Poult. Sci.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Google Scholar
Google Scholar
Right arrow Articles by Reddish, J.
Right arrow Articles by Wick, M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reddish, J.
Right arrow Articles by Wick, M
Poultry Science, Vol 84, Issue 3, 462-466
Copyright © 2005 by Poultry Science Association


Articles

Myosin heavy chain isoform expression is not altered in the pectoralis major muscle in selenium-deficient chickens recovering from exudative diathetic myopathy

JM Reddish, JD Latshaw, NR St-Pierre, C Pretzman, and M Wick

Department of Animal Sciences, The Ohio State University, 2029 Fyffe Road, Columbus, Ohio 43210, USA.

The recovery of broiler chickens experiencing skeletal muscle myopathy caused by a selenium deficiency was compared with control broiler chickens in an age matched study by ultrastructural analysis of the pectoralis major (PM) muscle and examination of the temporal expression of the developmental fast skeletal myosin heavy chain (MyHC) isoforms. Selenium-deficient chicks showing signs of exudative diathesis (ED) were injected subcutaneously with sodium selenite in water and allowed to recover. At 0, 2, 5, 10, 20, and 30 d after selenium injection, a sample of the PM muscle was removed from selenium-deficient and control chicks for analysis. Ultrastructural analysis revealed vacuolization in the PM of selenium-deficient chicks with little or no visible damage to the sarcomere. Relative amounts of chicken ventricular, embryonic, neonatal, and adult fast skeletal MyHC isoforms were determined using chicken fast skeletal MyHC isoform specific monoclonal antibodies. The temporal expression of the developmental MyHC isoforms was similar in all chickens (P > 0.05). There was no expression of chicken ventricular MyHC observed in the PM of either group. These results indicate that chicken fast muscle recovering from exudative diathetic myopathy does not use the same pathways as chicken skeletal fast muscle regenerating from physical or toxic injury in which temporal expression of the MyHC isoforms is initially predominantly ventricular, then predominantly embryonic, neonatal, and finally predominantly adult developmental MyHC isoform.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the Poultry Science Association.