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Mediators of SARS-CoV-2 entry are preferentially enriched in cardiomyocytes
Hereditas ( IF 2.7 ) Pub Date : 2021-01-04 , DOI: 10.1186/s41065-020-00168-4
Jing Yang , Tan Chen , Yafeng Zhou

Background The coronavirus disease 2019 (COVID-19) has spread rapidly around the world. In addition to common respiratory symptoms such as cough and fever, some patients also have cardiac injury, however, the mechanism of cardiac injury is not clear. In this study, we analyzed the RNA expression atlases of angiotensin-converting enzyme 2(ACE2), cathepsin B (CTSB) and cathepsin L (CTSL) in the human embryonic heart at single-cell resolution. Results The results showed that ACE2 was preferentially enriched in cardiomyocytes. Interestingly, serine protease transmembrane serine protease 2 (TMPRSS2) had less expression in cardiomyocytes, but CTSB and CTSL, which belonged to cell protease, could be found to be enriched in cardiomyocytes. The results of enrichment analysis showed that differentially expressed genes (DEGs) in ACE2-positive cardiomyocytes were mainly enriched in the processes of cardiac muscle contraction, regulation of cardiac conduction, mitochondrial respiratory chain, ion channel binding, adrenergic signaling in cardiomyocytes and viral transcription. Conclusions Our study suggests that both atrial and ventricular cardiomyocytes are potentially susceptible to severe acute respiratory syndrome coronavirus-2(SARS-CoV-2), and SARS-CoV-2 may enter ventricular cardiomyocytes using CTSB/CTSL for S protein priming. This may be the partial cellular mechanism of cardiac injury in patients with COVID-19.

中文翻译:

SARS-CoV-2进入的介质优先富集在心肌细胞中

背景 2019 年冠状病毒病 (COVID-19) 已在世界范围内迅速传播。部分患者除咳嗽、发热等常见呼吸道症状外,还有心脏损伤,但心脏损伤机制尚不明确。在这项研究中,我们以单细胞分辨率分析了人胚胎心脏中血管紧张素转换酶 2 (ACE2)、组织蛋白酶 B (CTSB) 和组织蛋白酶 L (CTSL) 的 RNA 表达图谱。结果结果显示ACE2优先富集在心肌细胞中。有趣的是,丝氨酸蛋白酶跨膜丝氨酸蛋白酶2(TMPRSS2)在心肌细胞中表达较少,但CTSB和CTSL属于细胞蛋白酶,在心肌细胞中富集。富集分析结果表明,ACE2阳性心肌细胞中差异表达基因(DEGs)主要富集在心肌收缩、心脏传导调节、线粒体呼吸链、离子通道结合、心肌细胞肾上腺素能信号传导和病毒转录等过程中。结论 我们的研究表明,心房和心室心肌细胞均可能对严重急性呼吸综合征冠状病毒-2(SARS-CoV-2)敏感,SARS-CoV-2 可能使用 CTSB/CTSL 进行 S 蛋白启动进入心室心肌细胞。这可能是 COVID-19 患者心脏损伤的部分细胞机制。心肌细胞中的肾上腺素能信号传导和病毒转录。结论 我们的研究表明,心房和心室心肌细胞均可能对严重急性呼吸综合征冠状病毒-2(SARS-CoV-2)敏感,SARS-CoV-2 可能使用 CTSB/CTSL 进行 S 蛋白启动进入心室心肌细胞。这可能是 COVID-19 患者心脏损伤的部分细胞机制。心肌细胞中的肾上腺素能信号传导和病毒转录。结论我们的研究表明,心房和心室心肌细胞都可能对严重急性呼吸综合征冠状病毒-2(SARS-CoV-2)敏感,并且 SARS-CoV-2 可能使用 CTSB/CTSL 进行 S 蛋白启动进入心室心肌细胞。这可能是 COVID-19 患者心脏损伤的部分细胞机制。
更新日期:2021-01-04
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