help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
This version published online on June 26, 2003
Endocrinology, doi:10.1210/en.2003-0046
A more recent version of this article appeared on October 1, 2003
This Article
Right arrow Author Manuscript (PDF)
Right arrow All Versions of this Article:
144/10/4586    most recent
Author Manuscript (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Calegari, V. C.
Right arrow Articles by Velloso, L. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Calegari, V. C.
Right arrow Articles by Velloso, L. A.

Submitted on January 9, 2003
Accepted on June 13, 2003

SOCS3 is induced by angiotensin II in heart and isolated cardiomyocytes and participates in desensitization

Vivian C. Calegari1, Rosangela M. N. Bezerra1, Márcio A. Torsoni1, Adriana S. Torsoni1, Kleber G. Franchini1, Mário J. A. Saad1, and Lício A. Velloso1*

1 Department of Internal Medicine, State University of Campinas, Campinas, SP, Brazil

* To whom correspondence should be addressed. E-mail: lavelloso{at}fcm.unicamp.br.

Angiotensin II exerts a potent growth stimulus on the heart and vascular wall. Activation of the JAK/STAT intracellular signaling pathway by angiotensin II mediates at least some of the mitogenic responses to this hormone. In other signaling systems that use the JAK/STAT pathway, proteins of the SOCS family participate in signal regulation. In the present study it is demonstrated that SOCS3 is constitutively expressed at a low level in rat heart and neonatal rat ventricular myocytes. Angiotensin II at physiological concentration enhances the expression of SOCS3 mRNA and protein, mainly via AT1 receptors. Following induction, SOCS3 associates with JAK2 and impairs further activation of the JAK2/STAT1 pathway. Pre-treatment of rats with a specific phosphorthioate antisense oligonucleotide to SOCS3, reverses the desensitization to angiotensin signaling, as detected by a fall in c-jun expression following repetitive infusions of the hormone. Thus, SOCS3 is induced by angiotensin II in rat heart and neonatal rat ventricular myocytes, and participate in the modulation of the signal generated by this hormone.
Key words: Angiotensin • SOCS • JAK2 • STAT • AT1 • c-jun • G protein-coupled-receptor • cardiomyocyte






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2003 by The Endocrine Society