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Verfasst von:Zappe, Maren [VerfasserIn]   i
 Feldner, Anja [VerfasserIn]   i
 Arnold, Caroline [VerfasserIn]   i
 Sticht, Carsten [VerfasserIn]   i
 Hecker, Markus [VerfasserIn]   i
 Korff, Thomas [VerfasserIn]   i
Titel:NFAT5 isoform C controls biomechanical stress responses of vascular smooth muscle cells
Verf.angabe:Maren Zappe, Anja Feldner, Caroline Arnold, Carsten Sticht, Markus Hecker and Thomas Korff
E-Jahr:2018
Jahr:23 August 2018
Fussnoten:Gesehen am 12.09.2018
Titel Quelle:Enthalten in: Frontiers in physiology
Ort Quelle:Lausanne : Frontiers Research Foundation, 2007
Jahr Quelle:2018
Band/Heft Quelle:9(2018) Artikel-Nummer 1190, 11 Seiten
ISSN Quelle:1664-042X
Abstract:Vascular cells are continuously exposed to mechanical stress that may wreak havoc if exceeding physiological levels. Consequently, mechanisms facing such a challenge are indispensable and contribute to the adaptation of the cellular phenotype. To this end, vascular smooth muscle cells (VSMCs) activate mechanoresponsive transcription factors promoting their proliferation and migration to initiate remodeling the arterial wall. In mechanostimulated VSMCs, we identified nuclear factor of activated T-cells 5 (NFAT5) as transcriptional regulator protein and intended to unravel mechanisms controlling its expression and nuclear translocation. In cultured human VSMCs, blocking RNA synthesis diminished both baseline and stretch-induced NFAT5 mRNA expression while inhibition of the proteasome promoted accumulation of the NFAT5 protein. Detailed PCR analyses indicated a decrease in expression of NFAT5 isoform A and an increase in isoform C in mechanoactivated VSMCs. Upon overexpression, only NFAT5c was capable to enter the nucleus in control- and stretch-stimulated VSMCs. As evidenced by analyses of NFAT5c mutants, nuclear translocation required palmitoylation, phosphorylation at Y143 and was inhibited by phosphorylation at S1197. On the functional level, overexpression of NFAT5c forces its accumulation in the nucleus as well as transcriptional activity and stimulated VSMC proliferation and migration. These findings suggest that NFAT5 is continuously expressed and degraded in resting VSMCs while expression and accumulation of isoform C in the nucleus is facilitated during biomechanical stress to promote an activated VSMC phenotype.
DOI:doi:10.3389/fphys.2018.01190
URL:kostenfrei: Volltext: http://dx.doi.org/10.3389/fphys.2018.01190
 kostenfrei: Volltext: https://www.frontiersin.org/articles/10.3389/fphys.2018.01190/full
 DOI: https://doi.org/10.3389/fphys.2018.01190
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Biomechanical stress
 Hypertension
 TonEBP/NFAT5
 Transcription Factors
 vascular smooth muscle cells
 Wall stress
K10plus-PPN:1580913369
Verknüpfungen:→ Zeitschrift
 
 
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