Skip Navigation

Cardiovascular Research 2007 73(1):57-65; doi:10.1016/j.cardiores.2006.09.016
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Frias, M. A.
Right arrow Articles by Lang, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Frias, M. A.
Right arrow Articles by Lang, U.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

Prostaglandin E2 activates Stat3 in neonatal rat ventricular cardiomyocytes: A role in cardiac hypertrophy

Miguel A. Frias*, Michela C. Rebsamen, Christine Gerber-Wicht and Ursula Lang

Division of Endocrinology, Diabetology and Nutrition, University Hospital, 24, rue Micheli-du-Crest, CH-1211 Geneva 14, Switzerland

* Corresponding author. Tel.: +41 22 3729322; fax: +41 22 3729330. Email address: Miguel.Frias{at}medecine.unige.ch

Objective: The purpose of this study was to investigate whether prostaglandin E2 (PGE2) induces Signal transducer and activator of transcription 3 (Stat3) activation in neonatal rat ventricular cardiomyocytes and if so to determine the possible role of this activation in PGE2-induced hypertrophic responses.

Methods: Stat3 activation and its nuclear phosphorylation were determined by electrophoretic mobility shift assay (EMSA) and by Western blots, respectively. Protein synthesis was assessed by [3H]-leucine incorporation into total protein and cell surface was quantified by microscopic analysis.

Results: We found that PGE2 induces a concentration- (1–100 nM) and time-dependent increase in Stat3 activation, reaching maximal values after 90 min of stimulation. Experiments with agonists and antagonists of the PGE2 receptor subtypes EP1–EP4 indicate that PGE2 activates Stat3 mainly through the EP4 receptor. We further observed that the extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor U0126 abolishes PGE2-induced Stat3 activation whereas the p38 MAP kinase blocker SB203580 has no effect. Nuclear Stat3 phosphorylation induced by PGE2 is also suppressed by the translation and transcription inhibitors, cycloheximide and actinomycin D, respectively. Transfecting ventricular cardiomyocytes with a small interfering RNA (siRNA) targeting rat Stat3, we obtained an approximately 70% reduction in Stat3 expression, 24 and 48 h after electroporation. In these Stat3-silenced cells, the PGE2-induced increase in protein synthesis and cell surface is strongly inhibited.

Conclusion: In ventricular cardiomyocytes, PGE2 induces the activation of Stat3 which plays an essential role in PGE2-induced increase in cell size and protein synthesis. The activation of Stat3 occurs mainly through EP4 and involves ERK1/2 as well as newly synthesized protein(s).

KEYWORDS Hypertrophy; Prostaglandins; Signal transduction

Time for primary review 27 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
M. A. Frias, U. Lang, C. Gerber-Wicht, and R. W. James
Native and reconstituted HDL protect cardiomyocytes from doxorubicin-induced apoptosis
Cardiovasc Res, September 18, 2009; (2009) cvp289v2.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. A. Frias, R. W. James, C. Gerber-Wicht, and U. Lang
Native and reconstituted HDL activate Stat3 in ventricular cardiomyocytes via ERK1/2: Role of sphingosine-1-phosphate
Cardiovasc Res, May 1, 2009; 82(2): 313 - 323.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. A. Frias, S. Somers, C. Gerber-Wicht, L. H. Opie, S. Lecour, and U. Lang
The PGE2-Stat3 interaction in doxorubicin-induced myocardial apoptosis
Cardiovasc Res, October 1, 2008; 80(1): 69 - 77.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
V. Brune, E. Tiacci, I. Pfeil, C. Doring, S. Eckerle, C. J.M. van Noesel, W. Klapper, B. Falini, A. von Heydebreck, D. Metzler, et al.
Origin and pathogenesis of nodular lymphocyte-predominant Hodgkin lymphoma as revealed by global gene expression analysis
J. Exp. Med., September 29, 2008; 205(10): 2251 - 2268.
[Abstract] [Full Text] [PDF]

Home page
 Exp. Biol. Med.Home page
X.-J. Zou, L. Yang, and S.-L. Yao
Propofol Depresses Angiotensin II-Induced Cardiomyocyte Hypertrophy In Vitro
Experimental Biology and Medicine, February 1, 2008; 233(2): 200 - 208.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
J.-Y. Qian, P. Harding, Y. Liu, E. Shesely, X.-P. Yang, and M. C. LaPointe
Reduced Cardiac Remodeling and Function in Cardiac-Specific EP4 Receptor Knockout Mice With Myocardial Infarction
Hypertension, February 1, 2008; 51(2): 560 - 566.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
M. M. Bamman
Take two NSAIDs and call on your satellite cells in the morning
J Appl Physiol, August 1, 2007; 103(2): 415 - 416.
[Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. C. Schaub and M. A. Hefti
The PGE2-Stat3 connection in cardiac hypertrophy
Cardiovasc Res, January 1, 2007; 73(1): 3 - 5.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.