Dissection of astrocyte-mediated cues in neuronal guidance and process extension

Powell, Elizabeth M.; Geller, Herbert M.

doi:10.1002/(sici)1098-1136(199903)26:1<73::aid-glia8>3.0.co;2-s

Cited by 105 publications

(73 citation statements)

References 59 publications

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“…Elimination of CSPG GAG chains with cABC reduces the inhibitory effects of Neu7 cells (Powell and Geller, 1999), and we found the same reduction in inhibition after treatment of Neu7 CM with cABC. With this in mind, Neu7 cells were used as a model system to test the hypothesis that interrupting polymerization of CSPG GAG chains could alleviate CSPGmediated inhibition of axon growth.…”

Section: Chpf Sirna Reduces Gag Chain Production By Astrocytessupporting

confidence: 75%

Inhibiting Glycosaminoglycan Chain Polymerization Decreases the Inhibitory Activity of Astrocyte-Derived Chondroitin Sulfate Proteoglycans

Laabs

Wang²,

Katagiri³

et al. 2007

J. Neurosci.

109

101

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Chondroitin sulfate proteoglycans (CSPGs) are upregulated in the CNS after injury and participate in the inhibition of axon regeneration mainly through their glycosaminoglycan (GAG) side chains. In the present study, we have identified a new way to alleviate the inhibition of axonal regeneration by CSPG GAGs. We have successfully decreased the amount of CSPG GAG produced by astrocytes by targeting chondroitin polymerizing factor (ChPF), a key enzyme in the CSPG biosynthetic pathway. Using short interfering RNA (siRNA), we reduced ChPF mRNA levels by 70% in both the Neu7 astrocyte cell line and primary rat astrocytes. This reduction leads to a decrease in ChPF protein levels and a reduced amount of CSPG GAG chains in the conditioned media (CM) of these cells. Secretion of neurocan by primary astrocytes and NG2 core protein by Neu7 cells transfected with ChPF siRNA is not decreased, suggesting that inhibiting GAG chain synthesis does not affect core protein trafficking from these cells. CM from siRNA-treated Neu7 cells is a less repulsive substrate for axons than CM from control cells. In addition, axonal outgrowth from cerebellar granule neurons is increased on or in CM from ChPF siRNA-treated Neu7 cells. These data indicate that targeting the biosynthesis of CSPG GAG is a potentially new therapeutic avenue for decreasing CSPG GAG produced by astrocytes after CNS injury.

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Section: Chpf Sirna Reduces Gag Chain Production By Astrocytessupporting

confidence: 75%

Inhibiting Glycosaminoglycan Chain Polymerization Decreases the Inhibitory Activity of Astrocyte-Derived Chondroitin Sulfate Proteoglycans

Laabs

Wang²,

Katagiri³

et al. 2007

J. Neurosci.

109

101

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“…correct extension (Banker, 1980;Powell and Geller, 1999) and elimination of neural processes (Barres, 2008). In FXS, as in other disorders that manifest with cognitive impairment (Kaufmann and Moser, 2000), the fine-tuning is often impaired.…”

Section: Discussionmentioning

confidence: 99%

Astrocytes Prevent Abnormal Neuronal Development in the Fragile X Mouse

Jacobs¹,

Doering²

2010

J. Neurosci.

151

123

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Astrocytes are now distinguished as major regulators of neuronal growth and synaptic development. Recently, they have been identified as key players in the progression of a number of developmental disorders; however, in fragile X syndrome (FXS), the role of astrocytes is not known. Using a coculture design, we found that hippocampal neurons exhibited abnormal dendritic morphology and a decreased number of presynaptic and postsynaptic protein aggregates when they were grown on astrocytes from a fragile X mouse. Moreover, we found that normal astrocytes could prevent the development of abnormal dendrite morphology and preclude the reduction of presynaptic and postsynaptic protein clusters in neurons from a fragile X mouse. These experiments are the first to establish a role for astrocytes in the altered neurobiology of FXS. Our results support the notion that astrocytes contribute to abnormal dendrite morphology and the dysregulated synapse development in FXS.

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“…Although the function of GFAP is not fully understood, its expression is increased in response to brain injury and inflammation [15]. During brain development, astrocytes take part in guiding axon development, neuroblast migration [19,20], and formation of developing synapses [21]. Thus, disruption of astrocyte function during development causes a wide variety of neurodevelopmental defects [22,23].…”

Section: Semi-quantitative Rt-pcrmentioning

confidence: 99%

The effect of low dose lipopolysaccharide on thyroid hormone-regulated actin cytoskeleton modulation and type 2 iodothyronine deiodinase activity in astrocytes

Iwasaki

Shimokawa

et al. 2013

Endocr J

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Dissection of astrocyte-mediated cues in neuronal guidance and process extension

Cited by 105 publications

References 59 publications

Inhibiting Glycosaminoglycan Chain Polymerization Decreases the Inhibitory Activity of Astrocyte-Derived Chondroitin Sulfate Proteoglycans

Inhibiting Glycosaminoglycan Chain Polymerization Decreases the Inhibitory Activity of Astrocyte-Derived Chondroitin Sulfate Proteoglycans

Astrocytes Prevent Abnormal Neuronal Development in the Fragile X Mouse

The effect of low dose lipopolysaccharide on thyroid hormone-regulated actin cytoskeleton modulation and type 2 iodothyronine deiodinase activity in astrocytes

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