help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Papoian, T.
Right arrow Articles by Lewis, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Papoian, T.
Right arrow Articles by Lewis, W.

American Journal of Pathology, Vol 136, 1201-1207, Copyright © 1990 by American Society for Investigative Pathology

REGULAR ARTICLES

Adriamycin cardiotoxicity in vivo. Selective alterations in rat cardiac mRNAs

T Papoian and W Lewis
Department of Pathology, UCLA School of Medicine, Center for the Health Sciences.

Adriamycin (ADR) is an antineoplastic agent with a side-effect of dilated cardiomyopathy. The present study examined ADR-induced changes in cardiac mRNA in vivo. Sprague-Dawley female rats (300 to 400 g) received from 2 to 8 mg/kg of ADR intraperitoneally. After 1 to 6 days, rats were killed and RNA was extracted from heart or gastrocnemius muscle by acid guanidinium-phenol-chloroform extraction. RNA underwent agarose electrophoresis, transfer to nitrocellulose, and hybridization with [32P]-cDNA probes specific to mRNA coding for alpha cardiac (alpha c) actin, alpha skeletal (alpha sk) actin, beta (beta) actin, and glyceraldehyde-3-phosphate dehydrogenase (G3PD). Results showed that alpha c actin mRNA levels in heart extracts were lowest at day 3 after injection, with a 60% decrease at 8 mg/kg ADR. beta actin and G3PD mRNAs decreased 28% and 21%, respectively. In gastrocnemius muscle extracts, both alpha sk actin and G3PD mRNAs decreased 30%. Results suggest a selective effect of ADR on depressing alpha c actin mRNA in the rat heart. Such changes may relate to clinical ADR-induced heart muscle disease.


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
C. C. Lim, C. Zuppinger, X. Guo, G. M. Kuster, M. Helmes, H. M. Eppenberger, T. M. Suter, R. Liao, and D. B. Sawyer
Anthracyclines Induce Calpain-dependent Titin Proteolysis and Necrosis in Cardiomyocytes
J. Biol. Chem., February 27, 2004; 279(9): 8290 - 8299.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1990 by the American Society for Investigative Pathology.