scholarly journals Conduction abnormality in gap junction protein connexin45-deficient embryonic stem cell-derived cardiac myocytes

2004 ◽  
Vol 280A (2) ◽  
pp. 973-979 ◽  
Author(s):  
Katsuko Egashira ◽  
Kiyomasa Nishii ◽  
Kei-Ichiro Nakamura ◽  
Madoka Kumai ◽  
Sachio Morimoto ◽  
...  
1999 ◽  
Vol 96 (26) ◽  
pp. 15127-15132 ◽  
Author(s):  
T. Minamino ◽  
T. Yujiri ◽  
P. J. Papst ◽  
E. D. Chan ◽  
G. L. Johnson ◽  
...  

2005 ◽  
Vol 289 (3) ◽  
pp. H1091-H1098 ◽  
Author(s):  
David E. Gutstein ◽  
Stephan B. Danik ◽  
Steve Lewitton ◽  
David France ◽  
Fangyu Liu ◽  
...  

Genetic studies in the mouse have demonstrated that conditional cardiac-restricted loss of connexin43 (Cx43), the major ventricular gap junction protein, is highly arrhythmogenic. However, whether more focal gap junction remodeling, as is commonly seen in acquired cardiomyopathies, influences the propensity for arrhythmogenesis is not known. We examined electrophysiological properties and the frequency of spontaneous and inducible arrhythmias in genetically engineered chimeric mice derived from injection of Cx43-deficient embryonic stem cells into wild-type recipient blastocysts. Chimeric mice had numerous well-circumscribed microscopic Cx43-negative foci in their hearts, comprising ∼15% of the total surface area as determined by immunohistochemical analysis. Systolic function in the chimeric mice was significantly depressed as measured echocardiographically (19.0% decline in fractional shortening compared with controls, P < 0.05) and by invasive hemodynamics (17.6% reduction in change of pressure over time, P < 0.01). Chimeras had significantly more spontaneous arrhythmic events than controls ( P < 0.01), including frequent runs of nonsustained ventricular tachycardia in some of the chimeric mice. However, in contrast to mice with conditional cardiac-resticted loss of Cx43 in the heart, no sustained ventricular tachyarrhythmias were observed. We conclude that focal areas of uncoupling in the myocardium increase the likelihood of arrhythmic triggers, but more widespread uncoupling is required to support sustained arrhythmias.


2006 ◽  
Vol 1080 (1) ◽  
pp. 207-215 ◽  
Author(s):  
I. ITZHAKI ◽  
J. SCHILLER ◽  
R. BEYAR ◽  
J. SATIN ◽  
L. GEPSTEIN

1996 ◽  
Vol 229 (2) ◽  
pp. 318-326 ◽  
Author(s):  
Yumiko Oyamada ◽  
Kiyoshi Komatsu ◽  
Hisakazu Kimura ◽  
Michio Mori ◽  
Masahito Oyamada

2002 ◽  
Vol 34 (7) ◽  
pp. A31
Author(s):  
Sarah Lodding ◽  
Michael Van Kanegan ◽  
Nancy Benkusky ◽  
Hector Valdivia ◽  
Gary Lyons

1997 ◽  
Vol 33 (4) ◽  
pp. 270-276 ◽  
Author(s):  
Elizabeth M. Rust ◽  
Margaret V. Westfall ◽  
Linda C. Samuelson ◽  
Joseph M. Metzger

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