Research Topics
Species | James HaorahSummaryAffiliation: University of Nebraska Medical Center Country: USA Publications
| Collaborators
|
Detail Information
Publications
The Mechanisms of Cerebral Vascular Dysfunction and Neuroinflammation by MMP-Mediated Degradation of VEGFR-2 in Alcohol IngestionP M Abdul Muneer
Laboratory of Neurovascular Oxidative Injury, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198
Arterioscler Thromb Vasc Biol 32:1167-77. 2012..We describe the mechanisms of BBB dysfunction and neuroinflammation as a result of MMP-3/9 activation and disruption of vascular endothelial growth factor (VEGF)-A/VEGFR-2 interaction, impairing effective angiogenesis...- Stabilization of superoxide dismutase by acetyl-l-carnitine in human brain endothelium during alcohol exposure: novel protective approachJames Haorah
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
Free Radic Biol Med 51:1601-9. 2011..The presence of enzymatic stabilizers favors the ROS-neutralizing antioxidant redox of the BBB, suggesting an underlying protective mechanism of NO for brain vascular tone and vasodilation... - Impairment of brain endothelial glucose transporter by methamphetamine causes blood-brain barrier dysfunctionP M Abdul Muneer
Laboratory of Neurovascular Oxidative Injury, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA
Mol Neurodegener 6:23. 2011..abstract:.. - Mechanism of alcohol-induced oxidative stress and neuronal injuryJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
Free Radic Biol Med 45:1542-50. 2008..Novel quantitative methods of ROS and NO detection help dissect the mechanisms of alcohol-induced neurodegeneration. Uncovering the basic mechanisms of oxidative neuronal injury will serve as the basis for development of new therapies... - Activation of protein tyrosine kinases and matrix metalloproteinases causes blood-brain barrier injury: Novel mechanism for neurodegeneration associated with alcohol abuseJames Haorah
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
Glia 56:78-88. 2008..These results provide better understanding of multifaceted effects of alcohol on the brain and could help develop new therapeutic interventions... - Oxidative stress activates protein tyrosine kinase and matrix metalloproteinases leading to blood-brain barrier dysfunctionJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Neurochem 101:566-76. 2007..These findings point to new therapeutic interventions ameliorating BBB dysfunction in neurological disorders such as stroke or neuroinflammation... - Alcohol-induced blood-brain barrier dysfunction is mediated via inositol 1,4,5-triphosphate receptor (IP3R)-gated intracellular calcium releaseJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198 5215, USA
J Neurochem 100:324-36. 2007..These putative events can lead to BBB dysfunction in the setting of alcoholism, and to neuro-inflammatory disorders promoting leukocyte migration across the BBB... - Ethanol consumption decreases the synthesis of the mannose 6-phosphate/insulin-like growth factor II receptor but does not decrease its messenger RNAJames Haorah
Liver Study Unit, Research Service 151, The Veterans Affairs VA Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105, USA
Biochem Pharmacol 65:637-48. 2003..Thus, the ethanol-elicited decline in receptor protein synthesis may be due to defective M6P/IGF-IIR mRNA translation... - Ethanol-induced activation of myosin light chain kinase leads to dysfunction of tight junctions and blood-brain barrier compromiseJames Haorah
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology, University of Nebraska Medical Center, Omaha, NE 68198, USA
Alcohol Clin Exp Res 29:999-1009. 2005..Cytoskeletal alterations (MLC) and TJ changes (occludin and claudin-5 phosphorylation) result in BBB impairment (decrease in TEER). TJ compromise is associated with increased monocyte migration across the BBB... - Alcohol abuse enhances neuroinflammation and impairs immune responses in an animal model of human immunodeficiency virus-1 encephalitisRaghava Potula
Center for Neurovirology and Neurodegenerative Disorders, Department of Pharmacology and Experimental Neuroscience, 985215 Nebraska Medical Center, Omaha, NE 68198-5215, USA
Am J Pathol 168:1335-44. 2006..Thus, alcohol abuse could be a co-factor in progression of HIV-1 infection of the brain... - Inhibitory effects of alcohol on glucose transport across the blood-brain barrier leads to neurodegeneration: preventive role of acetyl-L: -carnitineP M Abdul Muneer
Laboratory of Neurovascular Oxidative Injury, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA
Psychopharmacology (Berl) 214:707-18. 2011..Here we examined whether interference of glucose uptake and transport at the endothelium by alcohol leads to BBB dysfunction and neuronal degeneration... - Activation of peroxisome proliferator-activated receptor gamma (PPARgamma) suppresses Rho GTPases in human brain microvascular endothelial cells and inhibits adhesion and transendothelial migration of HIV-1 infected monocytesServio H Ramirez
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha 68198, USA
J Immunol 180:1854-65. 2008..These findings indicate that Rac1 and RhoA inhibition by PPARgamma agonists could be a new approach for treatment of neuroinflammation by preventing monocyte migration across the BBB... - Rho-mediated regulation of tight junctions during monocyte migration across the blood-brain barrier in HIV-1 encephalitis (HIVE)Yuri Persidsky
Center for Neurovirology and Neurodegenerative Disorders, Nebraska Medical Center, Omaha, NE 68198 5215, USA
Blood 107:4770-80. 2006..Thus, loss of TJ integrity was associated with Rho activation caused by monocyte brain migration, suggesting that Rho/RhoK activation in BMVECs could be an underlying cause of BBB impairment during HIVE... - Acetyl-L-carnitine protects neuronal function from alcohol-induced oxidative damage in the brainTravis J Rump
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA
Free Radic Biol Med 49:1494-504. 2010..These findings suggest the potential clinical utility of ALC as a neuroprotective agent that prevents alcohol-induced brain damage and development of neurological disorders... - Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune function during diseaseJames Haorah
Liver Study Unit, The Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198-5215, USA
Cell Immunol 229:139-48. 2004..The latter was restored by anti-oxidant. The data support the notion that HIV-1 infection and EtOH may work in concert to affect immune function including antigen presentation and thereby affect disease progression... - Methamphetamine inhibits the glucose uptake by human neurons and astrocytes: stabilization by acetyl-L-carnitineP M Abdul Muneer
Laboratory of Neurovascular Oxidative Injury, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America
PLoS ONE 6:e19258. 2011..These findings suggest that deprivation of glucose-derived energy may contribute to neurotoxicity of METH abusers... - Blood-brain barrier: structural components and function under physiologic and pathologic conditionsYuri Persidsky
Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Neuroimmune Pharmacol 1:223-36. 2006..Better understanding of tight junction regulation and factors affecting transport systems will allow the development of therapeutics to improve the BBB function in health and disease... - The inflammatory footprints of alcohol-induced oxidative damage in neurovascular componentsSaleena Alikunju
Laboratory of Neurovascular Oxidative Injury, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA
Brain Behav Immun 25:S129-36. 2011..These findings reveal the underlying mechanisms that ethanol-elicited BBB oxidative damage initiates the brain vascular inflammatory process, which ultimately leads to neuroinflammation... - Alcohol-induced interactive phosphorylation of Src and toll-like receptor regulates the secretion of inflammatory mediators by human astrocytesNicholas A Floreani
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198 5215, USA
J Neuroimmune Pharmacol 5:533-45. 2010..Experiments with small interfering RNA knockdown of TLR4 in human astrocytes confirmed that silencing expression also abolished the interactive phosphorylation of both TLR4 and Src in the presence of ethanol... - Proteasome activity and autophagosome content in liver are reciprocally regulated by ethanol treatmentPaul G Thomes
Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, United States
Biochem Biophys Res Commun 417:262-7. 2012..Conclusion: Our findings demonstrate that ethanol metabolism generates oxidants, the levels of which differentially influence the activities of the proteasome and autophagy... - Chronic ethanol administration decreases the ligand binding properties and the cellular content of the mannose 6-phosphate/insulin-like growth factor II receptor in rat hepatocytesJames Haorah
Liver Study Unit, Research Service 151, The Veterans Affairs VA Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105, USA
Biochem Pharmacol 63:1229-39. 2002..This reduction may account, in part, for the impaired processing and delivery of acid hydrolases to lysosomes previously observed in ethanol-fed rats... - Total N-nitroso compounds and their precursors in hot dogs and in the gastrointestinal tract and feces of rats and mice: possible etiologic agents for colon cancerSidney S Mirvish
Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE 68198 6805, USA
J Nutr 132:3526S-3529S. 2002..Feeding a similar hot dog mixture to mice did not affect normal 7-methyldeoxyguanosine level in colonic mucosal DNA. Overall, results support the hypothesis that colonic NOCs are a cause of colon cancer... - Partial purification from hot dogs of N-nitroso compound precursors and their mutagenicity after nitrosationLin Zhou
Eppley Institute for Research in Cancer and Department of Pharmaceutical Sciences, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA
J Agric Food Chem 54:5679-87. 2006..Hot dog patties prepared with or without sucrose or glucose showed similar ANC and ANCP levels. We discuss possible implications of these findings for the etiology of colon cancer... - N-nitroso compounds in the gastrointestinal tract of rats and in the feces of mice with induced colitis or fed hot dogs or beefSidney S Mirvish
Eppley Institute for Research in Cancer and Department of Pharmaceutical Sciences, University of Nebraska Medical Center, Omaha, NE 68198, USA
Carcinogenesis 24:595-603. 2003..Results should help evaluate the view that colonic NOC causes colon cancer associated with colitis and ingestion of red and nitrite-preserved meat... - Peroxynitrite alters the catalytic activity of rodent liver proteasome in vitro and in vivoNatalia A Osna
Liver Study Unit, The Omaha Veterans Affairs VA Medical Center, Omaha, NE 68105, USA
Hepatology 40:574-82. 2004..In conclusion, PN dose-dependently modulated proteasome activity, regulating protein degradation by the proteasome in liver cells... - Nitrosation of glycine ethyl ester and ethyl diazoacetate to give the alkylating agent and mutagen ethyl chloro(hydroximino)acetateLin Zhou
Eppley Institute for Research in Cancer, 6805 University of Nebraska Medical Center, Omaha, Nebraska 68198, USA
Chem Res Toxicol 17:416-23. 2004..In conclusion, gastric nitrosation of glycine derivatives such as peptides with a N-terminal glycine might produce ECHA analogues that alkylate bases of gastric mucosal DNA and thereby initiate gastric cancer...