| Autor: |
Pham TP; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands., van Bergen AS; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands., Kremer V; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands., Glaser SF; Institute of Cardiovascular Regeneration, Goethe University, 60590 Frankfurt am Main, Germany.; German Center for Cardiovascular Research DZHK, Partner Site Frankfurt Rhine-Main, 60590 Frankfurt am Main, Germany., Dimmeler S; Institute of Cardiovascular Regeneration, Goethe University, 60590 Frankfurt am Main, Germany.; German Center for Cardiovascular Research DZHK, Partner Site Frankfurt Rhine-Main, 60590 Frankfurt am Main, Germany., Boon RA; Department of Physiology, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands.; Institute of Cardiovascular Regeneration, Goethe University, 60590 Frankfurt am Main, Germany.; German Center for Cardiovascular Research DZHK, Partner Site Frankfurt Rhine-Main, 60590 Frankfurt am Main, Germany. |
| Abstrakt: |
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. |
