Skip Navigation

Cardiovascular Research 2006 72(2):303-312; doi:10.1016/j.cardiores.2006.08.003
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Liang, Y.-J.
Right arrow Articles by Shyu, K.-G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liang, Y.-J.
Right arrow Articles by Shyu, K.-G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

Mechanical stress enhances serotonin 2B receptor modulating brain natriuretic peptide through nuclear factor-{kappa}B in cardiomyocytes

Yao-Jen Lianga, Ling-Ping Laia, Bao-Wei Wangb, Shiow-Jen Juangc, Che-Ming Changd, Jyh-Gang Leud and Kou-Gi Shyud,e,*

aInstitute of Pharmacology, National Taiwan University, Taipei, Taiwan
bDepartment of Medical Education and Research, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
cDepartment of Family Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
dDepartment of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
eGraduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan

* Corresponding author. Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan. Tel.: +886 2 2833 2211x2094; fax: +886 2 2836 5775. Email address: shyukg{at}ms12.hinet.net

Objective: Serotonin via serotonin 2B receptors (SR2BR) regulates cardiac embryonic development and adult heart functions. However, the role of SR2BR in the failing heart due to pressure overload is not well understood.

Methods: Wistar rats of aortic banding and neonatal cardiomyocyte with mechanical stretch were used as cardiomyopathy models.

Results: After two weeks of aortic banding surgery, serum serotonin, mRNA and protein expression of SR2BR increased significantly. The selective SR2BR antagonist, SB215505 (SB), significantly reduced the increase in heart weight, decreased heart wall thickness, left ventricular mass and the expression of the brain natriuretic peptide (BNP) but did not attenuate the up-regulation of SR2BR protein expression in rats after aortic banding for three weeks. After following in vitro mechanical stretch of cardiomyocytes and incubation with serotonin 1 µM, the level of SR2BR and BNP protein increased time-dependently. When transfected by specific siRNA of SR2BR or pretreated with caffeic acid phenethyl ester in cardiomyocytes, the increase of nuclear factor-{kappa}B (NF-{kappa}B) translocation and BNP protein induced by serotonin incubation plus mechanical stretch were both reversed.

Conclusions: SR2BR expression is involved in pressure-induced cardiomyopathy and its downstream signaling may involve NF-{kappa}B to modulate BNP expression in cardiomyocyte.

KEYWORDS Serotonin (5-HT) 2B receptors; Hypertrophy; Cardiomyopathy; Mechanical stretch; Myocytes

Time for primary review 19 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
 Am. J. Physiol. Heart Circ. Physiol.Home page
T. Koyanagi, L. Y. Wong, K. Inagaki, O. V. Petrauskene, and D. Mochly-Rosen
Alteration of gene expression during progression of hypertension-induced cardiac dysfunction in rats
Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H220 - H226.
[Abstract] [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.