Abstract 607: Cardiac-specific Deletion Of ErbB4 In The Adult Mouse Increases Cardiac Cell Proliferation And Causes Physiological Cardiac Hypertrophy
| Autor: | Zhen Wang, Walter Thomas, Tamara Paravicini |
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| Rok vydání: | 2014 |
| Předmět: | |
| Zdroj: | Hypertension. 64 |
| ISSN: | 1524-4563 0194-911X |
| DOI: | 10.1161/hyp.64.suppl_1.607 |
| Popis: | The epidermal growth factor receptor type 4 (ErbB4) is a receptor tyrosine kinase that is activated by the growth factor neuregulin 1 (NRG1). ErbB4 is essential for cardiac development and promotes cardiomyocyte survival in culture. To investigate the physiological importance of ErbB4 in the adult heart, we generated a mouse model with conditional deletion of ErbB4 in cardiomyocytes using a tamoxifen-inducible Cre recombinase (MHC-MerCreMer). Adult MHC-MerCreMer/ErbB4 fl/fl (ErbB4 conditional knockout, cKO, n=6) and MHC-MerCreMer/ErbB4 WT/WT (control, n=8) animals were injected with tamoxifen (20 mg/kg/day ip for 10 days). Ten days after tamoxifen treatment, cardiac specific deletion of ErbB4 was confirmed by qPCR. At 3 months after ErbB4 deletion, echocardiography showed no differences in cardiac function (fractional shortening), however the heart weight:tibia length ratio was increased by 45% in the cKO animals (5.1±0.2 vs 7.4±0.6 mg/mm, P P P Conclusion: Cardiac-specific deletion of ErbB4 in the adult increases heart weight without altering cardiac function, cardiomyocyte size or fibrosis. ErbB4 deletion also increases NRG1 expression, which may contribute to the maintenance of cardiac function and the development of cardiac hypertrophy via cell proliferation. |
| Databáze: | OpenAIRE |
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