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Mechanical stretch and angiotensin II increase interleukin-13 production and interleukin-13 receptor alpha2 expression in rat neonatal cardiomyocytes.

Authors: Nishimura, Y  Inoue, T  Morooka, T  Node, K 
Citation: Nishimura Y, etal., Circ J. 2008 Apr;72(4):647-53.
Pubmed: (View Article at PubMed) PMID:18362439

BACKGROUND: The high affinity receptor for interleukin (IL)-13, IL-13 receptor alpha2 (IL-13Ralpha2), acts as a decoy receptor for IL-13, modulates fibrosis and has an anti-tumor effect. Recently, IL-13Ralpha2 has been considered as a therapeutic target for fibrosis and tumor growth. However, the mechanism of IL-13Ralpha2 expression in cardiomyocytes is unclear. METHODS AND RESULTS: The mechanism of IL-13Ralpha2 expression was examined using cultured rat neonatal cardiomyocytes. Cyclical mechanical stretch induced IL-13Ralpha2 mRNA expression in rat cardiomyocytes. Treatment with angiotensin II, which plays a pivotal role in mechanical stretch-induced cardiomyocyte hypertrophy, upregulated IL-13Ralpha2 mRNA expression in rat cardiomyocytes. IL-13Ralpha2 mRNA expression was also upregulated through IL-13 treatment. Furthermore, mechanical stretch and angiotensin II treatment caused IL-13 secretion from rat cardiomyocytes, which was suppressed by angiotensin type1 receptor (AT1R) RNA interference. Upregulation of IL-13Ralpha2 mRNA expression through mechanical stretch, angiotensin II treatment and IL-13 treatment was inhibited by anti-IL-13Ralpha1 antibody and STAT6 depletion through RNA interference. Positive immunohistochemical staining for IL-13Ralpha2 was observed in the myocardium of endomyocardial biopsy specimens from the failing human heart, but not in autopsy specimens from control subjects. CONCLUSION: IL-13 might act in an autocrine and paracrine fashion to upregulate IL-13Ralpha2 expression in cardiomyocytes.


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CRRD Object Information
CRRD ID: 2298568
Created: 2008-07-11
Species: All species
Last Modified: 2008-07-11
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.