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A recent study led by researchers at the University of California in Los Angeles Health Sciences (UCLA) determined that the fluid that runs with a protein similar to COVID-19 through a 3D printed model to explain how the virus increases the risk of stroke.
COVID-19 was initially identified as a disease with severe respiratory symptoms, but little is known about how it increases the risk of stroke.
To improve on the findings, the UCLA researchers used a 3D-printed silicone model of blood vessels in the brain to mimic the forces generated by blood pushing through an artery that is abnormally narrow, a condition called intracranial atherosclerosis. They showed that as these forces act on the cells lining the artery, they increase the production of a molecule called angiotensin-converting enzyme 2, or ACE2, that the coronavirus uses to enter cells on the surface of blood vessels.
Dr. Jason Hinman, assistant professor of neurology at the David Geffen School of Medicine at UCLA and lead author of the study, stated that flux directly influences ACE2 expression. In addition to Hinman, the study authors are neurologists from the Geffen School of Medicine and scientists from UC San Francisco and the Veterans Health Administration. The article was published (PDF) in Stroke.
The UCLA researchers created the model using data from CT scans of blood vessels in a human brain. They then coated the inner surfaces of the models with endothelial cells, the type of cells that line human blood vessels. The models allowed the researchers to mimic the same forces that would act on real blood vessels during a COVID-19 infection.
To confirm whether coronavirus floating in the bloodstream could adhere to ACE2 in endothelial cells in the brain, the researchers produced copycat ‘virus’ fat molecules peppered with the spike proteins that the coronavirus uses to bind to ACE2. Previous research indicated that the coronavirus binds to endothelial cells in other organs, but it was unknown if that was also happening in the brain.
After creating the new model, the researchers confirmed that the particles did indeed interact with cells lining blood vessels, primarily in regions of the brain with higher levels of ACE2.
“This finding could explain the higher incidence of stroke seen in COVID-19 infections,” Hinman said.
Another discovery shows that when scientists analyzed which genes were turned on in endothelial cells after the coronavirus spike proteins attached to them, they found that the genes that were turned on were a specific set of immune response genes found in the blood vessels of the brain. cells, but not in endothelial cells of other organs in the body.
“There is a unique brain endothelial response to the virus that may be helpful in identifying patients who are at increased risk for stroke,” Hinman said.
The researchers intend to conduct follow-up studies using a live coronavirus in the 3D-printed blood vessel model, which would further confirm the results of the current study and clarify which COVID-19 patients may be at increased risk of stroke. .
