دورية أكاديمية
Repetitive Transient Ischemia-Induced Cardiac Angiogenesis is Mediated by Camkii Activation
| العنوان: | Repetitive Transient Ischemia-Induced Cardiac Angiogenesis is Mediated by Camkii Activation |
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| المؤلفون: | Zhuobin Chen, Benlei Li, Qiaoqiao Dong, Cheng Qian, Jun Cheng, Yanggan Wang |
| المصدر: | Cellular Physiology and Biochemistry, Vol 47, Iss 3, Pp 914-924 (2018) |
| بيانات النشر: | Cell Physiol Biochem Press GmbH & Co KG, 2018. |
| سنة النشر: | 2018 |
| المجموعة: | LCC:Physiology LCC:Biochemistry |
| مصطلحات موضوعية: | Coronary angiogenesis, Ca2+/Calmodulin-dependent kinase II, Vascular endothelial growth factor, Ischemia, Physiology, QP1-981, Biochemistry, QD415-436 |
| الوصف: | Background/Aims: Coronary angiogenesis is an important protective mechanism in response to myocardial ischemia in coronary artery disease. However, the underlying mechanisms remain largely unclear. Here, we investigated the role of CaMKII activation in ischemia-induced cardiac angiogenesis. Methods: Repetitive transient ischemia model was established in C57/BL6 mice by daily multiple episodes (3 times/day) of short time (5 min) occlusion of the left anterior descending coronary artery for 7 days. Coronary angiogenesis was detected by immunofluorescent staining. RT-qPCR and Western blot analyses were used to detect the mRNA and protein levels of CaMKII, p-CaMKII and VEGF. Primary cardiac microvascular endothelial cells (CMECs) were isolated to investigate the effects of KN93 on cell proliferation and migration in hypoxic condition. Results: We found that angiogenesis was induced in the ischemic myocardium and suppressed by chronic intraperitoneal injection of CaMKII inhibitor KN93. RT-qPCR and Western blot analyses showed that myocardial ischemia induced an increased expression and autophosphorylation of CaMKII. VEGF expression was increased in the ischemia model but blunted by KN93. Moreover, KN93 suppressed the proliferation and migration of cardiac endothelial cells in hypoxic condition in which the protein expression of CaMKII, p-CaMKII and VEGF was increased. Conclusion: CaMKII is an important mediator for the ischemia-induced coronary angiogenesis, in which CaMKII-triggered VEGF expression plays a key role. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1015-8987 1421-9778 |
| العلاقة: | https://www.karger.com/Article/FullText/490133Test; https://doaj.org/toc/1015-8987Test; https://doaj.org/toc/1421-9778Test |
| DOI: | 10.1159/000490133 |
| الوصول الحر: | https://doaj.org/article/02ad2575a5e146ffa97c0b25f4442c23Test |
| رقم الانضمام: | edsdoj.02ad2575a5e146ffa97c0b25f4442c23 |
| قاعدة البيانات: | Directory of Open Access Journals |
| تدمد: | 10158987 14219778 |
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| DOI: | 10.1159/000490133 |