Single-cell analysis reveals transcriptomic and epigenomic impacts on the maternal-fetal interface following SARS-CoV-2 infection.
Lin GaoVrinda MathurSabrina Ka Man TamXuemeng ZhouMing Fung CheungLu Yan ChanGuadalupe Estrada GutierrezBo Wah LeungSakita MoungmaithongChi Chiu WangLiona Chiu Yee PoonDanny Chi Yeu LeungPublished in: Nature cell biology (2023)
During pregnancy the maternal-fetal interface plays vital roles in fetal development. Its disruption is frequently found in pregnancy complications. Recent studies show increased incidences of adverse pregnancy outcomes in patients with COVID-19; however, the mechanism remains unclear. Here we analysed the molecular impacts of SARS-CoV-2 infection on the maternal-fetal interface. Generating bulk and single-nucleus transcriptomic and epigenomic profiles from patients with COVID-19 and control samples, we discovered aberrant immune activation and angiogenesis patterns in distinct cells from patients. Surprisingly, retrotransposons were also dysregulated in specific cell types. Notably, reduced enhancer activities of LTR8B elements were functionally linked to the downregulation of pregnancy-specific glycoprotein genes in syncytiotrophoblasts. Our findings revealed that SARS-CoV-2 infection induced substantial changes to the epigenome and transcriptome at the maternal-fetal interface, which may be associated with pregnancy complications.
Keyphrases
- pregnancy outcomes
- single cell
- rna seq
- pregnant women
- high throughput
- end stage renal disease
- cell proliferation
- dna methylation
- genome wide
- ejection fraction
- risk factors
- gene expression
- birth weight
- respiratory syndrome coronavirus
- chronic kidney disease
- signaling pathway
- endothelial cells
- transcription factor
- high glucose
- emergency department
- body mass index
- peritoneal dialysis
- vascular endothelial growth factor
- sars cov
- drug induced
- binding protein