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In JoVE (1)
Other Publications (2)
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Articles by Jonathan L. Respress in JoVE
चूहे में Transthoracic इकोकार्डियोग्राफी
Jonathan L. Respress1, Xander H.T. Wehrens1,2
1Department of Molecular Physiology and Biophysics, Baylor College of Medicine (BCM), 2The Margaret M. and Albert B. Alkek Department of Medicine, Baylor College of Medicine (BCM)
Transthoracic इकोकार्डियोग्राफी चूहों में हृदय समारोह के मूल्यांकन के लिए एक noninvasive विधि प्रदान करता है. अल्ट्रासाउंड और डॉपलर इमेजिंग रूपात्मकता के एक संयोजन करने के लिए दिल और intracardiac रक्त प्रवाह, जो एक साथ हृदय systolic और diastolic प्रदर्शन के एक आकलन प्रदान आयामी माप प्राप्त करने के लिए इस्तेमाल किया जा सकता है.
Other articles by Jonathan L. Respress on PubMed
Accelerated Development of Pressure Overload-induced Cardiac Hypertrophy and Dysfunction in an RyR2-R176Q Knockin Mouse Model
Hypertension. Apr, 2010 | Pubmed ID: 20157052
In response to chronic hypertension, the heart compensates by hypertrophic growth, which frequently progresses to heart failure. Although intracellular calcium (Ca(2+)) has a central role in hypertrophic signaling pathways, the Ca(2+) source for activating these pathways remains elusive. We hypothesized that pathological sarcoplasmic reticulum Ca(2+) leak through defective cardiac intracellular Ca(2+) release channels/ryanodine receptors (RyR2) accelerates heart failure development by stimulating Ca(2+)-dependent hypertrophic signaling. Mice heterozygous for the gain-of-function mutation R176Q/+ in RyR2 and wild-type mice were subjected to transverse aortic constriction. Cardiac function was significantly lower, and cardiac dimensions were larger at 8 weeks after transverse aortic constriction in R176Q/+ compared with wild-type mice. R176Q/+ mice displayed an enhanced hypertrophic response compared with wild-type mice as assessed by heart weight:body weight ratios and cardiomyocyte cross-sectional areas after transverse aortic constriction. Quantitative PCR revealed increased transcriptional activation of cardiac stress genes in R176Q/+ mice after transverse aortic constriction. Moreover, pressure overload resulted in an increased sarcoplasmic reticulum Ca(2+) leak, associated with higher expression levels of the exon 4 splice form of regulator of calcineurin 1, and a decrease in nuclear factor of activated T-cells phosphorylation in R176Q/+ mice compared with wild-type mice. Taken together, our results suggest that RyR2-dependent sarcoplasmic reticulum Ca(2+) leak activates the prohypertrophic calcineurin/nuclear factor of activated T-cells pathway under conditions of pressure overload.
Ryanodine Receptor Phosphorylation by Calcium/calmodulin-dependent Protein Kinase II Promotes Life-threatening Ventricular Arrhythmias in Mice with Heart Failure
Circulation. Dec, 2010 | Pubmed ID: 21098440
approximately half of patients with heart failure die suddenly as a result of ventricular arrhythmias. Although abnormal Ca(2+) release from the sarcoplasmic reticulum through ryanodine receptors (RyR2) has been linked to arrhythmogenesis, the molecular mechanisms triggering release of arrhythmogenic Ca(2+) remain unknown. We tested the hypothesis that increased RyR2 phosphorylation by Ca(2+)/calmodulin-dependent protein kinase II is both necessary and sufficient to promote lethal ventricular arrhythmias.