Literature DB >> 15846800

Alterations in metabolism and gap junction expression may determine the role of astrocytes as "good samaritans" or executioners.

Reza Farahani1, Mara H Pina-Benabou2, Andreas Kyrozis3, Ayesha Siddiq2, Penha C Barradas4, Fung-Chow Chiu5, Leny A Cavalcante6, James C K Lai7, Patric K Stanton2,8, Renato Rozental2,9.   

Abstract

Our knowledge of astroglia and their physiological and pathophysiological role(s) in the central nervous system (CNS) has grown during the past decade, revealing a complex picture. It is becoming increasingly clear that glia play a significant role in the homeostasis and function of the CNS and that neurons should no longer be considered the only cell type that responds, both rapidly and slowly, to electrochemical activity. We discuss recent advances in the field with an emphasis on the impact of hypoxia and ischemia on astrocytic metabolism and the functional relationship between glucose metabolism and gap junctions in astrocytes. We also address the controversy over whether astrocytic gap junctions mediate protection or killing of neurons during or after hypoxic or ischemic insults. Copyright 2005 Wiley-Liss, Inc.

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Year:  2005        PMID: 15846800     DOI: 10.1002/glia.20213

Source DB:  PubMed          Journal:  Glia        ISSN: 0894-1491            Impact factor:   8.073


  32 in total

Review 1.  Gap junctions.

Authors:  Morten Schak Nielsen; Lene Nygaard Axelsen; Paul L Sorgen; Vandana Verma; Mario Delmar; Niels-Henrik Holstein-Rathlou
Journal:  Compr Physiol       Date:  2012-07       Impact factor: 9.090

2.  Astrocytes promote TNF-mediated toxicity to oligodendrocyte precursors.

Authors:  Sunja Kim; Andrew J Steelman; Hisami Koito; Jianrong Li
Journal:  J Neurochem       Date:  2010-12-02       Impact factor: 5.372

Review 3.  Glial connexins and gap junctions in CNS inflammation and disease.

Authors:  Tammy Kielian
Journal:  J Neurochem       Date:  2008-04-10       Impact factor: 5.372

4.  Protective effects of carbenoxolone are associated with attenuation of oxidative stress in ischemic brain injury.

Authors:  Lang Zhang; Yu-Min Li; Yu-Hong Jing; Shao-Yu Wang; Yan-Feng Song; Jie Yin
Journal:  Neurosci Bull       Date:  2013-05-07       Impact factor: 5.203

5.  Neuroprotective Role of Gap Junctions in a Neuron Astrocyte Network Model.

Authors:  Gemma Huguet; Anoushka Joglekar; Leopold Matamba Messi; Richard Buckalew; Sarah Wong; David Terman
Journal:  Biophys J       Date:  2016-07-26       Impact factor: 4.033

Review 6.  Disruption of ion homeostasis in the neurogliovascular unit underlies the pathogenesis of ischemic cerebral edema.

Authors:  Arjun Khanna; Kristopher T Kahle; Brian P Walcott; Volodymyr Gerzanich; J Marc Simard
Journal:  Transl Stroke Res       Date:  2013-11-22       Impact factor: 6.829

7.  Protection from ataxia-linked apoptosis by gap junction inhibitors.

Authors:  Dingbo Lin; Dolores J Takemoto
Journal:  Biochem Biophys Res Commun       Date:  2007-08-27       Impact factor: 3.575

8.  Treatment of human astrocytoma U87 cells with silicon dioxide nanoparticles lowers their survival and alters their expression of mitochondrial and cell signaling proteins.

Authors:  James C K Lai; Gayathri Ananthakrishnan; Sirisha Jandhyam; Vikas V Dukhande; Alok Bhushan; Mugdha Gokhale; Christopher K Daniels; Solomon W Leung
Journal:  Int J Nanomedicine       Date:  2010-10-05

9.  Protein kinase C gamma mutations in the C1B domain cause caspase-3-linked apoptosis in lens epithelial cells through gap junctions.

Authors:  Dingbo Lin; Denton Shanks; Om Prakash; Dolores J Takemoto
Journal:  Exp Eye Res       Date:  2007-03-31       Impact factor: 3.467

10.  Epileptogenic potential of mefloquine chemoprophylaxis: a pathogenic hypothesis.

Authors:  Remington L Nevin
Journal:  Malar J       Date:  2009-08-05       Impact factor: 2.979

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