A study conducted by the University of California- Los Angeles Health Sciences (UCLA) using 3D-printed ‘blood vessels’ has tried to explain how COVID-19 virus increases the risk of stroke.
Researchers did a study about the running fluid spiked with a COVID-19-like protein on a 3D-printed model of the arteries of a patient who had suffered a stroke. Although COVID-19 was first identified by its severe respiratory symptoms, little is understood about how the virus increases the danger for stroke.
To enhance the findings, UCLA researchers used a 3D-printed silicone model of blood vessels within the brain to mimic the forces generated by blood pushing through an artery that’s abnormally narrowed, a condition called intracranial atherosclerosis.
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They showed that as those forces act on the cells lining the artery, and increases the assembly of a molecule called angiotensin-converting enzyme 2, or ACE2, which the coronavirus uses to enter cells on the surface of blood vessels.
Dr Jason Hinman, an professor of neurology at the David Geffen School of drugs at UCLA and the study’s senior author claimed that the flow directly influences ACE2 expression.
The paper was published (PDF) in Stroke.
UCLA researchers created the model using data from CT scans of blood vessels during a human brain. They then lined the inner surfaces of the models with endothelial cells, the sort of cells that line human blood vessels.
The models enabled the researchers to mimic an equivalent forces that might act on real blood vessels during a COVID-19 infection. To verify whether coronavirus bobbing along within the bloodstream could latch onto the ACE2 on the endothelial cells within the brain, researchers produced imitation ‘viruses’ fatty molecules studded with the spike proteins that coronavirus uses to bind to ACE2.
Previous research works had indicated that the coronavirus binds to endothelial cells in other organs, but it had been unknown whether that was also happening within the brain.
After creating the new model, researchers confirmed the particles did indeed interact with the cells lining the vessel, mostly within the regions of the brain with higher levels of ACE2.
“This finding could explain the increased incidence of strokes seen in COVID-19 infections,” Hinman said.
Another discovery shows that when the scientists analyzed which genes were turned on in the endothelial cells after the coronavirus spike proteins bound to them, they found that the genes that were activated were a specific set of immune-response genes that are found in brain blood vessel cells, but not in endothelial cells from other organs of the body.
“There’s a singular brain endothelial response to the virus which will be helpful in identifying patients who have a better risk for stroke,” Hinman said.
The researchers aimed to conduct follow-up studies employing a live coronavirus within the 3D-printed vessel model, which might further confirm the results of the prevailing study and clarify which COVID-19 patients may have a better risk for stroke.