ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
The coordinated increased expression of biliverdin reductase and heme oxygenase-2 promotes cardiomyocyte survival: a reductase-based peptide counters β-adrenergic receptor ligand-mediated cardiac dysfunction.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Oxidative stress modulates heme synthesis and induces peroxiredoxin-2 as a novel cytoprotective response in β-thalassemic erythropoiesis.Haematologica · 2011Trial
- Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases.Nature reviews. Drug discovery · 2019Review
- Article
- Multiple short-chain dehydrogenases/reductases are regulated in pathological cardiac hypertrophy.FEBS open bio · 2018Article
- Article
- Nanoparticle Delivered Human Biliverdin Reductase-Based Peptide Increases Glucose Uptake by Activating IRK/Akt/GSK3 Axis: The Peptide Is Effective in the Cell and Wild-Type and Diabetic Ob/Ob Mice.Journal of diabetes research · 2016Article
- Translational Significance of Heme Oxygenase in Obesity and Metabolic Syndrome.Trends in pharmacological sciences · 2016Review
- Biliverdin reductase isozymes in metabolism.Trends in endocrinology and metabolism: TEM · 2015Review
- A review on hemeoxygenase-2: focus on cellular protection and oxygen response.Oxidative medicine and cellular longevity · 2014Review
- Expression of Biliverdin Reductase A in peripheral blood leukocytes is associated with treatment response in HCV-infected patients.PloS one · 2013Article
- Hypoxic regulation of cardiac Ca2+ channel: possible role of haem oxygenase.The Journal of physiology · 2012Article
- Molecular modeling to provide insight into the substrate binding and catalytic mechanism of human biliverdin-IXα reductase.The journal of physical chemistry. B · 2012Article
- The human biliverdin reductase-based peptide fragments and biliverdin regulate protein kinase Cδ activity: the peptides are inhibitors or substrate for the protein kinase C.The Journal of biological chemistry · 2012Article
- Nebivolol improves diastolic dysfunction and myocardial remodeling through reductions in oxidative stress in the transgenic (mRen2) rat.American journal of physiology. Heart and circulatory physiology · 2012Article
- Direct Antioxidant Properties of Bilirubin and Biliverdin. Is there a Role for Biliverdin Reductase?Frontiers in pharmacology · 2012Article
- Physiological antioxidative network of the bilirubin system in aging and age-related diseases.Frontiers in pharmacology · 2012Article
- Cardiac function dependence on carbon monoxide.Medical gas researchReview
- Sex-specific effects of heme oxygenase-2 deficiency on renovascular hypertension.Journal of the American Society of Hypertension : JASHArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
HO-2 oxidizes heme to CO and biliverdin; the latter is reduced to bilirubin by biliverdin reductase (BVR). In addition, HO-2 is a redox-sensitive K/Ca(2)-associated protein, and BVR is an S/T/Y kinase. The two enzymes are components of cellular defense mechanisms. This is the first reporting of regulation of HO-2 by BVR and that their coordinated increase in isolated myocytes and intact heart protects against cardiotoxicity of β-adrenergic receptor activation by isoproterenol (ISO). The induction of BVR mRNA, protein, and activity and HO-2 protein was maintained for ≥ 96 h; increase in HO-1 was modest and transient. In isolated cardiomyocytes, experiments with cycloheximide, proteasome inhibitor MG-132, and siBVR suggested BVR-mediated stabilization of HO-2. In both models, activation of BVR offered protection against the ligand's stimulation of apoptosis. Two human BVR-based peptides known to inhibit and activate the reductase, KKRILHC(281) and KYCCSRK(296), respectively, were tested in the intact heart. Perfusion of the heart with the inhibitory peptide blocked ISO-mediated BVR activation and augmented apoptosis; conversely, perfusion with the activating peptide inhibited apoptosis. At the functional level, peptide-mediated inhibition of BVR was accompanied by dysfunction of the left ventricle and decrease in HO-2 protein levels. Perfusion of the organ with the activating peptide preserved the left ventricular contractile function and was accompanied by increased levels of HO-2 protein. Finding that BVR and HO-2 levels, myocyte apoptosis, and contractile function of the heart can be modulated by small human BVR-based peptides offers a promising therapeutic approach for treatment of cardiac dysfunctions.
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