz; Pawlak, Robert; Frischknecht, Renato; Kaczmarek, Leszek

doi:10.1016/b978-0-444-63486-3.00006-2

Cited by 72 publications

(62 citation statements)

References 149 publications

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“…It seems that further studies regarding the significance of hNP in the aetiology and course of rDD should be aimed at finding out their impact on the cognitive efficiency of the affected (Lu et al 2009, Tsilibary et al 2014) and on their emotional functioning (Horii et al (2008) found increased anxiety in neuropsin-deficient mice, suggesting the involvement of this protease in emotional responses).…”

Section: Discussionmentioning

confidence: 99%

Human Neuropsin Gene in Depression

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Human Neuropsin Gene in Depression

et al. 2017

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“…MMP-9 activity has also been reported to be an important factor that shapes synaptic plasticity at the physiological and morphological levels. 1,3,56 Numerous unbiased highthroughput approaches indicated the possible involvement of synaptic proteins, including neuroligins and neurexins, and their genes in schizophrenia. 43,[57][58][59] A transsynaptic link that involves neurexins and extends from the presynaptic side to neuroligin-1 or dystroglycan at the postsynaptic side can be broken after MMP-9-driven cleavage of each of these proteins, and such MMP-9 activity may affect synaptic efficacy.…”

Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9 as a Novel Player in Synaptic Plasticity and Schizophrenia: Table 1.

Lepeta¹,

Kaczmarek²

2015

SCHBUL

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Recent findings implicate alterations in glutamate signaling, leading to aberrant synaptic plasticity, in schizophrenia. Matrix metalloproteinase-9 (MMP-9) has been shown to regulate glutamate receptors, be regulated by glutamate at excitatory synapses, and modulate physiological and morphological synaptic plasticity. By means of functional gene polymorphism, gene responsiveness to antipsychotics and blood plasma levels MMP-9 has recently been implicated in schizophrenia. This commentary critically reviews these findings based on the hypothesis that MMP-9 contributes to pathological synaptic plasticity in schizophrenia.Key words: synaptic plasticity/glutamate/extracellular matrix Matrix Metalloproteinase-9 in Animal Studies Matrix Metalloproteinase-9 Expression and Activity in the BrainMatrix metalloproteinase-9 (MMP-9) belongs to a family of zinc-dependent proteases, mostly secreted as inactive pro-enzymes, activated outside the cell upon proteolytic cleavage. MMPs degrade extracellular matrix constituents, other proteases, growth factors, and extracellular domains of transmembrane proteins, such as cell adhesion molecules and receptors. As a result, MMPs participate in remodeling the pericellular microenvironment and cell-signaling via either the release or processing (to reveal their binding domains) of cell-surface receptor ligands.

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“…Though, it is known that extracellular proteolysis provides an attractive mechanism controlling structural changes and neuronal plasticity in the brain, and products of protein limited digestion of extracellular matrix are believed to play a singificant role in CNS homeostasis and intercellular communications [32]. Among them, angiostatins are major endogenous angiogenesis inhibitors that are generated after serial enzymatic proteolysis of Pg/Pm by multiple enzymatic actions (MMPs, cathepsins, authoproteolysis of Pm) [6].…”

Section: Fig 2 Representative Fluorescence Micrographs Of Plasminogmentioning

confidence: 99%