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Verfasst von:Ghosh, Subhajit [VerfasserIn]   i
 Kollár, Branislav [VerfasserIn]   i
 Nahar, Taslima [VerfasserIn]   i
 Sticht, Carsten [VerfasserIn]   i
 Gretz, Norbert [VerfasserIn]   i
 Wagner, Andreas H. [VerfasserIn]   i
 Korff, Thomas [VerfasserIn]   i
 Hecker, Markus [VerfasserIn]   i
Titel:Loss of the mechanotransducer zyxin promotes a synthetic phenotype of vascular smooth muscle cells
Verf.angabe:Subhajit Ghosh, PhD; Branislav Kollar, MD; Taslima Nahar, MSc; Sahana Suresh Babu, PhD; Agnieszka Wojtowicz, PhD; Carsten Sticht, PhD; Norbert Gretz, MD, PhD; Andreas H. Wagner, PhD; Thomas Korff, PhD; Markus Hecker, PhD, DSc
E-Jahr:2015
Jahr:June 2015
Umfang:27 S.
Fussnoten:Gesehen am 04.01.2018
Titel Quelle:Enthalten in: American Heart AssociationJournal of the American Heart Association
Ort Quelle:New York, NY : Association, 2012
Jahr Quelle:2015
Band/Heft Quelle:4(2015,6) Artikel-Nummer e001712, 27 Seiten
ISSN Quelle:2047-9980
Abstract:Background 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 family. Analyzing zyxin function in VSMCs at the cellular level might thus offer a better mechanistic insight. We aimed to characterize zyxin‐dependent changes in gene expression in VSMCs exposed to biomechanical stretch and define the functional role of zyxin in controlling the resultant VSMC phenotype. Methods and Results DNA microarray analysis was used to identify genes and pathways that were zyxin regulated in static and stretched human umbilical artery-derived and mouse aortic VSMCs. Zyxin‐null VSMCs showed a remarkable shift to a growth‐promoting, less apoptotic, promigratory and poorly contractile phenotype with ≈90% of the stretch‐responsive genes being zyxin dependent. Interestingly, zyxin‐null cells already seemed primed for such a synthetic phenotype, with mechanical stretch further accentuating it. This could be accounted for by higher RhoA activity and myocardin‐related transcription factor‐A mainly localized to the nucleus of zyxin‐null VSMCs, and a condensed and localized accumulation of F‐actin upon stretch. Conclusions At the cellular level, zyxin is a key regulator of stretch‐induced gene expression. Loss of zyxin drives VSMCs toward a synthetic phenotype, a process further consolidated by exaggerated stretch.
DOI:doi:10.1161/JAHA.114.001712
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: http://dx.doi.org/10.1161/JAHA.114.001712
 kostenfrei: Volltext: http://jaha.ahajournals.org.ezproxy.medma.uni-heidelberg.de/content/4/6/e001712
 DOI: https://doi.org/10.1161/JAHA.114.001712
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:gene expression
 hypertension
 remodeling
 vascular smooth muscle cells
 zyxin
K10plus-PPN:1566870917
Verknüpfungen:→ Zeitschrift

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