Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Stretch-dependent genes in vascular smooth muscle cells


ABSTRACT: Vascular smooth muscle cells (VSMCs) respond to biomechanical stretch with specific changes in gene expression which govern the phenotype of these cells. The mechanotransducer zyxin is a potential candidate for regulating the expression of such genes. Using microarrays, we compared stretch-induced gene expression in wild type and zyxin-null VSMCs to define such changes in detail. Wild type (WT) and zyxin-null VSMCs were stretched at 10% cyclic elongation for 6 hours and the changes in gene expression were compared under static and stretched conditions. Up to 3 biological replicates were used for each of the 4 sample types.

ORGANISM(S): Mus musculus

SUBMITTER: Carsten Sticht 

PROVIDER: E-GEOD-60447 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Loss of the mechanotransducer zyxin promotes a synthetic phenotype of vascular smooth muscle cells.

Ghosh Subhajit S   Kollar Branislav B   Nahar Taslima T   Suresh Babu Sahana S   Wojtowicz Agnieszka A   Sticht Carsten C   Gretz Norbert N   Wagner Andreas H AH   Korff Thomas T   Hecker Markus M  

Journal of the American Heart Association 20150612 6


<h4>Background</h4>Exposure of vascular smooth muscle cells (VSMCs) to excessive cyclic stretch such as in hypertension causes a shift in their phenotype. The focal adhesion protein zyxin can transduce such biomechanical stimuli to the nucleus of both endothelial cells and VSMCs, albeit with different thresholds and kinetics. However, there is no distinct vascular phenotype in young zyxin-deficient mice, possibly due to functional redundancy among other gene products belonging to the zyxin famil  ...[more]

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