scholarly journals Evidence for the expression of TRPM6 and TRPM7 in cardiomyocytes from all four chamber walls of the human heart

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Inga Andriulė ◽  
Dalia Pangonytė ◽  
Mantė Almanaitytė ◽  
Vaiva Patamsytė ◽  
Milda Kuprytė ◽  
...  
Keyword(s):  
Heart Disease ◽  
Human Heart ◽  
Cardiac Tissue ◽  
Divalent Cations ◽  
Right Atrial ◽  
Mrna Levels ◽  
Isolated Cardiomyocytes ◽  
Extracellular Milieu ◽  
Cell Incubation ◽  
Tissue Homogenates

AbstractThe expression of the channels-enzymes TRPM6 and TRPM7 in the human heart remains poorly defined, and TRPM6 is generally considered not to be expressed in cardiomyocytes. We examined their expression at protein and mRNA levels using right atrial samples resected from patients (n = 72) with or without ischemic heart disease (IHD) and samples from all chamber walls of explanted human hearts (n = 9). TRPM6 and TRPM7 proteins were detected using immunofluorescence on isolated cardiomyocytes, ELISA on tissue homogenates, and immunostaining of cardiac tissue, whereas their mRNAs were detected by RT-qPCR. Both TRPM6 and TRPM7 were present in all chamber walls, with TRPM7 being more abundant. TRPM6 was co-expressed with TRPM7. The expression levels were dependent on cell incubation conditions (presence or absence of divalent cations, pH of the extracellular milieu, presence of TRP channel inhibitors 2-aminoethoxydiphenyl-borate and carvacrol). These drugs reduced TRPM7 immunofluorescence but increased that of TRPM6. TRPM6 and TRPM7 expression was increased in tissues from IHD patients. This is the first demonstration of the presence and co-expression of TRPM6 and TRPM7 in cardiomyocytes from all chamber walls of the human heart. The increased TRPM6 and TRPM7 expression in IHD suggests that the chanzymes are involved in the pathophysiology of the disease.

Abstract P603: Age and Angiotensin-(1-12) Expression in Human Atrial Tissue of Patients with Left Heart Disease

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jessica VonCannon ◽  
Jasmina Varagic ◽  
Sayaka Nagata ◽  
Sarfaraz Ahmad ◽  
Adair Locke ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ventricular Remodeling ◽  
Underlying Mechanism ◽  
Right Atrial ◽  
Mrna Levels ◽  
Ang Ii ◽  
Left Heart ◽  
Atrial Tissue ◽  
Left Heart Disease ◽  
Age Related

In the human heart formation of angiotensin (Ang) II results from the hydrolysis of an alternate angiotensin substrate, -Ang-(1-12)-, by chymase rather than angiotensin converting enzyme. In our recent study a higher Ang-(1-12) expression and upregulation of chymase mRNA and enzymatic activity was found in left (LAA) versus right atrial appendages (RAA) of subjects with left heart disease. Since aging is associated with prominent changes in cardiac structure and function, we assessed the relationships among age, Ang-(1-12), and chymase gene expression and activity in both LAA and RAA in 44 patients undergoing cardiac surgery for the correction of valvular heart disease, resistant atrial fibrillation or ischemic heart disease. Immunohistochemistry for Ang-(1-12) detection was performed using an affinity purified polyclonal antibody directed to the COOH terminus of the full length of the sequence of human Ang-(1-12). Quantitative real-time polymerase chain reaction was used to detect chymase mRNA levels whereas chymase activity was assessed by HPLC. We report that Ang-(1-12) immunostaining in atrial appendages (r=0.30; p<0.05), but not chymase mRNA expression or activity, correlated directly with patients age. While a tendency for higher Ang-(1-12) expression in LAA (Intensity: 5.88 ± 0.91 units; n=11) when compared to RAA (Intensity: 3.948 ± 0.55 units; n=15) was noted in patients younger than 65 yrs, this difference was more prominent and statistically significant in patients older than 65 yrs of age (LAA Intensity: (n=12): 7.39 ± 1.06 units versus RAA Intensity (n=13): 4.74 ±0.54 units; p < 0.05). The results of the present study suggest an age-related increase in Ang-(1-12) expression in human atrial tissue that may be more prominent in the LAA of patients with left heart disease. We suggest that higher availability of Ang-(1-12) for direct Ang II formation may be an underlying mechanism responsible, at least in part, for age- and disease-related atrial and ventricular remodeling and dysfunction.

Unaltered Fatty Acid Uptake, Utilization, and Mitochondrial Respiration in Right Atrial Appendage of Type 2 Diabetic Human Heart

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 335-OR
Author(s):  
NANDINI RJ ◽  
SR RAJI ◽  
VIVEK V. PILLAI ◽  
JAYAKUMAR K. ◽  
SRINIVAS GOPALA
Keyword(s):  
Fatty Acid ◽  
Mitochondrial Respiration ◽  
Human Heart ◽  
Fatty Acid Uptake ◽  
Atrial Appendage ◽  
Right Atrial ◽  
Acid Uptake ◽  
Right Atrial Appendage ◽  
Type 2 Diabetic

Human Heart–Infiltrating T-Cell Clones From Rheumatic Heart Disease Patients Recognize Both Streptococcal and Cardiac Proteins

Circulation ◽  
1995 ◽  
Vol 92 (3) ◽  
pp. 415-420 ◽  
Author(s):  
L. Guilherme ◽  
E. Cunha-Neto ◽  
V. Coelho ◽  
R. Snitcowsky ◽  
P. M. A. Pomerantzeff ◽  
...  
Keyword(s):  
Heart Disease ◽  
T Cell ◽  
Rheumatic Heart Disease ◽  
Human Heart ◽  
T Cell Clones ◽  
Cell Clones ◽  
Rheumatic Heart

scholarly journals Inducibility, but not stability, of atrial fibrillation is increased by NOX2 overexpression in mice

2021 ◽  
Author(s):  
Alexandra S Mighiu ◽  
Alice Recalde ◽  
Klemen Ziberna ◽  
Ricardo Carnicer ◽  
Jakub Tomek ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Superoxide Production ◽  
Right Atrial ◽  
Burst Stimulation ◽  
Lv Mass ◽  
Surface Ecg ◽  
Tissue Homogenates ◽  
Genotype Difference ◽  
Left And Right

Abstract Aims Gp91-containing NADPH oxidases (NOX2) are a significant source of myocardial superoxide production. An increase in NOX2 activity accompanies atrial fibrillation (AF) induction and electrical remodelling in animal models and predicts incident AF in humans; however, a direct causal role for NOX2 in AF has not been demonstrated. Accordingly, we investigated whether myocardial NOX2 overexpression in mice (NOX2-Tg) is sufficient to generate a favourable substrate for AF and further assessed the effects of atorvastatin, an inhibitor of NOX2, on atrial superoxide production and AF susceptibility. Methods and results NOX2-Tg mice showed a 2- to 2.5-fold higher atrial protein content of NOX2 compared with wild-type (WT) controls, which was associated with a significant (twofold) increase in NADPH-stimulated superoxide production (2-hydroxyethidium by HPLC) in left and right atrial tissue homogenates (P = 0.004 and P = 0.019, respectively). AF susceptibility assessed in vivo by transoesophageal atrial burst stimulation was modestly increased in NOX2-Tg compared with WT (probability of AF induction: 88% vs. 69%, respectively; P = 0.037), in the absence of significant alterations in AF duration, surface ECG parameters, and LV mass or function. Mechanistic studies did not support a role for NOX2 in promoting electrical or structural remodelling, as high-resolution optical mapping of atrial tissues showed no differences in action potential duration and conduction velocity between genotypes. In addition, we did not observe any genotype difference in markers of fibrosis and inflammation, including atrial collagen content and Col1a1, Il-1β, Il-6, and Mcp-1 mRNA. Similarly, NOX2 overexpression did not have consistent effects on RyR2 Ca2+ leak nor did it affect PKA or CaMKII-mediated RyR2 phosphorylation. Finally, treatment with atorvastatin significantly inhibited atrial superoxide production in NOX2-Tg but had no effect on AF induction in either genotype. Conclusion Together, these data indicate that while atrial NOX2 overexpression may contribute to atrial arrhythmogenesis, NOX2-derived superoxide production does not affect the electrical and structural properties of the atrial myocardium.

scholarly journals Flow-driven right-to-left cardiac shunting in a patient with carcinoid heart disease and patent foramen ovale without elevated right atrial pressure: a case report and literature review

2020 ◽  
Author(s):  
Parinita Dherange ◽  
Nelson Telles ◽  
Kalgi Modi
Keyword(s):  
Heart Disease ◽  
Patent Foramen Ovale ◽  
Atrial Septum ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Heart Catheterization ◽  
Carcinoid Heart Disease ◽  
Foramen Ovale ◽  
Arterial Blood

Abstract Background Carcinoid heart disease is present in approximately 20% of the patients with carcinoid syndrome and is associated with poor prognosis. It usually manifests with right-sided valvular involvement including tricuspid insufficiency and pulmonary stenosis. Patent foramen ovale (PFO) is present in approximately 50% of the patients with carcinoid heart disease which is twice higher than the general population. Right-to-left shunting through a PFO can occur either due to higher right atrial pressure than left (pressure-driven) or when the venous flow is directed towards the PFO (flow-driven) in the setting of normal intracardiac pressures. We report a rare case of flow-driven right-to-left atrial shunting via PFO in a patient with carcinoid heart disease. Case summary A 54-year-old male with a metastatic neuroendocrine tumour to liver presented with progressive shortness of breath for 5 months. Patient was found to be hypoxic with oxygen saturation of 78% and examination revealed a holosystolic murmur. Arterial blood gas showed oxygen tension of 43 mmHg. A transthoracic and transoesophageal echocardiogram showed aneurysmal inter-atrial septum with a PFO, severe tricuspid regurgitation directed anteriorly towards the inter-atrial septum leading to a marked right-to-left shunt. Right heart catheterization showed right atrial pressure of 8 mmHg, mean pulmonary artery pressure of 12 mmHg, and normal oxygen saturations in the right atrium, right ventricle, and pulmonary arteries. The patient then underwent closure of the PFO along with tricuspid valve and pulmonary valve replacement at an experienced cardiovascular surgical centre and has been asymptomatic since. Conclusion Right-to-left shunting through a PFO in patients with normal right atrial pressure can be successfully treated with closure of the PFO. Thus, understanding the mechanism of intracardiac shunts is important to accurately diagnose and treat this rare and fatal condition.

Influence of atrial fibrillation on microRNA expression profiles in left and right atria from patients with valvular heart disease

2012 ◽  
Vol 44 (3) ◽  
pp. 211-219 ◽  
Author(s):  
Nicola Cooley ◽  
Mark J. Cowley ◽  
Ruby C. Y. Lin ◽  
Silvana Marasco ◽  
Chiew Wong ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Mirna Expression ◽  
Valvular Heart Disease ◽  
Left Atrial ◽  
Expression Profiles ◽  
Artery Bypass ◽  
Expression Patterns ◽  
Right Atrial ◽  
Detectable Effect

Chronic atrial fibrillation (AF) is a complication associated with the dilated atria of patients with valvular heart disease and contributes to worsened pathology. We examined microRNA (miRNA) expression profiles in right and left atrial appendage tissue from valvular heart disease (VHD) patients. Right atrial (RA) appendage from patients undergoing coronary artery bypass grafting and left atrial (LA) appendage from healthy hearts, not used for transplant, were used as controls. There was no detectable effect of chronic AF on miRNA expression in LA tissue, but miRNA expression in RA was strongly influenced by AF, with 47 miRNAs (15 higher, 32 lower) showing differential expression between the AF and control sinus rhythm groups. VHD induced different changes in miRNA expression in LA compared with RA. Fifty-three (12 higher, 41 lower) miRNAs were altered by VHD in LA, compared with 5 (4 higher, 1 lower) in RA tissue. miRNA profiles also differed between VHD-LA and VHD-RA (13 higher, 26 lower). We conclude that VHD and AF influence miRNA expression patterns in LA and RA, but these are affected differently by disease progression and by the development of AF. These findings provide new insights into the progression of VHD.

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