heme oxygenase is a heat shock protein and pest protein in rat astroglial cells pdf Tuesday, March 23, 2021 4:45:49 AM

Heme Oxygenase Is A Heat Shock Protein And Pest Protein In Rat Astroglial Cells Pdf

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Reperfusion in ischemia is believed to generate cytotoxic oxidative stress, which mediates reperfusion injury.

Protective Effects of Inducible HO-1 on Oxygen Toxicity in Rat Brain Endothelial Microvessel Cells

Intracerebral hemorrhage ICH is a fatal acute cerebrovascular disease, with a high morbidity and mortality. Following ICH, erythrocytes release heme and several of its metabolites, thereby contributing to brain edema and secondary brain damage. Heme oxygenase is the initial and rate-limiting enzyme of heme catabolism, and the expression of heme oxygenase-1 HO-1 is rapidly induced following acute brain injury. Therefore, in-depth studies regarding the role of HO-1 in secondary brain damage following ICH may provide a theoretical basis for neuroprotective function after ICH. Relative to ischemic stroke, ICH is associated with increased morbidity and mortality, severely impairing physical and mental health and negatively influencing patient quality of life 6 — 9.

The mechanisms involved in brain edema formation following intracerebral hemorrhage ICH have not been fully elucidated. The authors have found that red blood cell lysis plays an important role in edema development after ICH. In the present study, they sought to determine whether degradation products of hemoglobin cause brain edema. Hemoglobin, hemin, bilirubin, or FeCl 2 were infused with stereotactic guidance into the right basal ganglia of Sprague—Dawley rats. The animals were killed 24 hours later to determine brain water and ion contents. Western blot analysis and immunohistochemistry were applied for heme oxygenase-1 HO-1 measurement. The effects of an HO inhibitor, tin-protoporphyrin SnPP , and the iron chelator deferoxamine, on hemoglobin-induced brain edema were also examined.

Glial HO-1 expression, iron deposition and oxidative stress in neurodegenerative diseases

Heat shock proteins show remarkable variations in their expression levels under a variety of toxic conditions. A research span expanded over five decades has revealed their molecular characterization, gene regulation, expression patterns, vast similarity in diverse groups, and broad range of functional capabilities. Their functions include protection and tolerance against cytotoxic conditions through their molecular chaperoning activity, maintaining cytoskeleton stability, and assisting in cell signaling. However, their role as biomarkers for monitoring the environmental risk assessment is controversial due to a number of conflicting, validating, and nonvalidating reports. The current knowledge regarding the interpretation of HSPs expression levels has been discussed in the present review.

Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. Chronic hypoxia increases the expression of a set of stress proteins oxygen regulated proteins or ORPs which is implicated in the development of drug resistance and radiation sensitivity in tumour cells. We report here that ORP 33 is a form of the heme catabolic enzyme, heme oxygenase, using evidence obtained from northern blotting, two-dimensional polyacrylamide gel electrophoresis and western analysis. Heme oxygenase is believed to be an important component of the cellular response to oxidative stress. The significance of heme oxygenase as a hypoxia-induced stress protein is discussed. Read article at publisher's site DOI :

In rat primary astrocyte cultures, we demonstrated that dopamine, cysteamine, H 2 O 2 and menadione rapidly induce heme oxygenase-1 HO-1 expression mRNA and protein followed by sequestration of non-transferrin-derived 55 Fe by the mitochondrial compartment. The effects of dopamine on HO-1 expression were inhibited by ascorbate implicating a free radical mechanism of action. Dopamine-induced mitochondrial iron trapping was abrogated by administration of the heme oxygenase inhibitors, tin mesoporphyrin SnMP or dexamethasone DEX indicating that HO-1 up-regulation is necessary for subsequent mitochondrial iron deposition in these cells. Over-expression of the human HO-1 gene in cultured rat astroglia by transient transfection also stimulated mitochondrial 55 Fe deposition, an effect that was again preventible by SnMP or DEX administration. We hypothesize that free ferrous iron and carbon monoxide generated by HOmediated heme degradation promote mitochondrial membrane injury and the deposition of redox-active iron within this organelle. We have shown that the percentages of GFAP-positive astrocytes that co-express HO-1 in Parkinson-affected substantia nigra and Alzheimer-diseased hippocampus are significantly increased relative to age-matched controls.

Glial HO-1 expression, iron deposition and oxidative stress in neurodegenerative diseases

In rat primary astrocyte cultures, we demonstrated that dopamine, cysteamine, H 2 O 2 and menadione rapidly induce heme oxygenase-1 HO-1 expression mRNA and protein followed by sequestration of non-transferrin-derived 55 Fe by the mitochondrial compartment. The effects of dopamine on HO-1 expression were inhibited by ascorbate implicating a free radical mechanism of action. Dopamine-induced mitochondrial iron trapping was abrogated by administration of the heme oxygenase inhibitors, tin mesoporphyrin SnMP or dexamethasone DEX indicating that HO-1 up-regulation is necessary for subsequent mitochondrial iron deposition in these cells.

Alexandria M. Palaferri Schieber, Janelle S. Physiological responses that occur during infection are most often thought of in terms of effectors of microbial destruction through the execution of resistance mechanisms, due to a direct action of the microbe, or are maladaptive consequences of host—pathogen interplay.

Brain edema after experimental intracerebral hemorrhage: role of hemoglobin degradation products

Heme oxygenase-1 HO-1 is a highly inducible and ubiquitous cellular enzyme that subserves cytoprotective responses to toxic insults, including inflammation and oxidative stress. In contrast, we have found that in human immunodeficiency virus HIV infection of the brain, which is also associated with inflammation, oxidative stress and neurodegeneration, HO-1 expression is decreased, likely reflecting a unique role for HO-1 deficiency in neurodegeneration pathways activated by HIV infection. We have also shown that HO-1 expression is significantly suppressed by HIV replication in cultured macrophages which represent the primary cellular reservoir for HIV in the brain. HO-1 deficiency is associated with release of neurotoxic levels of glutamate from both HIV-infected and immune-activated macrophages; this glutamate-mediated neurotoxicity is suppressed by pharmacological induction of HO-1 expression in the macrophages. Thus, HO-1 induction could be a therapeutic strategy for neuroprotection against HIV infection and other neuroinflammatory brain diseases.

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Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. Chronic hypoxia increases the expression of a set of stress proteins oxygen regulated proteins or ORPs which is implicated in the development of drug resistance and radiation sensitivity in tumour cells. We report here that ORP 33 is a form of the heme catabolic enzyme, heme oxygenase, using evidence obtained from northern blotting, two-dimensional polyacrylamide gel electrophoresis and western analysis.

Intracerebral hemorrhage ICH is a fatal acute cerebrovascular disease, with a high morbidity and mortality. Following ICH, erythrocytes release heme and several of its metabolites, thereby contributing to brain edema and secondary brain damage. Heme oxygenase is the initial and rate-limiting enzyme of heme catabolism, and the expression of heme oxygenase-1 HO-1 is rapidly induced following acute brain injury. Therefore, in-depth studies regarding the role of HO-1 in secondary brain damage following ICH may provide a theoretical basis for neuroprotective function after ICH.

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