Destruction of extracellular matrix proteoglycans is pervasive in simian retroviral neuroinfection

Medina‐Flores, Rafael; Wang, Guoji; Bissel, Stephanie J.; Murphey‐Corb, Michael; Wiley, Clayton A.

doi:10.1016/j.nbd.2004.04.011

Cited by 29 publications

(19 citation statements)

References 91 publications

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“…The main agents of this remodeling process are three families of metalloproteases collectively known as metzincin family, i.e. ‘matrix metalloproteases’ (MMPs), ‘a disintegrin and matrix metalloproteases’ (ADAMS), and ‘ADAMS with a thrombospondin domain’ (ADAMTS), which cleave ECM molecules, including those that compose PNNs (Fig.2) (Abdolmaleky et al, 2005b; Hobohm et al, 2005; Medina-Flores et al, 2004; Muir et al, 2002; Rivera et al, 2010). For instance, ADAMTSs are known to cleave multiple PNN components including the CSPGs aggrecan, brevican, neurocan, versican, and phosphacan (Fig.…”

Section: Potential Causes Of Pnn Abnormalitiesmentioning

confidence: 99%

“…Thus, expression of several metalloproteases may be altered in subjects with SZ as a result of genetic predisposition. Second, PNN integrity and expression of metalloproteases are markedly affected by stress and immune responses (Fillman et al, 2014; Franklin et al, 2008; Gray et al, 2008; Medina-Flores et al, 2004). These responses have been linked to the pathogenesis of SZ, with a very recent study pointing to a genetic contribution to immune factors involvement (Arion et al, 2007; Fillman et al, 2013; Horvath and Mirnics, 2014; Ripke and Schizophrenia Working Group of the Psychiatric Genomics, 2014; Saetre et al, 2007; Smith et al, 2007).…”

Section: Potential Causes Of Pnn Abnormalitiesmentioning

confidence: 99%

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Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia

Berretta

Pantazopoulos

Markota

et al. 2015

Schizophrenia Research

131

119

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Perineuronal nets (PNNs) were shown to be markedly altered in subjects with schizophrenia. In particular, decreases of PNNs have been detected in the amygdala, entorhinal cortex and prefrontal cortex. The formation of these specialized extracellular matrix (ECM) aggregates during postnatal development, their functions and association with distinct populations of GABAergic interneurons, bear great relevance to the pathophysiology of schizophrenia. PNNs gradually mature in an experience-dependent manner during late stages of postnatal development, overlapping with the prodromal period/age of onset of schizophrenia. Throughout adulthood, PNNs regulate neuronal properties, including synaptic remodeling, cell membrane compartmentalization and subsequent regulation of glutamate receptors and calcium channels, and susceptibility to oxidative stress. With the present paper, we discuss evidence for PNN abnormalities in schizophrenia, the potential functional impact of such abnormalities on inhibitory circuits and, in turn, cognitive and emotion processing. We integrate these considerations with results from recent genetic studies showing genetic susceptibility for schizophrenia associated with genes encoding for PNN components, matrix-regulating molecules and immune system factors. Notably, the composition of PNNs is regulated dynamically in response to factors such as fear, reward, stress, and immune response. This regulation occurs through families of matrix metalloproteinases that cleave ECM components, altering their functions and affecting plasticity. Several metalloproteinases have been proposed as vulnerability factors for schizophrenia. We speculate that the physiological process of PNN remodeling may be disrupted in schizophrenia as a result of interactions between matrix remodeling processes and immune system dysregulation. In turn, these mechanisms may contribute to dysfunction of GABAergic neurons.

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Section: Potential Causes Of Pnn Abnormalitiesmentioning

confidence: 99%

Section: Potential Causes Of Pnn Abnormalitiesmentioning

confidence: 99%

Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia

Berretta

Pantazopoulos

Markota

et al. 2015

Schizophrenia Research

131

119

View full text Add to dashboard Cite

show abstract

“…Proteolysis of proteoglycans by ADAMTS enzymes can have destructive effects, producing matrices with disrupted cell-matrix communication, matrices with impaired fibrillary networks, or matrices with altered biomechanical properties [11]. After numerous comprehensive studies, ADAMTS expression has been found in the CNS [49][50][51][52][53][54][55][56][57][58][59][60] and is known to be changed in disease conditions [44,51,53].…”

Section: The Proposed Functions Of Adamts In Cnsmentioning

confidence: 99%

Pathophysiological Function of ADAMTS Enzymes on Molecular Mechanism of Alzheimer’s Disease

Gürses¹,

Ural²,

Güleç³

et al. 2016

Aging and disease

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The extracellular matrix (ECM) is an environment that has various enzymes attended in regeneration and restoration processes which is very important to sustain physiological and biological functions of central nervous system (CNS). One of the participating enzyme systems in ECM turnover is matrix metalloproteinases. A disintegrin-like and metalloproteinase with thrombospondin type 1 motifs (ADAMTS) is a unique family of ECM proteases found in mammals.Components of this family may be distinguished from the ADAM (A Disintegrin and Metalloproteinase) family based on the multiple copies of thrombospondin 1-like repeats. The considerable role of the ADAMTS in the CNS continues to develop. Evidences indicate that ADAMTS play an important role in neuroplasticity as well as nervous system pathologies such as Alzheimer's disease (AD). It is hopeful and possible that ADAMTS family members may be utilized to develop therapies for CNS pathologies, ischemic injuries, neurodegenerative and neurological diseases. To understand and provide definitive data on ADAMTS to improve structural and functional recovery in CNS injury and diseases, this review aimed to enlighten the subject extensively to reach certain information on metalloproteinases and related molecules/enzymes. It will be interesting to examine how ADAMTS expression and action would affect the initiation/progression of above-mentioned clinical situations, especially AD.

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“…One possible mechanism of neurodegeneration is that the neuroinflammatory cascade initiated by infiltrating monocytes disrupts the neuronal extracellular matrix (ECM) that normally provides physical support as well as a repository of growth and survival factors. 4 To elucidate mechanisms leading to neurodegeneration in lentiviral encephalitis, we used mass spectrometrybased proteomics to identify proteins that are differentially expressed in the cerebrospinal fluid (CSF) of simian immunodeficiency virus (SIV)-infected macaques that do or do not develop encephalitis. Among the proteins that showed differential up-regulation in the CSF of SIVE cases was YKL-40.…”

Section: Human Immunodeficiency Virus (Hiv)-1-associated Dementia [Acmentioning

confidence: 99%

YKL-40, a Marker of Simian Immunodeficiency Virus Encephalitis, Modulates the Biological Activity of Basic Fibroblast Growth Factor

Bonneh‐Barkay

Bissel

Wang

et al. 2008

The American Journal of Pathology

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120

100

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Destruction of extracellular matrix proteoglycans is pervasive in simian retroviral neuroinfection

Cited by 29 publications

References 91 publications

Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia

Losing the sugar coating: Potential impact of perineuronal net abnormalities on interneurons in schizophrenia

Pathophysiological Function of ADAMTS Enzymes on Molecular Mechanism of Alzheimer’s Disease

YKL-40, a Marker of Simian Immunodeficiency Virus Encephalitis, Modulates the Biological Activity of Basic Fibroblast Growth Factor

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