Unusual partners aid blood vessel growth


Insufficient oxygen to an area like the heart or legs, called hypoxia, is a cue to our bodies to make more blood vessels, and scientists have found some unusual partners are key to making that happen. They’ve found that two receptors on the surface of those cells come together then dive inside to enable the new growth, called angiogenesis, scientists report.

The endothelial cells that line existing blood vessels are essential to making new blood vessels, and they’ve found that two receptors on the surface of those cells come together then dive inside to enable the new growth, called angiogenesis, the Medical College of Georgia scientists report in the journal Nature Cell Biology.

As the name implies, vascular endothelial growth factor receptor 2, or VEGFR2, typically binds to VEGF, a signaling protein that enables new blood vessel growth, to go inside the cells. CTR1 enables copper, an essential mineral key to many important body functions, including angiogenesis, to also go inside.

Corresponding authors Dr. Masuko Ushio-Fukai, vascular biologist, and Dr. Tohru Fukai, vascular biologist and cardiologist, say that in the face of hypoxia, VEGF is naturally stimulated outside the cell, then in turn activates NADPH oxidase, a family of enzymes that generate reactive oxygen species, or ROS — in this case the good kind that enables cell signaling.

They’ve shown for the first time the step that happens next: ROS then quickly modifies CTR1, which prompts the VEGF receptor and this copper transporter to bind to each other on the cell surface and move inside the cell so the sustained VEGFR2 signaling that is essential to new blood vessel development happens.

When they knocked down the copper transporter, angiogenesis was severely impaired, Fukai says. They’ve also used the gene editing ability of CRISPR-Cas9 to make CTR1 unmodifiable and angiogenesis was again significantly reduced.


Story Source:
Materials provided by Medical College of Georgia at Augusta University. Original written by Toni Baker. Note: Content may be edited for style and length.


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