scholarly journals Fructose during pregnancy provokes fetal oxidative stress: The key role of the placental heme oxygenase-1

2016 ◽  
Vol 60 (12) ◽  
pp. 2700-2711 ◽  
Author(s):  
Silvia Rodrigo ◽  
Lourdes Rodríguez ◽  
Paola Otero ◽  
María I. Panadero ◽  
Antonia García ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

scholarly journals Defense and protection mechanisms in lung exposed to asbestiform fiber: the role of macrophage migration inhibitory factor and heme oxygenase-1

2020 ◽  
Vol 64 (2) ◽  
Author(s):  
Carla Loreto ◽  
Rosario Caltabiano ◽  
Adriana Carol Eleonora Graziano ◽  
Sergio Castorina ◽  
Claudia Lombardo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Lung Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Macrophage Migration

Fluoro-edenite (FE), an asbestiform fiber, is responsible for many respiratory pathologies: chronic obstructive diseases, pleural plaques, fibrosis, and malignant mesothelioma. Macrophage migration inhibitory factor (MIF) is one of the first cytokines produced in response to lung tissue damage. Heme oxygenase-1 (HO-1) is a protein with protective effects against oxidative stress. It is up regulated by several stimuli including pro-inflammatory cytokines and factors that promote oxidative stress. In this research, the in vivo model of sheep lungs naturally exposed to FE was studied in order to shed light on the pathophysiological events sustaining exposure to fibers, by determining immunohistochemical lung expression of MIF and HO-1. Protein levels expression of HO-1 and MIF were also evaluated in human primary lung fibroblasts after exposure to FE fibers in vitro. In exposed sheep lungs, MIF and HO-1 immunoexpression were spread involving the intraparenchymal stroma around bronchioles, interstitium between alveoli, alveolar epithelium and macrophages. High MIF immunoexpression prevails in macrophages. Similar results were obtained in vitro, but significantly higher values were only detected for HO-1 at concentrations of 50 and 100 μg/mL of FE fibers. MIF and HO-1 expressions seem to play a role in lung self-protection against uncontrolled chronic inflammation, thus counteracting the strong link with cancer development, induced by exposure to FE. Further studies will be conducted in order to add more information about the role of MIF and HO-1 in the toxicity FE-induced.

scholarly journals The Role of Heme Oxygenase 1 in the Protective Effect of Caloric Restriction against Diabetic Cardiomyopathy

2019 ◽  
Vol 20 (10) ◽  
pp. 2427 ◽  
Author(s):  
Maayan Waldman ◽  
Vadim Nudelman ◽  
Asher Shainberg ◽  
Romy Zemel ◽  
Ran Kornwoski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beneficial Effect ◽  
Heme Oxygenase ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Heme Oxygenase 1 ◽  
Ros Production ◽  
Diabetic Mice ◽  
Protein Levels

Type 2 diabetes mellitus (DM2) leads to cardiomyopathy characterized by cardiomyocyte hypertrophy, followed by mitochondrial dysfunction and interstitial fibrosis, all of which are exacerbated by angiotensin II (AT). SIRT1 and its transcriptional coactivator target PGC-1α (peroxisome proliferator-activated receptor-γ coactivator), and heme oxygenase-1 (HO-1) modulates mitochondrial biogenesis and antioxidant protection. We have previously shown the beneficial effect of caloric restriction (CR) on diabetic cardiomyopathy through intracellular signaling pathways involving the SIRT1–PGC-1α axis. In the current study, we examined the role of HO-1 in diabetic cardiomyopathy in mice subjected to CR. Methods: Cardiomyopathy was induced in obese diabetic (db/db) mice by AT infusion. Mice were either fed ad libitum or subjected to CR. In an in vitro study, the reactive oxygen species (ROS) level was determined in cardiomyocytes exposed to different glucose levels (7.5–33 mM). We examined the effects of Sn(tin)-mesoporphyrin (SnMP), which is an inhibitor of HO activity, the HO-1 inducer cobalt protoporphyrin (CoPP), and the SIRT1 inhibitor (EX-527) on diabetic cardiomyopathy. Results: Diabetic mice had low levels of HO-1 and elevated levels of the oxidative marker malondialdehyde (MDA). CR attenuated left ventricular hypertrophy (LVH), increased HO-1 levels, and decreased MDA levels. SnMP abolished the protective effects of CR and caused pronounced LVH and cardiac metabolic dysfunction represented by suppressed levels of adiponectin, SIRT1, PPARγ, PGC-1α, and increased MDA. High glucose (33 mM) increased ROS in cultured cardiomyocytes, while SnMP reduced SIRT1, PGC-1α levels, and HO activity. Similarly, SIRT1 inhibition led to a reduction in PGC-1α and HO-1 levels. CoPP increased HO-1 protein levels and activity, SIRT1, and PGC-1α levels, and decreased ROS production, suggesting a positive feedback between SIRT1 and HO-1. Conclusion: These results establish a link between SIRT1, PGC-1α, and HO-1 signaling that leads to the attenuation of ROS production and diabetic cardiomyopathy. CoPP mimicked the beneficial effect of CR, while SnMP increased oxidative stress, aggravating cardiac hypertrophy. The data suggest that increasing HO-1 levels constitutes a novel therapeutic approach to protect the diabetic heart. Brief Summary: CR attenuates cardiomyopathy, and increases HO-1, SIRT activity, and PGC-1α protein levels in diabetic mice. High glucose reduces adiponectin, SIRT1, PGC1-1α, and HO-1 levels in cardiomyocytes, resulting in oxidative stress. The pharmacological activation of HO-1 activity mimics the effect of CR, while SnMP increased oxidative stress and cardiac hypertrophy. These data suggest the critical role of HO-1 in protecting the diabetic heart.

scholarly journals Novel Insights into the Vasoprotective Role of Heme Oxygenase-1

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Emanuela Marcantoni ◽  
Luigia Di Francesco ◽  
Melania Dovizio ◽  
Annalisa Bruno ◽  
Paola Patrignani
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Vascular Wall ◽  
Heme Oxygenase 1 ◽  
Antiinflammatory Effect ◽  
Atherosclerotic Lesions ◽  
Inflammatory Processes ◽  
Cox 2 ◽  
Endogenous Antioxidant

Cardiovascular risk factors contribute to enhanced oxidative stress which leads to endothelial dysfunction. These events trigger platelet activation and their interaction with leukocytes and endothelial cells, thus contributing to the induction of chronic inflammatory processes at the vascular wall and to the development of atherosclerotic lesions and atherothrombosis. In this scenario, endogenous antioxidant pathways are induced to restrain the development of vascular disease. In the present paper, we will discuss the role of heme oxygenase (HO)-1 which is an enzyme of the heme catabolism and cleaves heme to form biliverdin and carbon monoxide (CO). Biliverdin is reduced enzymatically to the potent antioxidant bilirubin. Recent evidence supports the involvement of HO-1 in the antioxidant and antiinflammatory effect of cyclooxygenase(COX)-2-dependent prostacyclin in the vasculature. Moreover, the role of HO-1 in estrogen vasoprotection is emerging. Finally, possible strategies to develop novel therapeutics against cardiovascular disease by targeting the induction of HO-1 will be discussed.

Wood smoke extract promotes both apoptosis and proliferation in rat alveolar epithelial type II cells: The role of oxidative stress and heme oxygenase-1*

2008 ◽  
Vol 36 (9) ◽  
pp. 2597-2606 ◽  
Author(s):  
Tzong-Shyuan Lee ◽  
Yu-Ju Liu ◽  
Gau-Jun Tang ◽  
Huey-Wen Yien ◽  
Yuh-Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Wood Smoke ◽  
Heme Oxygenase 1 ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Induction of hepatic heme oxygenase-1 by diclofenac in rodents: role of oxidative stress and cytochrome P-450 activity

2003 ◽  
Vol 38 (6) ◽  
pp. 776-783 ◽  
Author(s):  
Lavinia Cantoni ◽  
Rea Valaperta ◽  
Xavier Ponsoda ◽  
José V Castell ◽  
Davide Barelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Cytochrome P 450

Dialysis Membrane-Induced Oxidative Stress: Role of Heme Oxygenase-1

2006 ◽  
Vol 105 (1) ◽  
pp. e24-e32 ◽  
Author(s):  
Madhu Bhaskaran ◽  
Neetu Radhakrishnan ◽  
Hitesh Patni ◽  
Priyanka Singh ◽  
Ahmad N. Chaudhary ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Dialysis Membrane

Role of heme oxygenase-1 protein in the neuroprotective effects of cyclopentenone prostaglandin derivatives under oxidative stress

2003 ◽  
Vol 17 (11) ◽  
pp. 2249-2255 ◽  
Author(s):  
Takumi Satoh ◽  
Megumi Baba ◽  
Daisaku Nakatsuka ◽  
Yasuyuki Ishikawa ◽  
Hiroyuki Aburatani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Neuroprotective Effects ◽  
Cyclopentenone Prostaglandin

scholarly journals Role of ATM in Oxidative Stress-mediated c-Jun Phosphorylation in Response to Ionizing Radiation and CdCl2

2001 ◽  
Vol 276 (15) ◽  
pp. 11783-11790 ◽  
Author(s):  
Sung A. Lee ◽  
Anatoly Dritschilo ◽  
Mira Jung
Keyword(s):  
Oxidative Stress ◽  
Ionizing Radiation ◽  
Heme Oxygenase ◽  
Redox Homeostasis ◽  
Heme Oxygenase 1 ◽  
Second Phase ◽  
Radiation Induced ◽  
Factor C ◽  
And Control

Ionizing radiation-induced phosphorylation of the transcription factor c-Jun is impaired in cells derived from individuals with ataxia telangiectasia (AT), in which theATMgene is mutated. We demonstrate here that ATM modulates c-Jun phosphorylation following exposure to ionizing radiation as well as treatment with CdCl2, a potent pro-oxidant. Exposure of AT and control fibroblasts to CdCl2induced a biphasic increase in c-Jun phosphorylation on serine residues 63 and 73, with the extent of the second phase being markedly greater in AT cells than in control cells. Heme oxygenase-1, a marker of oxidative stress, was also significantly induced in AT fibroblasts. Expression of recombinant ATM in AT fibroblasts, however, reduced the extent of the effects of CdCl2on both c-Jun phosphorylation and heme oxygenase-1 induction. Our data suggest that ATM contributes to oxidative stress-mediated signaling that leads to c-Jun phosphorylation by acting as a sensor of ionizing radiation-induced oxidative stress and by modulating intracellular redox homeostasis.

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