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Papers In Press, published online ahead of print January 29, 2001
Cardiovascular Division, Dept. of Medicine, Brigham and Women's Hospital, Boston, MA 02115
Corresponding Author: rlee{at}rics.bwh.harvard.edu
In the mechanically active environment of the artery, cells sense mechanical stimuli and regulate extracellular matrix structure. In this study, we explored the changes in synthesis of proteoglycans by vascular smooth muscle cells in response to precisely controlled mechanical strains. Strain increased mRNA for versican (3.2 fold), biglycan (2.0 fold), and perlecan (2.0 fold), while decorin mRNA levels decreased to a third of control levels. Strain also increased versican, biglycan, and perlecan core proteins, with a concomitant decrease in decorin core protein. Deformation did not alter the hydrodynamic size of proteoglycans as evidenced by molecular sieve chromatography, but increased sulfate incorporation in both chondroitin/dermatan sulfate proteoglycans and heparan sulfate proteoglycans (p<0.05 for both). Using DNA microarrays, we also identified the gene for the hyaluronan linking protein TSG-6 as mechanically-induced in smooth muscle cells. Northern analysis confirmed a 4.0 fold increase in steady state mRNA for TSG-6 following deformation. Size exclusion chromatography under associative conditions showed that versican-hyaluronan aggregation was enhanced following deformation. These data demonstrate that mechanical deformation increases specific vascular smooth muscle cell proteoglycan synthesis and aggregation, indicating a highly coordinated extracellular matrix response to biomechanical stimulation.
J. Biol. Chem, 10.1074/jbc.M010556200
Submitted on November 22, 2000
Revised on January 11, 2001
Accepted on January 29, 2001
Mechanical strain induces specific changes in the synthesis and organization of proteoglycans by vascular smooth muscle cells
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