Volume 89 Issue 50 | p. 27 | Concentrates
Issue Date: December 12, 2011

Hardened Arteries Have Leaky Tissue

Gaps between cells in stiff blood vessels could be new target for atherosclerosis therapies
Department: Science & Technology
Keywords: hardened arteries, atherosclerosis, cell contractility, Rho-associated kinase, cell mechanics
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Immune cells can sneak between blood-vessel cells that have pulled apart from each other on stiff tissue scaffolding. The enzyme ROCK regulates cell contraction via proteins such as actin.
Credit: B. Strauch/Sci. Transl. Med.
Immune cells can sneak between blood vessel cells that have pulled apart from each other on stiff tissue scaffolding; the enzyme ROCK regulates cell contraction via proteins such as actin.
 
Immune cells can sneak between blood-vessel cells that have pulled apart from each other on stiff tissue scaffolding. The enzyme ROCK regulates cell contraction via proteins such as actin.
Credit: B. Strauch/Sci. Transl. Med.

Closing the gaps between cells that line patients’ arteries could be a new strategy to treat atherosclerosis, a condition that often leads to heart attacks and strokes (Sci. Transl. Med., DOI: 10.1126/scitranslmed.3002761). Increased permeability between arterial cells allows cholesterol and immune cells to accumulate in blood-vessel walls, leading to dangerous plaque formation. Using fluorescent dyes, engineered tissue, and aortas from mice, Cynthia A. Reinhart-King and coworkers at Cornell University showed that hardened arteries—those with stiff tissue scaffolding—cause cells embedded within them to increase their contractile forces and pull apart from one another. To prevent this cell contraction, the researchers focused on rho-associated kinase (ROCK), an enzyme that helps regulate cell forces and movement via structural proteins such as actin. By inhibiting ROCK with the small molecule Y-27632, Reinhart-King’s group decreased the average cell-cell gap in hardened synthetic tissue by about 2 µm. Whether ROCK itself is the best target for future therapeutics rather than other molecules further downstream in the ROCK signaling pathway remains to be seen, comments biological engineer Douglas A. Lauffenburger of MIT, but the results of this study are “enticing.”

 
Chemical & Engineering News
ISSN 0009-2347
Copyright © American Chemical Society

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