Human cardiac myocytes undergo degeneration, cytolysis, and necrosis in a number of clinical disease conditions such as myocarditis, dilated cardiomyopathy, and during episodes of cardiac allograft rejection. The precise cellular, biochemical, and molecular mechanisms that lead to such abnormalities in myocytes have been difficult to investigate because at present it is not possible to obtain and maintain viable cell cultures of human adult cardiac myocytes in vitro. However, human fetal cardiac myocytes are relatively easy to maintain and culture in vitro, but their limited availability and growth, variability from one preparation to another, and varying degrees of contamination with endothelial and epithelial cell types have made it difficult to obtain reliable data on the effect of cardiotropic viruses and cardiotoxic drugs on such myocytes. These thoughts prompted us to attempt to derive a cell line of human cardiac origin. Highly enriched human fetal cardiac myocytes were transfected with the plasmids pSV2Neo and pRSVTAg and gave rise to a cell line (W1) which has been maintained in culture for 1 yr. Morphologic and phenotypic analyses of W1 cells by flow microfluorometry and immunoperoxidase techniques indicate that the W1 cell line shares many properties of human fetal cardiac myocytes, but appears not to react with specific antibodies known to react with markers unique to human endothelial, epithelial, skeletal muscle, and dendritic cells. These preliminary data suggest that the W1 cells may provide a unique source of an established cell line that shares many properties ascribed to human cardiac myocytes.
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http://dx.doi.org/10.1007/BF02630896 | DOI Listing |
Circ Res
January 2025
Center for Genetic Medicine, the Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, China (X.H., J.Z., C.X., R.C., P.J., X.J., P.H.).
Background: Cardiac ischemia/reperfusion disrupts plasma membrane integrity and induces various types of programmed cell death. The ESCRT (endosomal sorting complex required for transport) proteins, particularly AAA-ATPase Vps4a (vacuolar protein sorting 4a), play an essential role in the surveillance of membrane integrity. However, the role of ESCRT proteins in the context of cardiac injury remains unclear.
View Article and Find Full Text PDFBackground: Patients with arrhythmogenic cardiomyopathy (ACM) due to pathogenic variants in , the gene for the desmosomal protein plakophilin-2, are being enrolled in gene therapy trials designed to replace the defective allele via adeno-associated viral (AAV) transduction of cardiac myocytes. Evidence from experimental systems and patients indicates that ventricular myocytes in ACM have greatly reduced electrical coupling at gap junctions and reduced Na current density. In previous AAV gene therapy trials, <50% of ventricular myocytes have generally been transduced.
View Article and Find Full Text PDFArrhythmogenic cardiomyopathy (ACM) is a genetic form of heart failure that affects 1 in 5000 people globally and is caused by mutations in cardiac desmosomal proteins including , and Individuals with ACM suffer from ventricular arrhythmias, sudden cardiac death, and heart failure. There are few effective treatments and heart transplantation remains the best option for many affected individuals. Here we performed single nucleus RNA sequencing (snRNAseq) and spatial transcriptomics on myocardial samples from patients with ACM and control donors.
View Article and Find Full Text PDFJ Transl Med
January 2025
State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, School of Medicine, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.
Background: Dilated cardiomyopathy (DCM) is one of the most common causes of heart failure. Infiltration and alterations in non-cardiomyocytes of the human heart involve crucially in the occurrence of DCM and associated immunotherapeutic approaches.
Methods: We constructed a single-cell transcriptional atlas of DCM and normal patients.
Zhonghua Bing Li Xue Za Zhi
January 2025
Department of Pathology, the Seventh Medical Center of People's Liberation Army of China General Hospital, Beijing100700, China.
To analyze the morphologic changes and the extent of severity in end-stage heart disease; and to explore the correlation with their clinical features. Twelve cases of recipients who underwent pediatric cardiac allograft transplantation were collected from May 2022 to November 2023 at the Seventh Medical Center of People's Liberation Army of China General Hospital. Gross pathologic examinations were performed and morphological changes were observed under a light microscope after HE, Masson's trichrome, and reticulin staining.
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