Hallmarks of ion channel gene expression in end‐stage heart failure

2003 ◽  
Vol 17 (12) ◽  
pp. 1592-1608 ◽  
Author(s):  
Jürgen Borlak ◽  
Thomas Thum
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Ion Channel ◽  
Channel Gene ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Ion Channel Gene

scholarly journals Changes in Ion Channel Gene Expression Underlying Heart Failure-Induced Sinoatrial Node Dysfunction

2011 ◽  
Vol 4 (4) ◽  
pp. 496-508 ◽  
Author(s):  
Joseph Yanni ◽  
James O. Tellez ◽  
Michal Mączewski ◽  
Urszula Mackiewicz ◽  
Andrzej Beresewicz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Ion Channel ◽  
Sinoatrial Node ◽  
Channel Gene ◽  
Sinoatrial Node Dysfunction ◽  
Ion Channel Gene

scholarly journals Ion Channel Gene Expression in Lung Adenocarcinoma: Potential Role in Prognosis and Diagnosis

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e86569 ◽  
Author(s):  
Jae-Hong Ko ◽  
Wanjun Gu ◽  
Inja Lim ◽  
Hyoweon Bang ◽  
Eun A. Ko ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Adenocarcinoma ◽  
Ion Channel ◽  
Potential Role ◽  
Channel Gene ◽  
Ion Channel Gene

scholarly journals Troponin I gene expression during human cardiac development and in end-stage heart failure.

1993 ◽  
Vol 72 (5) ◽  
pp. 932-938 ◽  
Author(s):  
S Sasse ◽  
N J Brand ◽  
P Kyprianou ◽  
G K Dhoot ◽  
R Wade ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Troponin I ◽  
Cardiac Development ◽  
End Stage Heart Failure ◽  
End Stage ◽  
I Gene

scholarly journals The Transcription Factors Islet and Lim3 Combinatorially Regulate Ion Channel Gene Expression

2014 ◽  
Vol 34 (7) ◽  
pp. 2538-2543 ◽  
Author(s):  
V. Wolfram ◽  
T. D. Southall ◽  
C. Gunay ◽  
A. A. Prinz ◽  
A. H. Brand ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Ion Channel ◽  
Channel Gene ◽  
Ion Channel Gene

scholarly journals A Novel Model for Studying Voltage-Gated Ion Channel Gene Expression during Reversible Ischemic Stroke

2019 ◽  
Vol 16 (1) ◽  
pp. 60-67 ◽  
Author(s):  
Yun-Shen Tai ◽  
Shih-Chieh Yang ◽  
Yi-Chun Hsieh ◽  
Yaw-Bin Huang ◽  
Pao-Chu Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ischemic Stroke ◽  
Ion Channel ◽  
Voltage Gated ◽  
Channel Gene ◽  
Novel Model ◽  
Ion Channel Gene

Myocardial Gene Expression of Regulators of Myocyte Apoptosis and Myocyte Calcium Homeostasis During Hemodynamic Unloading by Ventricular Assist Devices in Patients With End-Stage Heart Failure

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Babett Bartling ◽  
Hendrik Milting ◽  
Heike Schumann ◽  
Dorothea Darmer ◽  
Lativ Arusoglu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Calcium Homeostasis ◽  
Cardiac Transplantation ◽  
Left Ventricular ◽  
Ventricular Assist ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Myocardial Gene Expression

Background —In patients with end-stage heart failure, characterized by an increased susceptibility to cardiomyocyte apoptosis and a labile cardiomyocyte calcium homeostasis, a ventricular assist device (VAD) is implanted for bridging to cardiac transplantation and results in myocardial unloading. Although phenotype changes in the failing heart are assumed to result from hemodynamic overload, the reversibility of these changes under unloading is unknown. Methods and Results —By use of quantitative reverse-transcription polymerase chain reaction, mRNA expression analyses were performed on left ventricular specimens obtained from 10 nonfailing donor hearts (from 8 patients with dilated cardiomyopathy and 2 patients with coronary heart disease) at the time of VAD implantation and 36 to 169 days later during VAD removal with subsequent cardiac transplantation. In terminally failing hearts before VAD support, left ventricular mRNA analyses revealed increased Pro-ANP, reduced antiapoptotic Bcl-x L and antiapoptotic Fas isoform FasExo6Del, and a decreased ratio of sarcoplasmic reticulum Ca 2+ -ATPase per sarcolemmal Na + -Ca 2+ exchanger in comparison with nonfailing ventricles. After VAD unloading, ventricular transcription of Pro-ANP was immediately normalized, and apoptotic DNA fragmentation was attenuated. In patients with dilated cardiomyopathy, mRNAs of Bcl-x L and FasExo6Del/Fas were enhanced depending on time on VAD. The Bcl-x L mRNA level correlated positively with that of the Bcl-x L protein. Transcription of sarcoplasmic reticulum Ca 2+ -ATPase/Na + -Ca 2+ exchanger demonstrated recovery in only 4 of 10 patients. Conclusions —Mechanical support of the failing heart induces a time-dependent change in myocardial gene expression compatible with a decreased susceptibility to apoptosis.

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