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Search results for: Total RNA Human Adult Normal Tissue Heart Atrium (right)

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#31731197   2019/11/12 To Up

Analysis of long non-coding RNA and mRNA profiles in epicardial adipose tissue of patients with atrial fibrillation.

Accumulating studies have suggested that epicardial adipose tissue (EAT) play an important role in the pathogenesis of atrial fibrillation (AF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that bioactive molecules secreted from EAT, including exosomes carrying long non-coding RNAs (lncRNAs), may modulate atrial remodeling. LncRNAs are associated with cardiovascular disorders, including AF, but their roles in EAT remain elusive. The aim of the present study was to investigate the expression profile of lncRNAs in EAT with AF. Differentially expressed lncRNAs and nearby mRNAs interaction networks were constructed. Epicardial adipose samples were collected from patients with persistent non-valvular AF (n = 6) and sinus rhythm (SR) (n = 6), and the expression of lncRNAs and mRNAs were profiled using RNA-sequencing method. A total of 46,577 transcripts, including 35,552 protein-coding pattern, corresponding to 15,404 genes in EAT, among which, 655 mRNAs (265 upregulated and 390 downregulated) and 57 lncRNAs (17 upregulated and 40 downregulated) were differentially expressed between AF and SR (P < 0.05; fold change>1.5). GO enrichment, KEGG pathway analysis and interaction network construction showed that these differentially expressed lncRNAs were enriched in functional categories, including metabolism and stress response, which might contribute to the pathogenesis of AF. Our study demonstrated a differentially expressed lncRNA profile in EAT with AF, and provide a novel insight into the interactions between EAT and AF.
Lei Zhao, Zheng Ma, Zongsheng Guo, Meili Zheng, Kuibao Li, Xinchun Yang

2745 related Products with: Analysis of long non-coding RNA and mRNA profiles in epicardial adipose tissue of patients with atrial fibrillation.



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#30402860   // To Up

Long non-coding RNA expression profile in permanent atrial fibrillation patients with rheumatic heart disease.

Atrial fibrillation (AF) is the most common type of arrhythmia, especially in rheumatic heart disease (RHD) patients. The differences in structural remodeling and electrical remodeling between the left and right atrium associated with AF in RHD patients are well known, and alterations in the expression profiles of long noncoding RNAs (lncRNAs) in the left atrium have also been investigated. However, the role of lncRNAs in the right atrium (RA) remains largely unknown.
B Mei, H Liu, S Yang, M-Y Liang, Y Yue, S-Q Huang, J Hou, G-X Chen, Z-K Wu

2724 related Products with: Long non-coding RNA expression profile in permanent atrial fibrillation patients with rheumatic heart disease.

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#28495464   2017/03/12 To Up

MicroRNA-21 via Dysregulation of WW Domain-Containing Protein 1 Regulate Atrial Fibrosis in Atrial Fibrillation.

microRNAs (miRs) have been reported to regulate cell biological functions. To explore the underlying mechanism of miR-21 involvement in patients with atrial fibrosis and atrial fibrillation (AF).
Hui Tao, Meng Zhang, Jing-Jing Yang, Kai-Hu Shi

2421 related Products with: MicroRNA-21 via Dysregulation of WW Domain-Containing Protein 1 Regulate Atrial Fibrosis in Atrial Fibrillation.

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#26974694   2016/03/02 To Up

MicroRNA deep sequencing reveals chamber-specific miR-208 family expression patterns in the human heart.

Heart chamber-specific mRNA expression patterns have been extensively studied, and dynamic changes have been reported in many cardiovascular diseases. MicroRNAs (miRNAs) are also important regulators of normal cardiac development and functions that generally suppress gene expression at the posttranscriptional level. Recent focus has been placed on circulating miRNAs as potential biomarkers for cardiac disorders. However, miRNA expression levels in human normal hearts have not been thoroughly studied, and chamber-specific miRNA expression signatures in particular remain unclear.
Yu Kakimoto, Masayuki Tanaka, Hiroshi Kamiguchi, Hideki Hayashi, Eriko Ochiai, Motoki Osawa

1259 related Products with: MicroRNA deep sequencing reveals chamber-specific miR-208 family expression patterns in the human heart.

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#25500755   2014/11/20 To Up

Unraveling regulatory mechanisms of atrial remodeling of mitral regurgitation pigs by gene expression profiling analysis: role of type I angiotensin II receptor antagonist.

Left atrial enlargement associated with mitral regurgitation (MR) predicts a poor prognosis. However, the underlying regulatory mechanisms of atrial remodeling remain unclear. We used high-density oligonucleotide microarrays and enrichment analysis to identify the alteration of RNA expression pattern and biological processes involved in the atrial remodeling of pigs with and without MR. Gene arrays from left atria tissues were compared in 13 pigs (iatrogenic MR pigs [n = 6], iatrogenic MR pigs treated with valsartan [n = 4], and pigs without MR [n = 3]). A total of 22 genes were differentially upregulated by altered fold change >2.0 (Log2FC > 1), and 49 genes were differentially downregulated by altered fold change <0.5 (Log2FC < -1) in the left atria of the MR pigs compared with the pigs without MR. Enrichment analysis showed that renin-angiotensin system was identified in the Kyoto Encyclopedia of Genes and Genomes pathway. Notably, 12 of the 22 upregulated genes were identified to be downregulated by valsartan and 10 of the 49 downregulated genes were identified to be upregulated by valsartan. The tissue concentrations of angiotensin II and gene expression of hypertrophic gene, myosin regulatory light chain 2, ventricular isoforms, and fibrosis-related genes were significantly increased in the MR pigs compared with pigs without MR. In conclusion, differentially expressed transcriptome and related biological pathways have been identified in the left atria of the MR pigs compared with pigs without MR. Additionally, some of the differentially expressed genes could be regulated by type I angiotensin II receptor blocker.
Mien-Cheng Chen, Jen-Ping Chang, Tzu-Hao Chang, Sheng-Da Hsu, Hsien-Da Huang, Wan-Chun Ho, Feng-Sheng Wang, Chang-Chun Hsiao, Wen-Hao Liu

1785 related Products with: Unraveling regulatory mechanisms of atrial remodeling of mitral regurgitation pigs by gene expression profiling analysis: role of type I angiotensin II receptor antagonist.

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#23355885   2013/01/23 To Up

Gender differences in electrophysiological gene expression in failing and non-failing human hearts.

The increasing availability of human cardiac tissues for study are critically important in increasing our understanding of the impact of gender, age, and other parameters, such as medications and cardiac disease, on arrhythmia susceptibility. In this study, we aimed to compare the mRNA expression of 89 ion channel subunits, calcium handling proteins, and transcription factors important in cardiac conduction and arrhythmogenesis in the left atria (LA) and ventricles (LV) of failing and nonfailing human hearts of both genders. Total RNA samples, prepared from failing male (n = 9) and female (n = 7), and from nonfailing male (n = 9) and female (n = 9) hearts, were probed using custom-designed Taqman gene arrays. Analyses were performed to explore the relationships between gender, failure state, and chamber expression. Hierarchical cluster analysis revealed chamber specific expression patterns, but failed to identify disease- or gender-dependent clustering. Gender-specific analysis showed lower expression levels in transcripts encoding for K(v)4.3, KChIP2, K(v)1.5, and K(ir)3.1 in the failing female as compared with the male LA. Analysis of LV transcripts, however, did not reveal significant differences based on gender. Overall, our data highlight the differential expression and transcriptional remodeling of ion channel subunits in the human heart as a function of gender and cardiac disease. Furthermore, the availability of such data sets will allow for the development of disease-, gender-, and, most importantly, patient-specific cardiac models, with the ability to utilize such information as mRNA expression to predict cardiac phenotype.
Christina M Ambrosi, Kathryn A Yamada, Jeanne M Nerbonne, Igor R Efimov

1689 related Products with: Gender differences in electrophysiological gene expression in failing and non-failing human hearts.

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#22752749   2012/06/30 To Up

Molecular pathology of natriuretic peptides in the myocardium with special regard to fatal intoxication, hypothermia, and hyperthermia.

The present study investigated the molecular pathology of atrial and brain natriuretic peptides (ANP and BNP) in the myocardium to evaluate terminal cardiac function in routine forensic casework with particular regard to fatal drug intoxication (n = 18; sedative-hypnotics, n = 10; methamphetamine, n = 8), hypothermia (cold exposure, n = 13), and hyperthermia (heatstroke, n = 10), compared with that in acute ischemic heart disease (AIHD, n = 35) and congestive heart disease (CHD, n = 11) as controls (total n = 87; within 48 h postmortem). Quantitative analyses of myocardial ANP and BNP messenger RNA demonstrated that their expressions in bilateral atrial and ventricular walls were high in methamphetamine intoxication and hypothermia, comparable to those in AIHD and CHD, but were low in sedative-hypnotic intoxication and hyperthermia. In pericardial fluid, both ANP and BNP levels were increased in hypothermia, while CHD cases had an elevated BNP level, and ANP level showed a tendency to increase in hyperthermia; however, immunohistochemistry showed no evident differences in myocardial ANP and BNP among the causes of death. These findings suggest terminal high cardiac strain in methamphetamine intoxication, decreased cardiac strain in sedative-hypnotic intoxication and hyperthermia (heatstroke), and persistent congestion in hypothermia (cold exposure).
Jian-Hua Chen, Tomomi Michiue, Takaki Ishikawa, Hitoshi Maeda

2689 related Products with: Molecular pathology of natriuretic peptides in the myocardium with special regard to fatal intoxication, hypothermia, and hyperthermia.

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#19660384   2009/06/23 To Up

Warm-blood cardioplegic arrest induces selective mitochondrial translocation of protein kinase Cepsilon followed by interaction with 6.1 inwardly rectifying potassium channel subunit in viable myocytes overexpressing urocortin.

This study investigates the cardioprotective role and mechanism of action of urocortin in patients undergoing cardiac surgery, with respect to protein kinase Cepsilon expression, activation, and relocation.
Carol Chen-Scarabelli, Giuseppe Faggian, Zhaokan Yuan, Maddalena Tessari, Alessio Rungatscher, Justin Di Rezze, Gabriele M Scarabelli, Kadija Abounit, Roy McCauley, Louis Saravolatz, Alessandro Mazzucco, Tiziano M Scarabelli

2193 related Products with: Warm-blood cardioplegic arrest induces selective mitochondrial translocation of protein kinase Cepsilon followed by interaction with 6.1 inwardly rectifying potassium channel subunit in viable myocytes overexpressing urocortin.

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#17961532   2007/09/21 To Up

Expression profile of total VEGF, VEGF splice variants and VEGF receptors in the myocardium and arterial vasculature of diabetic and non-diabetic patients with coronary artery disease.

Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis and is implicated in the development of diabetic microvascular and macrovascular disease.
Eleni Zygalaki, Loukas Kaklamanis, Nikolaos I Nikolaou, Stamatis Kyrzopoulos, Mazen Houri, Zenon Kyriakides, Evi S Lianidou, Dimitrios Th Kremastinos

2325 related Products with: Expression profile of total VEGF, VEGF splice variants and VEGF receptors in the myocardium and arterial vasculature of diabetic and non-diabetic patients with coronary artery disease.

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#17560756   2007/05/22 To Up

Thyroid hormone receptor and IGF1/IGFR systems: possible relations in the human heart.

Thyroid hormone (TH) and insulin growth factor 1 (IGF1) systems both play crucial roles in the regulation of cardiac remodeling and hypertrophy processes. The mediation of this regulation is attributed to specific thyroid hormone receptors (TRs) and to the IGF1 receptor (IGF1R). In humans, two TR genes are expressed in the heart, TRalpha and TRbeta. Each gene generates two isoforms: TRalpha1, TRalpha2 and TRbeta1, TRbeta2. The aim of the present work was to study the local thyroid hormone and IGF1 signaling in human myocardium through the evaluation of the gene expression of TRalpha1, TRalpha2, TRbeta1 and IGF1R among atrial and ventricular biopsies obtained from patients undergoing cardiac surgery. Moreover, we evaluated possible correlations between TR and IGF1/IGF1R systems. Eighteen clinically and biochemically euthyroid patients (aged 68.3+/-3.2years, mean+/-SEM) without overt heart failure (Ejection Fraction (EF), 46.4+/-2.8%; Left Ventricular End Diastolic Diameter (LVEDD), 54.3+/-1.2mm, mean+/-SEM; NYHA I-II) were enrolled in the study: 13 undergoing aorto-coronary bypass and 5 undergoing valve replacement (aortic/mitral valve). The examination of total RNA, using real time PCR (LightCycler Technology) confirmed the expression of specific mRNAs encoding TRalpha1, TRalpha2, TRbeta1 and both IGF1 and IGF1R. We found that the three TR genes are co-expressed in the human atrium and ventricle. The finding of a strong correlation among IGF1R and the three TR genes expressed in the atrium (p<0.001) and among the three TRs in the atrium (p<0.001) suggests the interesting possibility that the two systems, TRs and IGF1R could also be functionally associated.
Laura Sabatino, Enri Gliozheni, Sabrina Molinaro, Alessandra Bonotti, Sienne Azzolina, Georges Popoff, Angelo Carpi, Giorgio Iervasi

1527 related Products with: Thyroid hormone receptor and IGF1/IGFR systems: possible relations in the human heart.

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