1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1346-7</a>
Pages
313–313
Issue
1
Volume
15
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Reduced AMPK activation and increased HCAR activation drive anti-inflammatory response and neuroprotection in glaucoma.
Publisher
An entity responsible for making the resource available
Journal of neuroinflammation
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-11
Subject
The topic of the resource
AMP-activated protein kinase; AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Pathology; Diet; Disease Models; Eye Proteins/genetics; Female; G-Protein-Coupled – Metabolism; G-Protein-Coupled/*metabolism; Glaucoma; Glaucoma – Complications; Glaucoma – Pathology; Glaucoma/*complications/pathology; Impact of Events Scale; Inbred DBA; Inflammation – Etiology; Inflammation – Prevention and Control; Inflammation hydroxycarboxylic acid receptor; Inflammation/*etiology/*prevention & control; Ketogenic diet; Ketogenic/methods; Male; Membrane Glycoproteins; Membrane Glycoproteins/genetics; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia/drug effects/pathology; Models; Mutation; Mutation/genetics; Neuroprotection/drug effects/*physiology; NLR Family; Optic Nerve – Pathology; Optic Nerve/pathology; Phosphotransferases – Metabolism; Proteins; Pyrin Domain-Containing 3 Protein/genetics/metabolism; Receptors; Retina – Drug Effects; Retina – Pathology; Retinal Ganglion Cells/drug effects/*pathology; Transgenic
Creator
An entity primarily responsible for making the resource
Harun-Or-Rashid Mohammad; Inman Denise M
Description
An account of the resource
BACKGROUND: Glaucoma is a chronic degenerative disease for which inflammation is considered to play a pivotal role in the pathogenesis and progression. In this study, we examined the impact of a ketogenic diet on the inflammation evident in glaucoma as a follow-up to a recent set of experiments in which we determined that a ketogenic diet protected retinal ganglion cell structure and function. METHODS: Both sexes of DBA/2J (D2) mice were placed on a ketogenic diet (keto) or standard rodent chow (untreated) for 8 weeks beginning at 9 months of age. DBA/2J-Gpnmb(+) (D2G) mice were also used as a non-pathological genetic control for the D2 mice. Retina and optic nerve (ON) tissues were micro-dissected and used for the analysis of microglia activation, expression of pro- and anti-inflammatory molecules, and lactate- or ketone-mediated anti-inflammatory signaling. Data were analyzed by immunohistochemistry, quantitative RT-PCR, ELISA, western blot, and capillary tube-based electrophoresis techniques. RESULTS: Microglia activation was observed in D2 retina and ON as documented by intense microglial-specific Iba1 immunolabeling of rounded-up and enlarged microglia. Ketogenic diet treatment reduced Iba1 expression and the activated microglial phenotype. We detected low energy-induced AMP-activated protein kinase (AMPK) phosphorylation in D2 retina and ON that triggered NF-kappaB p65 signaling through its nuclear translocation. NF-kappaB induced pro-inflammatory TNF-alpha,
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1346-7</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
AMP-activated protein kinase
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Biological
Calcium Binding Proteins – Metabolism
Calcium-Binding Proteins/metabolism
Cells – Drug Effects
Cells – Pathology
Department of Pharmaceutical Sciences
Diet
Disease Models
Eye Proteins/genetics
Female
G-Protein-Coupled – Metabolism
G-Protein-Coupled/*metabolism
Glaucoma
Glaucoma – Complications
Glaucoma – Pathology
Glaucoma/*complications/pathology
Harun-Or-Rashid Mohammad
Impact of Events Scale
Inbred DBA
Inflammation – Etiology
Inflammation – Prevention and Control
Inflammation hydroxycarboxylic acid receptor
Inflammation/*etiology/*prevention & control
Inman Denise M
Journal of neuroinflammation
Ketogenic diet
Ketogenic/methods
Male
Membrane Glycoproteins
Membrane Glycoproteins/genetics
Mice
Microfilament Proteins – Metabolism
Microfilament Proteins/metabolism
Microglia/drug effects/pathology
Models
Mutation
Mutation/genetics
NEOMED College of Pharmacy
Neuroprotection/drug effects/*physiology
NLR Family
Optic Nerve – Pathology
Optic Nerve/pathology
Phosphotransferases – Metabolism
Proteins
Pyrin Domain-Containing 3 Protein/genetics/metabolism
Receptors
Retina – Drug Effects
Retina – Pathology
Retinal Ganglion Cells/drug effects/*pathology
Transgenic
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.113.301591</a>
Pages
1911–1919
Issue
8
Volume
33
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Mitochondrial oxidative stress corrupts coronary collateral growth by activating adenosine monophosphate activated kinase-alpha signaling.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Body Weight/physiology; Cells; collateral circulation; coronary circulation; Coronary Vessels/cytology/*enzymology; Cultured; Disease Models; Endothelial Cells/cytology/*enzymology; Humans; Inbred WKY; Ischemia/metabolism/pathology; mitochondria; Mitochondria/drug effects/*metabolism; Myocardium/enzymology/pathology; Oxidative Stress/*physiology; Rats; reactive oxygen species; Rotenone/pharmacology; Signal Transduction/*physiology; TOR Serine-Threonine Kinases/metabolism; Uncoupling Agents/pharmacology
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Sam Wai Johnn; Stevanov Kelly; Enrick Molly; Chen Chwen-Lih; Kolz Christopher; Thakker Prashanth; Hardwick James P; Chen Yeong-Renn; Dyck Jason R B; Yin Liya; Chilian William M
Description
An account of the resource
OBJECTIVE: Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart. APPROACH AND RESULTS: Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/mL vascular endothelial growth factor, 1 micromol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (P\textless0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-alpha and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-alpha suggested impairments in energy production, which was reflected by decrease in O2 consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-alpha (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-alpha. Conversely, expression of a constitutively active AMPK-alpha blocked tube formation. CONCLUSIONS: We conclude that activation of AMPK-alpha during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.113.301591" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.113.301591</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2013
AMP-Activated Protein Kinases/*metabolism
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Body Weight/physiology
Cells
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Collateral Circulation
Coronary Circulation
Coronary Vessels/cytology/*enzymology
Cultured
Department of Integrative Medical Sciences
Disease Models
Dyck Jason R B
Endothelial Cells/cytology/*enzymology
Enrick Molly
Hardwick James P
Humans
Inbred WKY
Ischemia/metabolism/pathology
Kolz Christopher
Mitochondria
Mitochondria/drug effects/*metabolism
Myocardium/enzymology/pathology
NEOMED College of Medicine
Oxidative Stress/*physiology
Pung Yuh Fen
Rats
reactive oxygen species
Rotenone/pharmacology
Sam Wai Johnn
Signal Transduction/*physiology
Stevanov Kelly
Thakker Prashanth
TOR Serine-Threonine Kinases/metabolism
Uncoupling Agents/pharmacology
Yin Liya