JOE Society for Endocrinology Archive
HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Journal of Endocrinology (1998) 158, 27-33       DOI: 10.1677/joe.0.1580027
© 1998 Society for Endocrinology
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (10)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fryer, L.
Right arrow Articles by Sugden, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fryer, L.
Right arrow Articles by Sugden, M.
Journal of Endocrinology, Vol 158, Issue 1, 27-33
Copyright © 1998 by Society for Endocrinology


Articles

Cardiac protein kinase C expression in two models of cardiac hypertrophy associated with an activated cardiac renin-angiotensin system: effects of experimental hyperthyroidism and genetic hypertension (the mRen-2 rat)

LG Fryer, MJ Holness, JB Decock, and MC Sugden


There is evidence for a role of protein kinase C (PKC) in the development of cardiac hypertrophy. We examined the expression of individual PKC isoforms in the adult rat heart in two distinct, well-characterised in vivo models of cardiac hypertrophy associated with an activated cardiac renin-angiotensin system, namely experimental hyperthyroidism and the TGR(mRen2)27 rat. The cardiac expression of a range of PKC isoforms (PKC-alpha, PKC-omega, PKC-epsilon, PKC-gamma, and PKC-tau) was examined by immuno-blotting. Our work demonstrates that the expression of total cardiac nPKC-omega and nPKC-epsilon relative to protein is selectively and differentially modified in these models. A consistent up-regulation of nPKC-omega in conjunction with overall down-regulation of nPKC-epsilon was observed in both models. The expression of other PKC isoforms was unaffected. The divergent responses of the expression of the two nPKC isoforms to an activated cardiac renin-angiotensin system in vivo in adulthood suggest that these individual nPKC isoforms subserve specific roles in the response.


This article has been cited by other articles:


Home page
Journal of Renin-Angiotensin-Aldosterone SystemHome page
Yi Xu, V. Menon, and B. I Jugdutt
Cardioprotection after angiotensin II type 1 blockade involves angiotensin II type 2 receptor expression and activation of protein kinase C-{varepsilon} in acutely reperfused myocardial infarction in the dog: Effect of UP269-6 and losartan on AT1- and AT2-receptor expression and IP3 receptor and PKC{varepsilon} proteins
Journal of Renin-Angiotensin-Aldosterone System, June 1, 2000; 1(2): 184 - 195.
[Abstract] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
K. L. Butler, A. H. Huang, and J. K. Gwathmey
AT1-receptor blockade enhances ischemic preconditioning in hypertrophied rat myocardium
Am J Physiol Heart Circ Physiol, December 1, 1999; 277(6): H2482 - H2487.
[Abstract] [Full Text] [PDF]




HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 by the Society for Endocrinology.