scholarly journals Differential regulation of K Ca 2.1 ( KCNN1 ) K + channel expression by histone deacetylases in atrial fibrillation with concomitant heart failure

2021 ◽  
Vol 9 (11) ◽  
Author(s):  
Ann‐Kathrin Rahm ◽  
Teresa Wieder ◽  
Dominik Gramlich ◽  
Mara Elena Müller ◽  
Maximilian N. Wunsch ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Histone Deacetylases ◽  
Differential Regulation ◽  
K Channel ◽  
Channel Expression

scholarly journals Inhibition of Histone Deacetylases Induces K+ Channel Remodeling and Action Potential Prolongation in HL-1 Atrial Cardiomyocytes

2018 ◽  
Vol 49 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Patrick Lugenbiel ◽  
Katharina Govorov ◽  
Ann-Kathrin Rahm ◽  
Teresa Wieder ◽  
Dominik Gramlich ◽  
...  
Keyword(s):  
Action Potential ◽  
Ion Channel ◽  
Action Potential Duration ◽  
Histone Deacetylases ◽  
Trichostatin A ◽  
Class I ◽  
K Channel ◽  
Hdac Inhibition ◽  
Atrial Cardiomyocytes ◽  
Channel Expression

Background/Aims: Cardiac arrhythmias are triggered by environmental stimuli that may modulate expression of cardiac ion channels. Underlying epigenetic regulation of cardiac electrophysiology remains incompletely understood. Histone deacetylases (HDACs) control gene expression and cardiac integrity. We hypothesized that class I/II HDACs transcriptionally regulate ion channel expression and determine action potential duration (APD) in cardiac myocytes. Methods: Global class I/II HDAC inhibition was achieved by administration of trichostatin A (TSA). HDAC-mediated effects on K+ channel expression and electrophysiological function were evaluated in murine atrial cardiomyocytes (HL-1 cells) using real-time PCR, Western blot, and patch clamp analyses. Electrical tachypacing was employed to recapitulate arrhythmia-related effects on ion channel remodeling in the absence and presence of HDAC inhibition. Results: Global HDAC inhibition increased histone acetylation and prolonged APD90 in atrial cardiomyocytes compared to untreated control cells. Transcript levels of voltage-gated or inwardly rectifying K+ channels Kcnq1, Kcnj3 and Kcnj5 were significantly reduced, whereas Kcnk2, Kcnj2 and Kcnd3 mRNAs were upregulated. Ion channel remodeling was similarly observed at protein level. Short-term tachypacing did not induce significant transcriptional K+ channel remodeling. Conclusion: The present findings link class I/II HDAC activity to regulation of ion channel expression and action potential duration in atrial cardiomyocytes. Clinical implications for HDAC-based antiarrhythmic therapy and cardiac safety of HDAC inhibitors require further investigation.

Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation

2017 ◽  
Vol 112 (4) ◽  
Author(s):  
Stefanie Meyer-Roxlau ◽  
Simon Lämmle ◽  
Annett Opitz ◽  
Stephan Künzel ◽  
Julius P. Joos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Protein Phosphatase ◽  
Human Heart ◽  
Differential Regulation ◽  
Protein Phosphatase 1 ◽  
Human Heart Failure

scholarly journals Erratum to: Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation

2017 ◽  
Vol 112 (5) ◽  
Author(s):  
Stefanie Meyer-Roxlau ◽  
Simon Lämmle ◽  
Annett Opitz ◽  
Stephan Künzel ◽  
Julius P. Joos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Protein Phosphatase ◽  
Human Heart ◽  
Differential Regulation ◽  
Protein Phosphatase 1 ◽  
Human Heart Failure
Sign in / Sign up

Export Citation Format

Share Document