Response of Glial Cells to Ischemia: Roles of Reactive Oxygen Species and Glutathione

Juurlink, Bernhard H.J.

doi:10.1016/s0149-7634(96)00005-x

Cited by 151 publications

(95 citation statements)

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“…Several recent publications have demonstrated that hydrogen peroxide (H 2 O 2 ) induces typical VRAC currents in the absence of cell swelling in HeLa and hepatoma cell lines (15,16) and positively regulates swelling-activated organic osmolyte release in NIH3T3 fibroblasts (17). Because H 2 O 2 and other reactive oxygen species are abundantly produced in ischemia and during reperfusion (18,19), it is plausible that H 2 O 2 causes the activation or positive modulation of excitatory amino acid release in the ischemic brain. In line with such a suggestion, reactive oxygen species positively modulate the activity of a number of protein kinases, such as tyrosine kinases, mitogen-activated protein kinases (MAPKs), protein kinase C (PKC), and Ca 2ϩ /calmodulin-dependent protein kinase II (CaMKII) (20 -22).…”

mentioning

confidence: 99%

Hydrogen Peroxide Potentiates Volume-sensitive Excitatory Amino Acid Release via a Mechanism Involving Ca2+/Calmodulin-dependent Protein Kinase II

Haskew-Layton

Mongin

Kimelberg³

2005

Journal of Biological Chemistry

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confidence: 99%

Hydrogen Peroxide Potentiates Volume-sensitive Excitatory Amino Acid Release via a Mechanism Involving Ca2+/Calmodulin-dependent Protein Kinase II

Haskew-Layton

Mongin

Kimelberg³

2005

Journal of Biological Chemistry

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“…We have demonstrated a significant decrease in GSH in primary cultured oligodendrocytes when exposed to hypoxia and also when exposed to conditioned medium from hypoxic microglial cells. In hypoxic-ischemic conditions, GSH depletion has been implicated in the vulnerability of developing oligodendrocytes (Back et al, 2002), leading to their death by free radical-mediated mechanisms (Juurlink, 1997). Free radical production in the developing white matter in response to hypoxic-ischemic conditions has been reported (Welin et al, 2005) and microglial cells are known to be involved in free radical generation (Colton et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Iron and Iron Regulatory Proteins in Amoeboid Microglial Cells Are Linked to Oligodendrocyte Death in Hypoxic Neonatal Rat Periventricular White Matter through Production of Proinflammatory Cytokines and Reactive Oxygen/Nitrogen Species

Rathnasamy¹,

Ling²,

Kaur³

2011

J. Neurosci.

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This study was aimed to examine the role of iron in causing periventricular white matter (PWM) damage following a hypoxic injury in the developing brain. Along with iron, the expression of iron regulatory proteins (IRPs) and transferrin receptor (TfR), which are involved in iron acquisition, was also examined in the PWM by subjecting 1-d-old Wistar rats to hypoxia. Apart from an increase in iron levels in PWM, Perls' iron staining showed an increase of intracellular iron in the preponderant amoeboid microglial cells (AMCs) in the tissue. In response to hypoxia, the protein levels of IRP1, IRP2, and TfR in PWM and AMCs were significantly increased. In primary microglial cultures, administration of iron chelator deferoxamine reduced the generation of iron-induced reactive oxygen and nitrogen species and proinflammatory cytokines such as tumor necrosis factor-␣ and interleukin-1␤. Primary oligodendrocytes treated with conditioned medium from hypoxic microglia exhibited reduced glutathione levels, increased lipid peroxidation, upregulated caspase-3 expression, and reduced proliferation. This was reversed to control levels on treatment with conditioned medium from deferoxamine treated hypoxic microglia; also, there was reduction in apoptosis of oligodendrocytes. The present results suggest that excess iron derived primarily from AMCs might be a mediator of oligodendrocyte cell death in PWM following hypoxia in the neonatal brain.

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“…Astrocytes are involved in the normal maintenance of brain homeostasis, including several energy-dependent functions necessary for normal neuronal activity, e.g., regulation of extracellular K+, pH, and osmolality; export of metabolic intermediates; and rapid uptake of neurotransmitters (Kimelberg and Norenberg, 1989;Magistretti et al, 1993;Walz, 2000). The ability of astrocytes to maintain these functions may, in fact, be a critical determinant of neuronal survival after ischemia (Aschner et al, 1999;Juurlink, 1997;Marrif and Juurlink, 1999;Stanimirovic etal, 1997). Furthermore, metabolic imaging studies have suggested that mitochondrial function in post-ischemic brain may be impaired for hours to days after the ischemic insult (Heiss et al, 1997;Hoehn-Berlage, 1995;Ogasawara et al, 2001;Takamatsu et al, 2000;Wardlaw et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Extensive data indicate that astrocytes are involved in a number of processes that affect neuronal survival, such as glutamate uptake, maintenance of extracellular pH and potassium, Ca 2+ buffering, and transfer of lactate and/or pyruvate to neurons as energy substrates (Anderson and Swanson, 2000;Forsyth, 1996;Magistretti et al, 1993;Vernadakis, 1996;Walz, 2000). A number of these functions are dependent on mitochondrial membrane potential, and have been reported to be impaired early in ischemia (Benveniste et al, 1984;Montgomery, 1994;Juurlink, 1997).…”

Section: Decreased Energy Production and Altered Ion Homeostasismentioning

confidence: 99%

Perioperative Neuroprotection Symposium

Fiskum¹

2004

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Public reporting burden for this collection of information is estimated to average 1 hour par the data needed, and completing and reviewing this collection of information. Send conranls reducing this burden to Washington Headquarters Services. Directorate for Information Operations Management and Budget, Paperwork Reduction Protect (0704-01681. Washington, DC 20803Indudkig the «ma for reviewing instructions, searching existing data sources, gathering and maintaining tMs burden estimate or any other aspect of this ooHecMon of information, including suggestions for 1218 Jefferson Davis Highway, Suite 1204, Arttngton, VA 22202-4302, and to the Office of AGENCY USE ONLY (Leave blank) REPORT DATE June 2004 REPORT TYPE AND DATES COVERED Final Proceedings (13 Sep 03-22 May 04) TITLE AND SUBTITLE Perioperative Neuroprotection Symposium AUTHOR(S)Gary Fiskum, Ph.D. S. FUNDING NUMBERS DAMD17-03-1-0500 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Maryland, Baltimore Baltimore, MD 21201 E-Mail: gfisk001@umaryland.edu PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSORING / MONITORING AGENCY REPORT NUMBER SUPPLEMENTARY NOTESOriginal contains color plates: ALL DTIC reproductions will be in black and white 12a. DISTRIBUTION / AVAILABILITY STATEMENT Approved for Public Release; Distribution Unlimited 12b. DISTRIBUTION CODE A-TRACT IMaiiliwyiH 200 VVwW)The Perioperative Neuroprotection Symposium was held on April 16-19 in Ft. Lauderdale, Fl. The meeting was attended by approximately 140 registrant». Twenty four invited speakers made presentations in five sessions. An additional 40 poster presentations were^available for discussion throughout the meeting. Each participant received a symposium abstract book that included mini-reviews from each of the speakers and the short abstracts from the posters. The speakers also submitted formal manuscripts for peer-reviewed publication.Five of the poster presenters were also invited to submit short research manuscripts. Mitochondria and Neuroprotection Symposium April [16][17][18][19] 2004 Albert Lester Lehninger February 17,1917-March4,1986 Albert Lehninger was born in Bridgeport, Connecticut and received a B.A. in English from Wesleyan University in 1939. He received his Ph.D. in Physiological Chemistry from the University of Wisconsin in 1942. Lehninger stayed on at the Univ. of Wisconsin as an Instructor until 1945, when he was appointed Assistant Professor of Biochemistry and Surgery at the University of Chicago. At this juncture he had published 11 research articles. From 1945From -1952, he published an additional 33 articles. These studies included the discovery that fatty acid oxidation, ketone body metabolism, and the TCA cycle occur in the mitochondrion, some of the first investigations employing isolation of this organelle (see e.g., JBC1949 and 1950). Thus, while Lehninger was a chemist at heart, he was one of the founding father...

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Response of Glial Cells to Ischemia: Roles of Reactive Oxygen Species and Glutathione

Cited by 151 publications

References 163 publications

Hydrogen Peroxide Potentiates Volume-sensitive Excitatory Amino Acid Release via a Mechanism Involving Ca2+/Calmodulin-dependent Protein Kinase II

Hydrogen Peroxide Potentiates Volume-sensitive Excitatory Amino Acid Release via a Mechanism Involving Ca2+/Calmodulin-dependent Protein Kinase II

Iron and Iron Regulatory Proteins in Amoeboid Microglial Cells Are Linked to Oligodendrocyte Death in Hypoxic Neonatal Rat Periventricular White Matter through Production of Proinflammatory Cytokines and Reactive Oxygen/Nitrogen Species

Perioperative Neuroprotection Symposium

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