Journal
INTEGRATIVE BIOLOGY
Volume 3, Issue 11, Pages 1063-1070Publisher
OXFORD UNIV PRESS
DOI: 10.1039/c1ib00061f
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Funding
- Defense Advanced Research Projects Agency PREVENT through the Office of Naval Research [N66001-08-C-2036]
- Nanoscale Science and Engineering Center of the National Science Foundation under NSF [PHY-0117795]
- Harvard Materials Research Science and Engineering Center under NSF [DMR-0213805]
- NSF [1005022]
- NIH [1 R01 HL079126-01A2]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL079126] Funding Source: NIH RePORTER
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The physiologic role of smooth muscle structure in defining arterial function is poorly understood. We aimed to elucidate the relationship between vascular smooth muscle architecture and functional contractile output. Using microcontact printing and muscular thin film technology, we engineered in vitro vascular tissues with strictly defined geometries and tested their contractile function. In all tissues, vascular smooth muscle cells (VSMCs) were highly aligned with in vivo-like spindle architecture, and contracted physiologically in response to stimulation with endothelin-1. However, tissues wherein the VSMCs were forced into exaggerated spindle elongation exerted significantly greater contraction force per unit cross-sectional area than those with smaller aspect ratios. Moreover, this increased contraction did not occur in conjunction with an increase in traditionally measured contractile phenotype markers. These results suggest that cellular architecture within vascular tissues plays a significant role in conferring tissue function and that, in some systems, traditional phenotype characterization is not sufficient to define a functionally contractile population of VSMCs.
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