Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Logo for

Science 333 (6048): 1388-1390

Copyright © 2011 by the American Association for the Advancement of Science

Getting to the Heart of Mechanotransduction

Cecilia Hidalgo, and Paulina Donoso

Physiology and Biophysics Program, Institute of Biomedical Sciences, Brain Neuroscience Institute and Center of Molecular Studies of the Cell, Faculty of Medicine, Universidad de Chile, Santiago, Chile.

Figure 1
View larger version (222K):
[in this window]
[in a new window]

X-ROS signaling. In heart muscle cells, transverse tubule (T-T) membranes contain voltage-gated Ca2+ channels (VGCC, green). Influx of Ca2+ through the channels generates signals that open RyR2 channels (blue) in the neighboring sarcoplasmic reticulum (SR); the ensuing Ca2+ release promotes cell contraction. The T-T membrane also contains the NOX2 subunits p22 and gp91 (red). Before stretch (A), NOX2 activity, production of ROS (red dots), and Ca2+ sparks (blue dots) are low. A moderate stretch (B) causes an immediate activation of NOX2 by recruiting its regulatory subunits (p40, p47, p67, and rac1) to the T-T membrane via a mechanism that requires intact microtubules. The resulting increase in ROS production sensitizes RyR2 to activation by Ca2+, presumably by changing RyR2 redox state, causing a burst of Ca2+ sparks. Returning the cell to its initial length returns X-ROS signaling to its initial state. [Figure adapted from (2)]


To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882