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Single Cell RNAseq and VDJ sequence of ACE2 reactive and non-reactive B-cells isolated from COVID-19 patients peripheral blood

ABSTRACT: Single Cell RNAseq and VDJ sequence of ACE2 reactive and non-reactive B-cells isolated from COVID-19 patients peripheral blood

PROVIDER: PRJNA737416 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR14804700.fastq.gz	Fastqsanger.gz
	SRR14804701.fastq.gz	Fastqsanger.gz
	SRR14804702.fastq.gz	Fastqsanger.gz
	SRR14804703.fastq.gz	Fastqsanger.gz

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Single Cell RNAseq and VDJ sequence of ACE2 reactive and non-reactive B-cells isolated from COVID-19 patients peripheral blood

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The SARS-CoV-2 receptor ACE2 is expressed in mouse pericytes but not endothelial cells – implications for COVID-19 vascular research

Project description:Humanized mouse models and mouse-adapted SARS-CoV-2 virus are increasingly used to study COVID-19 pathogenesis, and it is therefore important to learn where the SARS-CoV-2 receptor ACE2 is expressed. Here we mapped ACE2 expression during mouse postnatal development and in adulthood. Pericytes in the central nervous system, heart and pancreas express ACE2 strongly, as do perineurial and adrenal fibroblasts, whereas endothelial cells do not at any location analyzed. In a number of other organs pericytes do not express ACE2, including in the lung where ACE2 instead is expressed in bronchial epithelium and alveolar type-II cells. The onset of ACE2 expression is organ-specific: in bronchial epithelium already at birth, in brain pericytes before and in heart pericytes after postnatal day 10.5. Establishing the vascular localization of ACE2 expression is central to correctly interpret data from modelling COVID-19 in the mouse and may shed light on the cause of vascular COVID-19 complications.

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Project description:Several humanized ACE2 (hACE2) mouse models have been developed for COVID-19 studies. Insertion of hACE2 at mouse Ace2 locus enables the utilization of endogenous promoter to drive its expression, better reflecting ACE2 abundance in various cell types and tissues. However, the relatively low expression of hACE2 in these mice may limit their fidelity in mimicking COVID-19 manifestations in humans and hinder their application in viral studies. In this study, we generated four hACE2 mouse models using different strategies for hACE2 expression. We found that the position of the β-globin intron within hACE2 cassette could have contrasting effects on hACE2 expression, with its placement downstream of hACE2 significantly increasing its transcription. Western blot analysis demonstrated that optimizing hACE2 codon usage further enhanced translation efficiency from all tested tissue. Consistent with elevated hACE2 expression, opt-hACE2 mice displayed more active immune response and severe COVID-19 phenotypes following SARS-CoV-2 challenging compared to other hACE2 mouse models. Thus, our study has elucidated the dual role of β-globin element in transgene expression, and highlighted that mice with optimized hACE2 codon preference could serve as a better model for SARS-CoV-2 studies.

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