Lncrna aerrie is required for sulfatase 1 expression, but not for endothelial‐to‐mesenchymal transition

Tan Phát Pham, Anke S. van Bergen, Veerle Kremer, Simone F. Glaser, Stefanie Dimmeler, Reinier A. Boon*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Endothelial cells can acquire a mesenchymal phenotype through a process called Endothelial‐to‐Mesenchymal transition (EndMT). This event is found in embryonic development, but also in pathological conditions. Blood vessels lose their ability to maintain vascular homeostasis and ultimately develop atherosclerosis, pulmonary hypertension, or fibrosis. An increase in inflammatory signals causes an upregulation of EndMT transcription factors, mesenchymal markers, and a decrease in endothelial markers. In our study, we show that the induction of EndMT results in an increase in long non‐coding RNA AERRIE expression. JMJD2B, a known EndMT regulator, induces AERRIE and subsequently SULF1. Silencing of AERRIE shows a partial regulation of SULF1 but showed no effect on the endothelial and mesenchymal markers. Additionally, the overexpression of AERRIE results in no significant changes in EndMT markers, suggesting that AERRIE is marginally regulating mesenchymal markers and transcription factors. This study identifies AERRIE as a novel factor in EndMT, but its mechanism of action still needs to be elucidated.
Original languageEnglish
Article number8088
JournalInternational Journal of Molecular Sciences
Volume22
Issue number15
DOIs
Publication statusPublished - 1 Aug 2021

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