Kimono

Hindawi Publishing Corporation
Journal of Biomedicine and Biotechnology
Volume 2011, Article ID 382586, 14 pages
doi:10.1155/2011/382586

Research Article
Dynamic Changes in SarcoplasmicReticulum Structure in
Ventricular Myocytes
Amanda L. Vega, Can Yuan, V. Scott Votaw, and Luis F. Santana
Department of Physiology & Biophysics, University of Washington, Box 357290, Seattle, WA 98195,USA
Correspondence should be addressed to Luis F. Santana, santana@u.washington.edu
Received 29 April 2011; Accepted 9 August 2011
Academic Editor: Xupei Huang
Copyright © 2011 Amanda L. Vega etal. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original workis properly
cited.
The fidelity of excitation-contraction (EC) coupling in ventricular myocytes is remarkable, with each action potential evoking a
[Ca2+ ]i transient. The prevalent model is that theconsistency in EC coupling in ventricular myocytes is due to the formation of
fixed, tight junctions between the sarcoplasmic reticulum (SR) and the sarcolemma where Ca2+ release is activated. Here,we tested
the hypothesis that the SR is a structurally inert organelle in ventricular myocytes. Our data suggest that rather than being static,
the SR undergoes frequent dynamic structural changes.SR boutons expressing functional ryanodine receptors moved throughout
the cell, approaching or moving away from the sarcolemma of ventricular myocytes. These changes in SR structure occurred in
theabsence of changes in [Ca2+ ]i during EC coupling. Microtubules and the molecular motors dynein and kinesin 1(Kif5b) were
important regulators of SR motility. These findings support a model in whichthe SR is a motile organelle capable of molecular
motor protein-driven structural changes.

1. Introduction
The sarcoplasmic reticulum (SR) is an intracellular organelle
that forms an intricate...