Excessive microtubules are not responsible for depressed force per cross-bridge in cardiac neural-crest-ablated embryonic chick hearts
Document Type
Article
Publication Date
1999
Abstract
Ablation of the cardiac neural crest (CNCA) in embryonic chicks results in a high incidence of persistent truncus arteriosus, a congenital heart defect associated with decreased myocardial contractility. Using left ventricular trabeculae from chicks at embryonic day (ED) 15, we have previously shown that the twitch force of intact preparations is significantly reduced whereas the maximal calcium-activated force of skinned preparations is not significantly different in CNCA and sham-operated animals. We also previously found that the ventricular content of myosin, as well as of actin and tropomyosin, was nearly doubled in ED 15 hearts after CNCA. Since the number of cross-bridges is proportional to the myosin concentration, these data suggest that the force exerted per cross-bridge is decreased in CNCA hearts. We investigated the possibility that the decrease in force per cross-bridge is caused by inhibition of the contractile apparatus by excessive microtubules. To the contrary, we found that the total β-tubulin content and the fraction of β-tubulin polymerized in microtubules measured by Western blotting was the same in ventricular muscle strips from CNCA and sham-operated embryos. Furthermore, exposure to microtubule- destabilizing agents did not improve the force-producing capability of the contractile apparatus in CNCA embryos. We conclude that depression of force per cross-bridge in hearts from CNCA embryos is not due to an excess of microtubules.
Publication Title
Pflugers Archiv European Journal of Physiology
Volume
438
Issue
3
First Page
307
Last Page
313
Recommended Citation
Hatcher, Cathy J.; Godt, Robert E.; and Nosek, T. M., "Excessive microtubules are not responsible for depressed force per cross-bridge in cardiac neural-crest-ablated embryonic chick hearts" (1999). PCOM Scholarly Works. 513.
https://digitalcommons.pcom.edu/scholarly_papers/513
Comments
This article was published in Pflugers Archiv European Journal of Physiology, Volume 438, Issue 3, Pages 307-313.
The published version is available at http://dx.doi.org/10.1007/s004240050914.Copyright © 1999 Springer.