In a new study from NYU Grossman School of Medicine, researchers found abnormal crosstalk between blood platelets and cells lining blood vessels is one cause of deadly organ damage in patients with severe COVID-19.
They revealed the protein signals given off by platelets, cell fragments that contribute to blood clotting, create inflammation, abnormal clotting, and damage to vessels when exposed to the pandemic virus.
The study identified two related genes, S1000A8 and S1000A9, which are turned up in the platelets of COVID-19 patients, causing them to make more of myeloid-related proteins (MRP) 8 and 14.
Higher levels of the two proteins, known to operate as a pair and be present in large amounts in immune cells, were linked to higher levels of clotting and inflammation in vessels, greater disease severity, and longer hospital stays.
In support of the theory that platelets are at the core of blood vessel damage in COVID-19, the team also showed evidence that approved medications are known to block platelet activation via the platelet surface protein P2Y12 (clopidogrel or ticagrelor) reduced COVID-19-related inflammation in vessels.
They also found that COVID-19-exposed platelets change cells lining blood vessels (endothelial cells) largely through a protein called p-selectin, which makes platelets stickier and more likely to form clots.
These findings reveal a new role for platelets in COVID-19 blood vessel damage and may explain in large part what makes the COVID-19 virus so much more deadly than its relatives that cause the common cold.
If you care about severe COVID-19, please read studies about the cause of severe inflammation in COVID-19 and findings of this drug is effective in treating severe COVID-19.
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The study is published in Science Advances. One author of the study is Tessa Barrett, Ph.D.
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