Neurotrophic Effects of Extracellular Guanosine

Rathbone, Michel P.; Pilutti, Lara A.; Caciagli, Francesco; Jiang, Shucui

doi:10.1080/15257770802143913

Cited by 67 publications

(69 citation statements)

References 33 publications

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“…Finally, also guanosine can induce reactive astrogliosis [29], through a yet-to-be identified G protein-coupled receptor, further confirming the key role played by extracellular nucleosides and nucleotides in modulating brain tissue response after injury…”

Section: Purines and Pyrimidinesmentioning

confidence: 71%

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Buffo

Rolando

Ceruti

2010

Biochemical Pharmacology

288

260

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 Running title: Beneficial and detrimental outcomes of astrogliosis after central nervous system injury. Abbreviations:Ado, adenosine; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate; AP1, activator protein1; AQP, acquaporin; BBB, blood-brain barrier; BDNF, brain-derived growth factor; bFGF, basic fibroblast growth factor; bHLH, basic helix loop helix; BMP, bone morphogenetic protein; CNS, central nervous system; CNTF, ciliary neurotrophic factor;COX-2, cyclooxigenase-2; CREB, cAMP response element binding; CSPGs, chondroitinsulphate proteoglycans; ERK, extracellular signal-regulated kinase; EGF, epidermal growth factor; Eph4A, ephrin 4A; Epo, erythropoietin; ET1, Endothelin 1; ET-R, endothelin receptor; GABA, gamma-aminobutyric acid; GDNF, glial cell-line derived neurotropic factor; GF, growth factor; GFAP, glial fibrillary acidic protein; GLAST, glutamate aspartate transporter; GLT1, glutamate transporter 1; GS, glutamine synthase; IFN , interferon-beta; IFNγ, interferon gamma; IGF1, insulin growth factor1; IL1β, interleukin 1 beta; IL2, interleukin 2; IL6, interleukin 6; IL10, interleukin 10; JAK, Janus protein tyrosine kinases; Lcn2, Lipocalin 2; MAPK, mitogen-activated protein kinase; MMP, matrix metalloprotease; mTOR, mammalian target of rapamycin; NFAT, nuclear factor of activated T cell; NFkB, nuclear factor kappa B; NGF, nerve growth factor; NT3, neurotrophin 3; p38MAPK, p38 mitogen-activated protein kinase; PTEN, phosphatase and tensin homolog; SOCS, suppressor of cytokine signaling; SOD, superoxide dismutase; STAT, signal transducers and activators of transcription; TGFα, transforming growth factor alpha;TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha; VCAM1, vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor. Page 4 of 63A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 4...

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Section: Purines and Pyrimidinesmentioning

confidence: 71%

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Buffo

Rolando

Ceruti

2010

Biochemical Pharmacology

288

260

View full text Add to dashboard Cite

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“…Involvement of the adenosinergic system in antiepileptic effects of Guo has been suggested because Guo induces stimulation of Ado release from astrocytes [379]. In addition, Guo, released mainly from astrocytes, stimulates astrocyte proliferation possibly via increased level of Ado [380,381]. However, (i) intraperitoneal administration of Ado enhanced [309], (ii) an Ado receptor (A 1 and A 2 ) antagonist (theophylline) decreased [382] and (iii) activation of A 2A receptor triggered/maintained [302] the absence epileptic activity in WAG/Rij rats.…”

Section: Non-adenosine Nucleosides: Uridine Guanosine and Inosinementioning

confidence: 99%

The Antiepileptic Potential of Nucleosides

Kovács¹,

Kékesi²,

Juhász³

et al. 2014

CMC

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Despite newly developed antiepileptic drugs to suppress epileptic symptoms, approximately one third of patients remain drug refractory. Consequently, there is an urgent need to develop more effective therapeutic approaches to treat epilepsy. A great deal of evidence suggests that endogenous nucleosides, such as adenosine (Ado), guanosine (Guo), inosine (Ino) and uridine (Urd), participate in the regulation of pathomechanisms of epilepsy. Adenosine and its analogues, together with non-adenosine (non-Ado) nucleosides (e.g., Guo, Ino and Urd), have shown antiseizure activity. Adenosine kinase (ADK) inhibitors, Ado uptake inhibitors and Ado-releasing implants also have beneficial effects on epileptic seizures. These results suggest that nucleosides and their analogues, in addition to other modulators of the nucleoside system, could provide a new opportunity for the treatment of different types of epilepsies. Therefore, the aim of this review article is to summarize our present knowledge about the nucleoside system as a promising target in the treatment of epilepsy.

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“…Guanosine administration increases both cholesterol and ApoE efflux from astrocytes in vitro, supporting a pharmacological role of guanosine in the modulation of cholesterol homeostasis in the brain [125]. Moreover, astrocytes that release guanosine can exert neurotrophic effects and promote neuritogenesis, possibly via MAP-kinase and PI3-kinase signaling pathways [127]. Previous studies failed to report an increase in synapse number in response to cholesterol administration in vitro [116], despite a strong enhancement in synaptic efficacy [119].…”

Section: Does Guanosine Enhance Corticocortical Synaptogenesis?mentioning

confidence: 90%