Andersen Group, Department of Clinical Biochemistry, Odense University Hospital, Odense, Denmark.
Clinical Institute, University of Southern Denmark, Odense, Denmark.
Basic Res Cardiol. 2023 Mar 2;118(1):8. doi: 10.1007/s00395-023-00979-2.
Whereas cardiomyocytes (CMs) in the fetal heart divide, postnatal CMs fail to undergo karyokinesis and/or cytokinesis and therefore become polyploid or binucleated, a key process in terminal CM differentiation. This switch from a diploid proliferative CM to a terminally differentiated polyploid CM remains an enigma and seems an obstacle for heart regeneration. Here, we set out to identify the transcriptional landscape of CMs around birth using single cell RNA sequencing (scRNA-seq) to predict transcription factors (TFs) involved in CM proliferation and terminal differentiation. To this end, we established an approach combining fluorescence activated cell sorting (FACS) with scRNA-seq of fixed CMs from developing (E16.5, P1, and P5) mouse hearts, and generated high-resolution single-cell transcriptomic maps of in vivo diploid and tetraploid CMs, increasing the CM resolution. We identified TF-networks regulating the G2/M phases of developing CMs around birth. ZEB1 (Zinc Finger E-Box Binding Homeobox 1), a hereto unknown TF in CM cell cycling, was found to regulate the highest number of cell cycle genes in cycling CMs at E16.5 but was downregulated around birth. CM ZEB1-knockdown reduced proliferation of E16.5 CMs, while ZEB1 overexpression at P0 after birth resulted in CM endoreplication. These data thus provide a ploidy stratified transcriptomic map of developing CMs and bring new insight to CM proliferation and endoreplication identifying ZEB1 as a key player in these processes.
虽然胎儿心脏中的心肌细胞 (CMs) 会分裂,但出生后的 CMs 无法进行核分裂和/或胞质分裂,从而成为多倍体或双核细胞,这是 CM 终末分化的关键过程。这种从二倍体增殖型 CM 向终末分化的多倍体 CM 的转变仍然是一个谜,似乎是心脏再生的一个障碍。在这里,我们使用单细胞 RNA 测序 (scRNA-seq) 来鉴定出生前后 CMs 的转录组图谱,以预测参与 CM 增殖和终末分化的转录因子 (TFs)。为此,我们建立了一种方法,将荧光激活细胞分选 (FACS) 与发育中 (E16.5、P1 和 P5) 小鼠心脏固定 CMs 的 scRNA-seq 相结合,并生成体内二倍体和四倍体 CMs 的高分辨率单细胞转录组图谱,从而提高了 CM 的分辨率。我们确定了调节出生前后发育中 CM 中 G2/M 期的 TF 网络。ZEB1(锌指 E-盒结合同源盒 1)是 CM 细胞周期中一个未知的 TF,在 E16.5 的有丝分裂期 CM 中被发现调控数量最多的细胞周期基因,但在出生前后下调。CM ZEB1 敲低减少了 E16.5 CM 的增殖,而出生后 P0 时 ZEB1 的过表达导致 CM 核内复制。这些数据因此提供了发育中 CM 的倍性分层转录组图谱,并为 CM 增殖和核内复制提供了新的见解,确定 ZEB1 是这些过程中的关键参与者。