Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death

被引:39
|
作者
Yoshida, Tadashi [1 ]
Friehs, Ingeborg [2 ]
Mummidi, Srinivas [3 ,4 ]
del Nido, Pedro J. [2 ]
Addulnour-Nakhoul, Solange [5 ,6 ]
Delafontaine, Patrice [1 ]
Valente, Anthony J. [2 ]
Chandrasekar, Bysani [1 ,6 ]
机构
[1] Tulane Univ, Sch Med, Inst Heart & Vasc, New Orleans, LA 70112 USA
[2] Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Cardiac Surg, Boston, MA 02115 USA
[3] Univ Texas Hlth Sci Ctr San Antonio, South Texas Vet Hlth Care Syst, San Antonio, TX 78229 USA
[4] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA
[5] Tulane Univ, Sch Med, Dept Med Gastroenterol, New Orleans, LA 70112 USA
[6] Southeast Louisiana Vet Hlth Care Syst, Res Serv, New Orleans, LA 70161 USA
关键词
Myocardial hypertrophy; Cardiac failure; Cyclical stretch; Interleukins; Inflammation; NF-KAPPA-B; CARDIAC FIBROBLAST MIGRATION; STRETCH-INDUCED HYPERTROPHY; HEART-FAILURE; INTERLEUKIN-18; EXPRESSION; BINDING-PROTEIN; ACTIVATION; DYSFUNCTION; INDUCTION; APOPTOSIS;
D O I
10.1016/j.yjmcc.2014.07.007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recurrent or sustained inflammation plays a causal role in the development and progression of left ventricular hypertrophy (LVH) and its transition to failure. Interleukin (IL)-18 is a potent pro-hypertrophic inflammatory cytokine. We report that induction of pressure overload in the rabbit, by constriction of the descending thoracic aorta induces compensatory hypertrophy at 4 weeks (mass/volume ratio: 1.7 +/- 0.11) and ventricular dilatation indicative of heart failure at 6 weeks (mass/volume ratio: 0.7 +/- 0.04). In concordance with this, fractional shortening was preserved at 4 weeks, but markedly attenuated at 6 weeks. We cloned rabbit IL-18, IL-18R alpha, IL-18R beta, and IL-18 binding protein (1-18BP) cDNA, and show that pressure overload, while enhancing IL-18 and IL-18R expression in hypertrophied and failing hearts, markedly attenuated the level of expression of the endogenous IL-18 antagonist IL-18BP. Cyclical mechanical stretch (10% cyclic equibiaxial stretch, 1 Hz) induced hypertrophy of primary rabbit cardiomyocytes in vitro and enhanced ANP, IL-18, and IL-18Ra expression. Further, treatment with rhIL-18 induced its own expression and that of IL-18Ra via AP-1 activation, and induced cardiomyocyte hypertrophy in part via PI3K/Akt/GATA4 signaling. In contrast, IL-18 potentiated TNF-alpha-induced cardiomyocyte death, and by itself induced cardiac endothelial cell death. These results demonstrate that pressure overload is associated with enhanced IL-18 and its receptor expression in hypertrophied and failingrabbit hearts. Since IL-18BP expression is markedly inhibited, our results indicate a positive amplification in IL-18 proinflammatory signaling during pressure overload, and suggest IL-18 as a potential therapeutic target in pathological hypertrophy and cardiac failure. Published by Elsevier Ltd.
引用
收藏
页码:141 / 151
页数:11
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