Key result
Rheumatoid arthritis iPSC-derived cardiomyocytes exhibit impaired calcium transients and decreased contractility versus controls.
Why the study?
Cardiovascular disease is a leading cause of morbidity in rheumatoid arthritis patients, motivating the generation and characterization of cardiomyocytes from RA patient-derived iPSCs.
Answers are grounded in this paper and cite their sources.
Functional cardiomyocytes can be successfully generated from pathogenic synovial cells of RA patients, revealing reduced contractility and altered calcium handling that may model RA-associated cardiac involvement.
Cardiovascular disease is a leading cause of morbidity in rheumatoid arthritis (RA) patients. This study aimed to generate and characterise cardiomyocytes from induced pluripotent stem cells (iPSCs) of RA patients. Fibroblast-like synoviocytes (FLSs) from patients with RA and osteoarthritis (OA) were successfully reprogrammed into RA-iPSCs and OA-iPSCs, respectively. The pluripotency of iPSCs was confirmed by quantitative reverse transcription-polymerase chain reaction and immunofluorescence staining. Established iPSCs were differentiated into cardiomyocytes using a small molecule-based monolayer differentiation protocol. Within 12 days of cardiac differentiation from patient-specific and control-iPSCs, spontaneously beating cardiomyocytes (iPSC-CMs) were observed. All iPSC-CMs exhibited a reliable sarcomeric structure stained with antibodies against cardiac markers and similar expression profiles of cardiac-specific genes. Intracellular calcium signalling was recorded to compare calcium-handling properties among cardiomyocytes differentiated from the three groups of iPSCs. RA-iPSC-CMs had a lower amplitude and a shorter duration of calcium transients than the control groups. Peak tangential stress and the maximum contractile rate were also decreased in RA-iPSC-CMs, suggesting that contractility was reduced. This study demonstrates the successful generation of functional cardiomyocytes from pathogenic synovial cells in RA patients through iPSC reprogramming. Research using RA-iPSC-CMs might provide an opportunity to investigate the pathophysiology of cardiac involvement in RA.
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Lee et al. (2016) studied Rheumatoid arthritis (n=9). iPSC reprogramming and cardiac differentiation vs. Osteoarthritis and healthy control cells was evaluated on Calcium-handling properties and contractility of iPSC-derived cardiomyocytes. Cardiomyocytes derived from rheumatoid arthritis patient-specific iPSCs exhibited a lower amplitude and shorter duration of calcium transients, as well as decreased contractility, compared to control cells.
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