ArticleJournal of cellular and molecular medicine2015
Interaction between connexin 43 and nitric oxide synthase in mice heart mitochondria.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- The Double-Edged Effect of Connexins and Pannexins of Glial Cells in Central and Peripheral Nervous System After Nerve Injury.Molecular neurobiology · 2025Review
- Made in the Womb: Maternal Programming of Offspring Cardiovascular Function by an Obesogenic Womb.Metabolites · 2023Review
- Preparation and Safety Evaluation ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Omacor Protects Normotensive and Hypertensive Rats Exposed to Continuous Light from Increased Risk to Malignant Cardiac Arrhythmias.Marine drugs · 2021Article
- Connexins in the Heart: Regulation, Function and Involvement in Cardiac Disease.International journal of molecular sciences · 2021Review
- Role of nitric oxide in mediating the cardioprotective effect of agomelatine against isoproterenol-induced myocardial injury in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases.Redox biology · 2020Review
- Mitochondrial ion channels as targets for cardioprotection.Journal of cellular and molecular medicine · 2020Review
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 2020Review
- Nitric oxide synthase inhibitors negatively regulate respiration in isolated rodent cardiac and brain mitochondria.American journal of physiology. Heart and circulatory physiology · 2020Article
- Review
- Mitochondrial Structural Changes in the Pathogenesis of Diabetic Retinopathy.Journal of clinical medicine · 2019Review
- Quantification of nitric oxide by high-performance liquid chromatography-fluorometric method in subgenomic hepatitis C virus-replicon expressing Huh7 cells upon treatment with acetylsalicylic acid.Experimental and therapeutic medicine · 2018Article
- The Novel Roles of Connexin Channels and Tunneling Nanotubes in Cancer Pathogenesis.International journal of molecular sciences · 2018Review
- Connexins and Nitric Oxide Inside and Outside Mitochondria: Significance for Cardiac Protection and Adaptation.Frontiers in physiology · 2018Review
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Disturbed expression and distribution of myocardial connexin 43 in sudden death patients with hyperthyroid heart disease.International journal of clinical and experimental pathology · 2017Article
- Nitric oxide synthetic pathway and cGMP levels are altered in red blood cells from end-stage renal disease patients.Molecular and cellular biochemistry · 2016Article
- Regulation of gap junction channels and hemichannels by phosphorylation and redox changes: a revision.BMC cell biology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Connexin 43 (Cx43), which is highly expressed in the heart and especially in cardiomyocytes, interferes with the expression of nitric oxide synthase (NOS) isoforms. Conversely, Cx43 gene expression is down-regulated by nitric oxide derived from the inducible NOS. Thus, a complex interplay between Cx43 and NOS expression appears to exist. As cardiac mitochondria are supposed to contain a NOS, we now investigated the expression of NOS isoforms and the nitric oxide production rate in isolated mitochondria of wild-type and Cx43-deficient (Cx43(Cre-ER(T)/fl) ) mice hearts. Mitochondria were isolated from hearts using differential centrifugation and purified via Percoll gradient ultracentrifugation. Isolated mitochondria were stained with an antibody against the mitochondrial marker protein adenine-nucleotide-translocator (ANT) in combination with either a neuronal NOS (nNOS) or an inducible NOS (iNOS) antibody and analysed using confocal laser scanning microscopy. The nitric oxide formation was quantified in purified mitochondria using the oxyhaemoglobin assay. Co-localization of predominantly nNOS (nNOS: 93 ± 4.1%; iNOS: 24.6 ± 7.5%) with ANT was detected in isolated mitochondria of wild-type mice. In contrast, iNOS expression was increased in Cx43(Cre-ER(T)/fl) mitochondria (iNOS: 90.7 ± 3.2%; nNOS: 53.8 ± 17.5%). The mitochondrial nitric oxide formation was reduced in Cx43(Cre-ER(T)/fl) mitochondria (0.14 ± 0.02 nmol/min./mg protein) in comparison to wild-type mitochondria (0.24 ± 0.02 nmol/min./mg). These are the first data demonstrating, that a reduced mitochondrial Cx43 content is associated with a switch of the mitochondrial NOS isoform and the respective mitochondrial rate of nitric oxide formation.
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