Arylsulfatase B modulates neurite outgrowth via astrocyte chondroitin‐4‐sulfate: Dysregulation by ethanol

Zhang, Xiaolu; Bhattacharyya, Sumit; Kusumo, Handojo; Goodlett, Charles R.; Tobacman, Joanne K.; Guizzetti, Marina

doi:10.1002/glia.22604

Cited by 56 publications

(75 citation statements)

References 63 publications

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“…Chronic ethanol exposure increases the activity of neurons by creating a hyper-glutamatergic state during withdrawal, which could result in increased transcription of aggrecan (Holmes et al, 2013). Ethanol is also known to profoundly impact the functioning of astrocytes and alters the production of astrocyte-derived PN components (Zhang et al, 2014). Thus, ethanol might affect the production of PN proteins in both neurons and glia.…”

Section: Discussionmentioning

confidence: 99%

Repeated Binge Drinking Increases Perineuronal Nets in the Insular Cortex

Lasek

2015

Alcohol Clin Exp Res

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Background Alcohol exposure leads to changes in the extracellular matrix (ECM) in the brain, which profoundly impacts neuronal plasticity. Perineuronal nets (PNs) are specialized ECM structures that enclose subpopulations of neurons in the cortex. Adolescent exposure to alcohol induces long-lasting increases in the expression of PN components in the cortex in adult mice. However, it has not been determined whether binge alcohol exposure in young adults alters PNs. Here, we examined PNs and their core components in the insula and primary motor cortex after repeated binge-like ethanol consumption in adult mice. Methods The 4 day drinking in the dark (DID) procedure was performed in mice for 1 or 6 weeks to model binge alcohol consumption. The impact of ethanol drinking on PNs was examined by fluorescent staining of brain sections using a marker for PNs, Wisteria floribunda agglutinin (WFA). In another set of experiments, cortex was dissected and Western blots and quantitative real-time PCR (qPCR) were performed to evaluate the expression of the PN proteins aggrecan, brevican, and phosphacan. Results Binge-like ethanol drinking for 6 weeks caused a significant increase in PNs in the insula, as measured by WFA binding. Aggrecan, brevican and phosphacan protein expression, and aggrecan mRNA expression, were also elevated in the insula after 6 weeks of ethanol drinking. In contrast, expression of PN components did not change after 1 week of DID. The increase in PNs appears to be specific to the insula, since alterations were not observed in the primary motor cortex. Conclusions Our results provide the first evidence that insular PNs increase after long-term binge drinking. The insula mediates compulsive alcohol use. Since PNs influence neuronal firing and plasticity, increased PNs in the insula after multiple binge cycles may contribute to restricted neuronal plasticity and lead to the development of compulsive alcohol use.

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Section: Discussionmentioning

confidence: 99%

Repeated Binge Drinking Increases Perineuronal Nets in the Insular Cortex

Lasek

2015

Alcohol Clin Exp Res

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“…Additional experiments such as rescue studies validating the role of C-6-S would be valuable but currently C-6-S is not commercially available. Both C-6-S and C-4-S disaccharides have been shown to inhibit neurite growth from embryonic neurons in cell culture however, their role with respect to adult neurons, such as those that innervate the adult IVD, are less clear [44, 45]. These studies suggest that free intact GAGs such as CS side-chains could be effective at inhibiting neurite growth and this is supported by work demonstrating that recombinant aggrecan depleted of chondroitin sulfated side-chains was unable to inhibit neurite extension [46].…”

Section: Discussionmentioning

confidence: 99%

Intact glycosaminoglycans from intervertebral disc-derived notochordal cell-conditioned media inhibit neurite growth while maintaining neuronal cell viability

et al. 2015

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BACKGROUND CONTEXT Painful human intervertebral discs (IVDs) exhibit nerve growth deep into the IVD. Current treatments for discogenic back pain do not address the underlying mechanisms propagating pain and are often highly invasive or only offer temporary symptom relief. The notochord produces factors during development that pattern the spine and inhibit growth of dorsal root ganglia (DRG) axons into the IVD. We hypothesize that notochordal cell (NC) conditioned medium (NCCM) includes soluble factors capable of inhibiting neurite growth and may represent a future therapeutic target. PURPOSE To test if NCCM can inhibit neurite growth and to determine if NC-derived Glycosaminoglycans (GAGs) are necessary candidates for this inhibition. STUDY DESIGN Human neuroblastoma (SH-SY5Y) cells and rat dorsal root ganglion (DRGs) cells were treated with NCCM in 2D culture in vitro and digestion and mechanistic studies determined if specific GAGs were responsible for inhibitory effects. METHODS NCCM was generated from porcine nucleus pulposus tissue that was cultured in DMEM for 4 days. A dose study was performed using SH-SY5Y cells that were seeded in basal medium for 24hrs and neurite outgrowth and cell viability were assessed following treatment with basal or NCCM (10% and 100%) media for 48hrs. GAGs from NCCM were characterized using multiple digestions and liquid chromatography mass spectroscopy (LC-MS). Neurite growth was assessed on both SH-SY5Y and DRG cells following treatment with NCCM with and without GAG digestion. RESULTS NCCM significantly inhibited neurite outgrowth from SH-SY5Y cells compared to Basal controls without dose or cytotoxic effects; % neurite expressing cells were 39.0±2.9, 27.3±3.6 & 30.2±2.7, and mean neurite length was 60.3±3.5μm, 50.8±2.4μm, 53.2±3.7μm for Basal, 10% NCCM & 100% NCCM, respectively. Digestions and LC-MS determined that Chondroitin-6-Sulfate was the major GAG chain in NCCM. Neurite growth from SH-SY5Y and DRG cells was not inhibited when cells were treated with NCCM with digested chondroitin sulfate (CS). CONCLUSIONS Soluble factors derived from NCCM were capable of inhibiting neurite outgrowth in multiple neural cell types without any negative effects on cell viability. Cleavage of GAGs via digestion was necessary to reverse the neurite inhibition capacity of NCCM. We conclude that intact GAGs such as CS secreted from NCs are potential candidates that could be useful to reduce neurite growth in painful IVDs.

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“…These precociously mature astrocytes would likely not be able to support normal neuritogenesis in neighboring neurons [92,196]. In support of this hypothesis, the pretreatment of astrocyte cultures with alcohol reduces neurite outgrowth of subsequently co-cultured neurons [197,198]. …”

Section: Fasd and Dna Methylationmentioning

confidence: 99%

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

Gavin

Grayson

Varghese

et al. 2017

Genes

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Prenatal alcohol exposure causes persistent neuropsychiatric deficits included under the term fetal alcohol spectrum disorders (FASD). Cellular identity emerges from a cascade of intrinsic and extrinsic (involving cell-cell interactions and signaling) processes that are partially initiated and maintained through changes in chromatin structure. Prenatal alcohol exposure influences neuronal and astrocyte development, permanently altering brain connectivity. Prenatal alcohol exposure also alters chromatin structure through histone and DNA modifications. However, the data linking alcohol-induced differentiation changes with developmental alterations in chromatin structure remain to be elucidated. In the first part of this review, we discuss the sequence of chromatin structural changes involved in neural cell differentiation during normal development. We then discuss the effects of prenatal alcohol on developmental histone modifications and DNA methylation in the context of neurogenesis and astrogliogenesis. We attempt to synthesize the developmental literature with the FASD literature, proposing that alcohol-induced changes to chromatin structure account for altered neurogenesis and astrogliogenesis as well as altered neuron and astrocyte differentiation. Together these changes may contribute to the cognitive and behavioral abnormalities in FASD. Future studies using standardized alcohol exposure paradigms at specific developmental stages will advance the understanding of how chromatin structural changes impact neural cell fate and maturation in FASD.

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Arylsulfatase B modulates neurite outgrowth via astrocyte chondroitin‐4‐sulfate: Dysregulation by ethanol

Cited by 56 publications

References 63 publications

Repeated Binge Drinking Increases Perineuronal Nets in the Insular Cortex

Repeated Binge Drinking Increases Perineuronal Nets in the Insular Cortex

Intact glycosaminoglycans from intervertebral disc-derived notochordal cell-conditioned media inhibit neurite growth while maintaining neuronal cell viability

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

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