Semaphorin 3A Binds to the Perineuronal Nets via Chondroitin Sulfate Type E Motifs in Rodent Brains

Dick, Gunnar; Tan, Chin Lik; Alves, João Nuno; Ehlert, Erich; Miller, Gregory M.; Hsieh‐Wilson, Linda C.; Sugahara, Kazuyuki; Oosterhof, Arie; Kuppevelt, Toin H. Van; Verhaagen, Joost; Fawcett, James W.; Kwok, Jerry

doi:10.1074/jbc.m111.310029

Cited by 126 publications

(143 citation statements)

References 57 publications

(79 reference statements)

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“…Vo et al recently demonstrated that Sema3A colocalized with parvalbumin-positive perineuronal nets (PNNs), which are extracellular matrix structures that circumvent inhibitory interneurons, as well as with the CS-DS proteoglycans aggrecan, versican, phosphacan, and tenascin-R [33] (Figure 2), and strongly interacted with CS-DS chains specifically containing E-units [34 ]. The inhibition of neurite outgrowth of dorsal root ganglia by Sema3A was previously shown to be enhanced by the addition of glycosaminoglycans from PNNs [34 ]. Furthermore, a treatment with chondroitinase ABC markedly facilitated plasticity in the visual cortex, injured cortical neurons, and spinal cord injury [35,36].…”

Section: Cs-pgs and Cs-e Are Involved In Neuronal Plasticitymentioning

confidence: 99%

Molecular interactions between chondroitin–dermatan sulfate and growth factors/receptors/matrix proteins

Mizumoto

Yamada

Sugahara

2015

Current Opinion in Structural Biology

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Section: Cs-pgs and Cs-e Are Involved In Neuronal Plasticitymentioning

confidence: 99%

Molecular interactions between chondroitin–dermatan sulfate and growth factors/receptors/matrix proteins

Mizumoto

Yamada

Sugahara

2015

Current Opinion in Structural Biology

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130

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“…1) are the most extensively investigated. Their components include chondroitin sulfate proteoglycans (CSPGs), hyaluronan, tenascin-R, link proteins, Reelin and semaphorin 3A (Carulli et al, 2013b; Deepa et al, 2006; Dick et al, 2013; Matthews et al, 2002; Vo et al, 2013a). CSPGs, the organizers of the ECM, are highly represented in PNNs, with aggrecan, neurocan, brevican, versican and phosphacan among the most abundant (Deepa et al, 2006; Giamanco and Matthews, 2012; Yamaguchi, 2000).…”

Section: Perineuronal Nets: Composition and Association With Distimentioning

confidence: 99%

“…We focus predominantly on evidence based on chondroitin sulfate proteoglycans (CSPGs), one of their main PNN components (Carulli et al, 2007; Deepa et al, 2006; Giamanco and Matthews, 2012). Importantly, other PNN elements, namely Reelin and semaphorin 3A, have been shown to be involved in the pathophysiology of SZ, although not directly as PNN components (Abdolmaleky et al, 2005a; Carulli et al, 2013a; Costa et al, 2001; Dick et al, 2013; Eastwood et al, 2003; Fatemi, 2005; Impagnatiello et al, 1998; Vo et al, 2013b). In particular, Reelin has been extensively investigated for its role in brain development, synaptic regulation during adulthood and involvement in several brain disorders, including SZ and bipolar disorder; although some of these aspects will be mentioned in this review, we refer to comprehensive publications by other groups for details (Abdolmaleky et al, 2005a; Akbarian and Huang, 2006; Barros et al, 2011; Campo et al, 2009; Chen et al, 2005; Costa et al, 2001; Curran and D’Arcangelo, 1998; Dityatev et al, 2006; Eastwood and Harrison, 2006; Fatemi, 2001; Flashner et al, 2013; Folsom and Fatemi, 2013; Franco and Muller, 2011; Frotscher, 2010; Frotscher et al, 2009a, b; Guidotti et al, 2011; Guidotti et al, 2000; Honda et al, 2011; Impagnatiello et al, 1998; Lakatosova and Ostatnikova, 2012; Pesold et al, 1999; Sinagra et al, 2005; Stranahan et al, 2013).…”

Section: Introductionmentioning

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

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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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“…1) [36]. Sema3A also co-localizes with cell surface CSPGs on cortical neurons, increasing the likelihood of Sema3A-neuropilin-1 interaction and axon repulsion [37][38][39]. This interaction can be augmented by the addition of glycosaminoglycans, which decreases neurite outgrowth and increases growth cone collapse [37,38].…”

Section: Semaphorinsmentioning

confidence: 99%

“…This interaction can be augmented by the addition of glycosaminoglycans, which decreases neurite outgrowth and increases growth cone collapse [37,38]. Conversely, digestion of the chondroitin sulfate side chains with chondroitinase ABC releases bound biologically active Sema3A, perhaps illuminating a mechanism contributing to the growth-promoting effects of chondroitinase ABC treatment [28,[37][38][39].…”

Section: Semaphorinsmentioning

confidence: 99%

Axon Guidance Molecules and Neural Circuit Remodeling After Spinal Cord Injury

Hollis

2016

Neurotherapeutics

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…once the development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably. Santiago Ramón y CajalCajal's neurotropic theory postulates that the complexity of the nervous system arises from the collaboration of neurotropic signals from neuronal and non-neuronal cells and that once development has ended, a paucity of neurotropic signals means that the pathways of the central nervous system are Bfixed, ended, immutable^. While the capacity for regeneration and plasticity of the central nervous system may not be quite as paltry as Cajal proposed, regeneration is severely limited in scope as there is no spontaneous regeneration of long-distance projections in mammals and therefore limited opportunity for functional recovery following spinal cord injury. It is not a far stretch from Cajal to hypothesize that reappropriation of the neurotropic programs of development may be an appropriate strategy for reconstitution of injured circuits. It has become clear, however, that a significant number of the molecular cues governing circuit development become re-active after injury and many assume roles that paradoxically obstruct the functional re-wiring of severed neural connections. Therefore, the problem to address is how individual neural circuits respond to specific molecular cues following injury, and what strategies will be necessary for instigating functional repair or remodeling of the injured spinal cord.

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Semaphorin 3A Binds to the Perineuronal Nets via Chondroitin Sulfate Type E Motifs in Rodent Brains

Cited by 126 publications

References 57 publications

Molecular interactions between chondroitin–dermatan sulfate and growth factors/receptors/matrix proteins

Molecular interactions between chondroitin–dermatan sulfate and growth factors/receptors/matrix proteins

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

Axon Guidance Molecules and Neural Circuit Remodeling After Spinal Cord Injury

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