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miR-98 Regulates TMPRSS2 Expression in Human Endothelial Cells: Key Implications for COVID-19
Alessandro Matarese1,2, Jessica Gambardella1,3,4, Celestino Sardu5,6
1Department of Medicine, Wilf Family Cardiovascular Research Institute, Einstein-Institute for Aging Research, Albert Einstein College of Medicine, New York, NY 10461, USA.
Abstract:
The two main co-factors needed by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to enter human cells are angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). Here, we focused on the study of microRNAs that specifically target TMPRSS2. Through a bioinformatic approach, we identified miR-98-5p as a suitable candidate. Since we and others have shown that endothelial cells play a pivotal role in the pathogenesis of the coronavirus disease 2019 (COVID-19), we mechanistically validated miR-98-5p as a regulator of TMPRSS2 transcription in two different human endothelial cell types, derived from the lung and from the umbilical vein. Taken together, our findings indicate that TMPRSS2 represents a valid target in COVID-19 treatment, which may be achieved by specific non-coding-RNA approaches.
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