التفاصيل البيبلوغرافية
| العنوان: |
Integrin-linked kinase is a central mediator in angiotensin II type 1- and chemokine receptor CXCR4 signaling in myocardial hypertrophy |
| المؤلفون: |
Bettink, Stephanie I.1, Werner, Christian1, Chen, Chia-Hui1, Müller, Patrick1, Schirmer, Stephan H.1, Walenta, Katrin L.1, Böhm, Michael1, Laufs, Ulrich1, Friedrich, Erik B. erikbfriedrich@hotmail.com |
| المصدر: |
Biochemical & Biophysical Research Communications. Jun2010, Vol. 397 Issue 2, p208-213. 6p. |
| مصطلحات موضوعية: |
*INTEGRINS, *PROTEIN kinases, *ANGIOTENSIN II, *CHEMOKINES, *CELL receptors, *CELLULAR signal transduction, *HYPERTROPHY, *CARDIOMYOPATHIES |
| مستخلص: |
Abstract: Inflammation and pro-hypertrophic signaling are important for development and progression of myocardial hypertrophy (LVH) and chronic heart failure (CHF). Here we investigated the relevance of integrin-linked kinase (ILK) for chemokine receptor CXCR4- and angiotensin II type 1-triggered signaling and its regulation and role in cardiac remodeling. Using ELISA, real-time-PCR, and Western blotting, the present study demonstrates that SDF-1 and its receptor CXCR4 are up-regulated in plasma and left ventricles, respectively, in mouse models of cardiac hypertrophy (transaortic constriction, transgenic cardiac-specific overexpression of rac1) and in human CHF in association with increased cardiac ILK-expression. In isolated cardiomyocytes, ILK is activated by CXCR4-ligation and necessary for SDF-1-triggered activation of rac1, NAD(P)H oxidase, and release of reactive oxygen species. Importantly, the pro-hypertrophic peptide angiotensin II induces ILK-activation dependent on rac1 in cardiomyocytes, where ILK is necessary for angiotensin II-mediated stimulation of hypertrophy genes and protein synthesis. We conclude that in both SDF-1- and angiotensin II-triggered signaling, ILK is a central mediator of rac1-induced oxidative stress and myocardial hypertrophy. [Copyright &y& Elsevier] |
| قاعدة البيانات: |
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