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Plos Biology : Intermolecular Failure of L-type CA2Þ Channel and Ryanodine Receptor Signaling in Hypertrophy, Volume 5

By Berridge, Michael

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Book Id: WPLBN0003927027
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos Biology : Intermolecular Failure of L-type CA2Þ Channel and Ryanodine Receptor Signaling in Hypertrophy, Volume 5  
Author: Berridge, Michael
Volume: Volume 5
Language: English
Subject: Journals, Science, Biology
Collections: Periodicals: Journal and Magazine Collection (Contemporary), PLoS Biology
Historic
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Publisher: Plos

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Berridge, M. (n.d.). Plos Biology : Intermolecular Failure of L-type CA2Þ Channel and Ryanodine Receptor Signaling in Hypertrophy, Volume 5. Retrieved from http://netlibrary.net/


Description
Description : Pressure overload–induced hypertrophy is a key step leading to heart failure. The Ca2þ-induced Ca2þ release (CICR) process that governs cardiac contractility is defective in hypertrophy/heart failure, but the molecular mechanisms remain elusive. To examine the intermolecular aspects of CICR during hypertrophy, we utilized loose-patch confocal imaging to visualize the signaling between a single L-type Ca2þ channel (LCC) and ryanodine receptors (RyRs) in aortic stenosis rat models of compensated (CHT) and decompensated (DHT) hypertrophy. We found that the LCC-RyR intermolecular coupling showed a 49% prolongation in coupling latency, a 47% decrease in chance of hit, and a 72% increase in chance of miss in DHT, demonstrating a state of ‘‘intermolecular failure.’’ Unexpectedly, these modifications also occurred robustly in CHT due at least partially to decreased expression of junctophilin, indicating that intermolecular failure occurs prior to cellular manifestations. As a result, cell-wide Ca2þ release, visualized as ‘‘Ca2þ spikes,’’ became desynchronized, which contrasted sharply with unaltered spike integrals and whole-cell Ca2þ transients in CHT. These data suggested that, within a certain limit, termed the ‘‘stability margin,’’ mild intermolecular failure does not damage the cellular integrity of excitation-contraction coupling. Only when the modification steps beyond the stability margin does global failure occur. The discovery of ‘‘hidden’’ intermolecular failure in CHT has important clinical implications.

 

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