Schulz Carl, Lemoine Marc D, Mearini Giulia, Koivumäki Jussi, Sani Jascha, Schwedhelm Edzard, Kirchhof Paulus, Ghalawinji Amer, Stoll Monika, Hansen Arne, Eschenhagen Thomas, Christ Torsten
Institute of Experimental Pharmacology and Toxicology (C.S., M.D.L., G.M., J.S., A.H., T.E., T.C.), University Medical Center Hamburg-Eppendorf, Germany.
German Center for Cardiovascular Research, Partner Site Hamburg/Kiel/Lübeck (C.S., M.D.L., G.M., J.S., E.S., P.K.).
Circ Arrhythm Electrophysiol. 2023 Mar;16(3):e011602. doi: 10.1161/CIRCEP.122.011602. Epub 2023 Feb 10.
Electrical remodeling in human persistent atrial fibrillation is believed to result from rapid electrical activation of the atria, but underlying genetic causes may contribute. Indeed, common gene variants in an enhancer region close to (paired-like homeodomain transcription factor 2) are strongly associated with atrial fibrillation, but the mechanism behind this association remains unknown. This study evaluated the consequences of deletion (PITX2) in human induced pluripotent stem cell-derived atrial cardiomyocytes.
CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/clustered regularly interspaced short palindromic repeat-associated 9) was used to delete in a healthy human iPSC line that served as isogenic control. Human induced pluripotent stem cell-derived atrial cardiomyocytes were differentiated with unfiltered retinoic acid and cultured in atrial engineered heart tissue. Force and action potential were measured in atrial engineered heart tissues. Single human induced pluripotent stem cell-derived atrial cardiomyocytes were isolated from atrial engineered heart tissue for ion current measurements.
PITX2 atrial engineered heart tissue beats slightly slower than isogenic control without irregularity. Force was lower in PITX2 than in isogenic control (0.053±0.015 versus 0.131±0.017 mN, n=28/3 versus n=28/4, PITX2 versus isogenic control; <0.0001), accompanied by lower expression of CACNA1C and lower L-type Ca current density. Early repolarization was weaker (action potential duration at 20% repolarization; 45.5±13.2 versus 8.6±5.3 ms, n=18/3 versus n=12/4, PITX2 versus isogenic control; <0.0001), and maximum diastolic potential was more negative (-78.3±3.1 versus -69.7±0.6 mV, n=18/3 versus n=12/4, PITX2 versus isogenic control; =0.001), despite normal inward rectifier currents (both I and I) and carbachol-induced shortening of action potential duration.
Complete PITX2 deficiency in human induced pluripotent stem cell-derived atrial cardiomyocytes recapitulates some findings of electrical remodeling of atrial fibrillation in the absence of fast beating, indicating that these abnormalities could be primary consequences of lower PITX2 levels.
人类持续性心房颤动的电重构被认为是由心房快速电激活引起的,但潜在的遗传原因可能也起作用。事实上,靠近PITX2(成对样同源域转录因子2)的增强子区域中的常见基因变异与心房颤动密切相关,但其背后的机制仍不清楚。本研究评估了人类诱导多能干细胞衍生的心房心肌细胞中PITX2缺失的后果。
使用CRISPR/Cas9(成簇规律间隔短回文重复序列/成簇规律间隔短回文重复序列相关蛋白9)在一个健康的人类诱导多能干细胞系中删除PITX2,该细胞系用作同基因对照。人类诱导多能干细胞衍生的心房心肌细胞用未过滤的视黄酸进行分化,并在心房工程心脏组织中培养。在心房工程心脏组织中测量力和动作电位。从心房工程心脏组织中分离出单个的人类诱导多能干细胞衍生的心房心肌细胞用于离子电流测量。
PITX2心房工程心脏组织的搏动比同基因对照稍慢,但无节律异常。PITX2组的力低于同基因对照组(0.053±0.015对0.131±0.017 mN,n = 28/3对n = 28/4,PITX2组对同基因对照组;<0.0001),同时伴有CACNA1C表达降低和L型钙电流密度降低。早期复极化较弱(复极化20%时的动作电位时程;45.5±13.2对8.6±5.3 ms,n = 18/3对n = 12/4,PITX2组对同基因对照组;<0.0001),最大舒张电位更负(-78.3±3.1对-69.7±0.6 mV,n = 18/3对n = 12/4,PITX2组对同基因对照组;=0.001),尽管内向整流电流(I和I)正常且卡巴胆碱诱导动作电位时程缩短。
人类诱导多能干细胞衍生的心房心肌细胞中完全缺乏PITX2可重现心房颤动电重构的一些发现,即在无快速搏动的情况下出现异常,这表明这些异常可能是PITX2水平降低的主要后果。