Transcriptomes in healthy and CHB fetal hearts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA498116 | ENA |
REPOSITORIES: ENA
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Project description:Given that diseases associated with anti-SSA/Ro autoantibodies such as systemic lupus erythematosus and Sjögren’s syndrome are linked with an upregulation of IFN and type I IFN-stimulated genes, including Sialic Acid-Binding Ig-Like Lectin 1 (Siglec-1), a receptor on monocytes/macrophages, recent attention has focused on a potential role for IFN and IFN-stimulated genes in the pathogenesis of congenital heart block (CHB). Accordingly, three approaches were leveraged to address the association of IFN, IFN-stimulated genes, and the phenotype of macrophages in affected fetal cardiac tissue: a) cultured healthy human macrophages transfected with hY3, an anti-SSA/Ro-associated single-stranded RNA, b) RNA isolated from freshly sorted human leukocytes/macrophages after Langendorff perfusion of three fetal hearts dying with CHB and three healthy gestational age-matched hearts, and c) autopsy tissue from three additional human CHB hearts and one healthy heart. TLR ligation of macrophages with hY3 led to the upregulation of a panel of IFN transcripts, including SIGLEC1, a result corroborated using qPCR. Utilizing independent and agnostic bioinformatics approaches, CD45+CD11c+ and CD45+CD11c- human leukocytes flow sorted from the CHB hearts highly expressed type I IFN response genes inclusive of SIGLEC1. Furthermore, Siglec-1 expression was identified in the septal region of several affected fetal hearts. These data now provide a link between IFN, IFN-stimulated genes, and the inflammatory and possibly fibrosing components of CHB, positioning Siglec-1-positive macrophages as integral to the process.
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