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Two hundred fifty ng of total RNA per sample was used for cRNA production by the RiboPure TMRNA extraction kit (Ambion, Grand Island, NY, USA). Samples with optical density ratio 260/280 > 1.8 and RNA integrity number > 7.0 were selected and sent for microarray processing. RNA quality was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies Inc, Santa Clara, CA, USA). RNAs were extracted from the myocardial samples by using a RiboPureTM kit (Ambion, Grand Island, NY, USA) according to the manufacturer's protocol. After excision, some atrial tissues were immediately frozen in liquid nitrogen and stored at –80 Celsius, and some were immediately fixed in 3.7% buffered formalin, then embedded in paraffin, and stored until later study for hematoxylin/eosin staining.
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Specimen StorageĪtrial tissues of non-ischemic MR patients and aortic valve disease patients with heart failure were sampled from the left atrial free wall during surgery. Six normal adult left atrial tissue samples (24-year-old Caucasian male, 27-year-old Caucasian male, 30-year-old Asian male, 60-year-old Caucasian female, 76-year-old Caucasian female and 77-year-old Caucasian male) were purchased from BioChain, Newark, CA, USA, and these 6 normal atrial tissues were used as the normal controls for gene analysis. Written informed consent was obtained from each study patient, and the study protocol conforms to the ethical guidelines of the 1975 Declaration of Helsinki as reflected in a priori approval by the Institutional Review Board of Chang Gung Memorial Hospital (100-0067C). Exclusion factors include previous myocardial infarction, febrile disorder, infectious or inflammatory disease, autoimmune disease, malignancy, acute or chronic viral hepatitis or use of immunosuppressive drugs. This study enrolled 14 patients with symptomatic severe non-ischemic MR in sinus rhythm (age: 58☙ years), and 7 age-matched patients with symptomatic severe aortic valve disease in sinus rhythm (age: 63☗ years aortic stenosis in 1, aortic regurgitation in 4, combined aortic stenoregurgitation in 2). The results of this study may recognize some of the differentially expressed genes and related pathways that contribute to the left atrial myocyte hypertrophy in patients with MR. The left atrial myocardium of patients with severe aortic valve disease was also used as a reference for gene analysis of the significant pathways as the left atrial size was smaller in patients with aortic valve disease compared to MR patients. In this study, we aimed to systemically explore the crucial differences in the RNA expression pattern between the left atrial myocardium of MR patients and normal subjects, and the molecular regulatory mechanisms and functional biological pathways related to the atrial myocyte hypertrophy using high-density oligonucleotide microarrays and enrichment analysis. However, the molecular regulatory mechanisms and functional biological pathways related to the left atrial myocyte hypertrophy of MR patients remain unclear. Structural remodeling associated with atrial enlargement, especially pathological hypertrophy of myocytes, developed in the left atrial myocardium of patients with MR. Left atrial enlargement has prognostic significance in MR patients undergoing mitral valve surgery. Mitral regurgitation (MR) is an important cause of heart failure related to valvular heart disease.