β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia

Hahnova, Klara; Brabcová, Iveta; Neckář, Jan; Weissova, Romana; Svatoňová, Anna; Nováková, Olga; Žurmanová, Jitka; Kalous, Martin; Šilhavý, Jan; Pravenec, Michal; Kolář, František; Novotný, Jiřı́

doi:10.1007/s12576-017-0546-8

Cited by 4 publications

(3 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study was performed to improve our understanding about the contribution of the 5-HT metabolizing enzyme MAO-A to cardiac hypertrophy and function. Induction of MAOA has been shown before in several studies as a response to hypoxia, volume load, ageing, or pressure load [ 37 , 38 , 39 , 40 , 41 , 42 ]. Similarly, 5-HT has been associated with myocardial hypertrophy and heart failure.…”

Section: Discussionmentioning

confidence: 95%

Monoamine Oxidase A Contributes to Serotonin—But Not Norepinephrine-Dependent Damage of Rat Ventricular Myocytes

et al. 2023

View full text Add to dashboard Cite

Serotonin effects on cardiac hypertrophy, senescence, and failure are dependent either on activation of specific receptors or serotonin uptake and serotonin degradation by monoamine oxidases (MAOs). Receptor-dependent effects are specific for serotonin, but MAO-dependent effects are nonspecific as MAOs also metabolize other substrates such as catecholamines. Our study evaluates the role of MAO-A in serotonin- and norepinephrine-dependent cell damage. Experiments were performed in vivo to study the regulation of MAOA and MAOB expression and in vitro on isolated cultured adult rat ventricular cardiomyocytes (cultured for 24 h) to study the function of MAO-A. MAOA but not MAOB expression increased in maladaptive hypertrophic stages. Serotonin and norepinephrine induced morphologic cell damage (loss of rod-shaped cell structure). However, MAO-A inhibition suppressed serotonin-dependent but not norepinephrine-dependent damages. Serotonin but not norepinephrine caused a reduction in cell shortening in nondamaged cells. Serotonin induced mitochondria-dependent oxidative stress. In vivo, MAOA was induced during aging and hypertension but the expression of the corresponding serotonin uptake receptor (SLC6A4) was reduced and enzymes that reduce either oxidative stress (CAT) or accumulation of 5-hydroxyindolacetaldehyde (ALDH2) were induced. In summary, the data show that MAO-A potentially affects cardiomyocytes’ function but that serotonin is not necessarily the native substrate.

show abstract

Section: Discussionmentioning

confidence: 95%

Monoamine Oxidase A Contributes to Serotonin—But Not Norepinephrine-Dependent Damage of Rat Ventricular Myocytes

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Wang et al [ 59 ] discovered that MAOs desensitize the β 1 -adrenergic pathway in mice injected intraperitoneally with the β-agonist isoproterenol to induce heart failure (HF). The inhibition of MAO-A in isolated adult cardiomyocytes of HF hearts salvaged the signaling pathway and led to the activation of the protein kinase A [ 60 ]. Thus, more studies are needed to explain the differences in the mortality rate between cardiomyocyte-specific MAO-B knockout male and female mice following I/R.…”

Section: Discussionmentioning

confidence: 99%

Sex Difference in Cardioprotection against Acute Myocardial Infarction in MAO-B Knockout Mice In Vivo

Heger

Szabados

Brosinsky

et al. 2023

IJMS

View full text Add to dashboard Cite

The cardiomyocyte-specific knockout (KO) of monoamine oxidase (MAO)-B, an enzyme involved in the formation of reactive oxygen species (ROS), reduced myocardial ischemia/reperfusion (I/R) injury in vitro. Because sex hormones have a strong impact on MAO metabolic pathways, we analyzed the myocardial infarct size (IS) following I/R in female and male MAO-B KO mice in vivo. Method and Results: To induce the deletion of MAO-B, MAO-B KO mice (Myh6 Cre+/MAO-Bfl/fl) and wild-type (WT, Cre-negative MAO-Bfl/fl littermates) were fed with tamoxifen for 2 weeks followed by 10 weeks of normal mice chow. Myocardial infarction (assessed by TTC staining and expressed as a percentage of the area at risk as determined by Evans blue staining)) was induced by 45 min coronary occlusion followed by 120 min of reperfusion. Results: The mortality following I/R was higher in male compared to female mice, with the lowest mortality found in MAO-B KO female mice. IS was significantly higher in male WT mice compared to female WT mice. MAO-B KO reduced IS in male mice but had no further impact on IS in female MAO-B KO mice. Interestingly, there was no difference in the plasma estradiol levels among the groups. Conclusion: The cardiomyocyte-specific knockout of MAO-B protects male mice against acute myocardial infarction but had no effect on the infarct size in female mice.

show abstract

“…Conplastic mouse models and murine cells offer means to investigate links between mitochondrial variation, disease manifestation, and cellular fitness in well‐controlled conditions. Interestingly, intraspecies conplastic murine models of metabolic diseases such as diabetes and obesity have not yet been widely employed in this setting, with the majority of studies having focused on studying cardiac health, especially hypertension (94‐98). Nevertheless, from the studies reviewed herein, it appears that combining nuclear and mitochondrial genomes from different strains and which, therefore, have not coevolved for longer periods of time could increase the risk for developing diabetes and obesity.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial genome variations, mitochondrial‐nuclear compatibility, and their association with metabolic diseases

Ludwig-Słomczyńska

Rehm

2022

Obesity

View full text Add to dashboard Cite

INTRODUC TI ON Origin, structure of, and protein coding by the mitochondrial genomeAround 2 to 3 billion years ago, the rise in atmospheric oxygen (i.e., the "Great Oxygen Event") altered the atmospheric conditions on the earth. At this time, the class of α-proteobacteria acquired the ability to use oxygen for energy production (1). Through uptake into and endosymbiosis with a host microorganism, eventually mitochondria developed as novel organelles that are typically found in all eukaryotes today. As the symbiotic relationship matured, the majority of endosymbiont genes transferred into the host nucleus (endosymbiotic gene transfer), whereas mitochondria today still retain control over crucial genes essential for mitochondrial energy production (2).The mitochondrial genome encodes only 37 genes. Among these, 13 code for polypeptides, 2 code for ribosomal RNAs (rRNAs) (12S and 16S), and 22 code for transfer RNAs (tRNAs) necessary for mitochondrial protein synthesis. All mRNAs code for subunits of the multiprotein complexes involved in mitochondrial oxidative phosphorylation. Mitochondrially encoded NADH dehydrogenase (mt-ND1, mt-ND2, mt-ND3, mt-ND4, mt-ND4L, mt-ND5, and mt-ND6) codes for seven out of forty-six polypeptides that compose complex I. Mitochondrially encoded cytochrome b (mt-CYB) is one of 11 polypeptides necessary to form complex III. Mitochondrially encoded cytochrome c oxidase (mt-CO1 , mt-CO2, and mt-CO3), along with 10 other nuclear-coded polypeptides,

show abstract

β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia

Cited by 4 publications

References 56 publications

Monoamine Oxidase A Contributes to Serotonin—But Not Norepinephrine-Dependent Damage of Rat Ventricular Myocytes

Monoamine Oxidase A Contributes to Serotonin—But Not Norepinephrine-Dependent Damage of Rat Ventricular Myocytes

Sex Difference in Cardioprotection against Acute Myocardial Infarction in MAO-B Knockout Mice In Vivo

Mitochondrial genome variations, mitochondrial‐nuclear compatibility, and their association with metabolic diseases

Contact Info

Product

Resources

About