Activation of insulin-like growth factor II receptor induces mitochondrial-dependent apoptosis through Gαq and downstream calcineurin signaling in myocardial cells
Endocrinology, ISSN: 0013-7227, Vol: 150, Issue: 6, Page: 2723-2731
2009
- 55Citations
- 15Captures
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Metrics Details
- Citations55
- Citation Indexes55
- 55
- CrossRef48
- Captures15
- Readers15
- 15
Article Description
In previous studies, we have found that IGF-II and IGF-II receptor (IGF-IIR) dose dependently correlated with the progression of pathological hypertrophy after complete abdominal aorta ligation, which may play a critical role in angiotensin II-induced cardiomyocyte apoptosis. However, the detail mechanisms of IGF-IIR in the regulation of cell apoptosis in response to IGF-II remain unclear. By using IGF-IR short hairpin RNA to inhibit IGF-IR expression and using Leu27 IGF-II analog to activate specifically the IGF-IIR, we investigated the role of IGF-II/IGF-IIR activation and its downstream signaling. Our results revealed that IGF-II synergistically increased the cell apoptosis induced by suppressing of IGF-IR in neonatal rat ventricular myocytes. After binding of Leu27IGF-II, IGF-IIR became associated with α-q polypeptide, acted like a protein-coupled receptor to activate calcineurin, led to the translocation of Bad into mitochondria and release of cytochrome c into cytoplasm, and contributed to mitochondrial-dependent apoptosis in neonatal rat ventricular myocytes. Furthermore, inhibition of IGF-IIR, α-q polypeptide, or calcineurin by RNA interference could block the Leu27IGF-II-induced cell apoptosis. Together, this study provides a new insight into the effects of the IGF-IIR and its downstream signaling in myocardial apoptosis. Suppression of IGF-IIR signaling pathways may be a good strategy for both the protection against myocardial cell apoptosis and the prevention of heart failure progression. Copyright © 2009 by The Endocrine Society.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=66649095587&origin=inward; http://dx.doi.org/10.1210/en.2008-0975; http://www.ncbi.nlm.nih.gov/pubmed/19095737; https://academic.oup.com/endo/article/150/6/2723/2456178; https://dx.doi.org/10.1210/en.2008-0975; https://academic.oup.com/endo/article-abstract/150/6/2723/2456178?redirectedFrom=fulltext
The Endocrine Society
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