دورية أكاديمية

CREB Negatively Regulates IGF2R Gene Expression and Downstream Pathways to Inhibit Hypoxia-Induced H9c2 Cardiomyoblast Cell Death

التفاصيل البيبلوغرافية
العنوان: CREB Negatively Regulates IGF2R Gene Expression and Downstream Pathways to Inhibit Hypoxia-Induced H9c2 Cardiomyoblast Cell Death
المؤلفون: Wei-Kung Chen, Wei-Wen Kuo, Dennis Jine-Yuan Hsieh, Hsin-Nung Chang, Pei-Ying Pai, Kuan-Ho Lin, Lung-Fa Pan, Tsung-Jung Ho, Vijaya Padma Viswanadha, Chih-Yang Huang
المصدر: International Journal of Molecular Sciences, Vol 16, Iss 11, Pp 27921-27930 (2015)
بيانات النشر: MDPI AG, 2015.
سنة النشر: 2015
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: CREB, hypoxia, apoptosis, IGF2R signaling, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: During hypoxia, gene expression is altered by various transcription factors. Insulin-like growth factor-II (IGF2) is known to be induced by hypoxia, which binds to IGF2 receptor IGF2R that acts like a G protein-coupled receptor, might cause pathological hypertrophy or activation of the mitochondria-mediated apoptosis pathway. Cyclic adenosine monophosphate (cAMP) responsive element-binding protein (CREB) is central to second messenger-regulated transcription and plays a critical role in the cardiomyocyte survival pathway. In this study, we found that IGF2R level was enhanced in H9c2 cardiomyoblasts exposed to hypoxia in a time-dependent manner but was down-regulated by CREB expression. The over-expression of CREB in H9c2 cardiomyoblasts suppressed the induction of hypoxia-induced IGF2R expression levels and reduced cell apoptosis. Gel shift assay results further indicated that CREB binds to the promoter sequence of IGF2R. With a luciferase assay method, we further observed that CREB represses IGF2R promoter activity. These results suggest that CREB plays an important role in the inhibition of IGF2R expression by binding to the IGF2R promoter and further suppresses H9c2 cardiomyoblast cell apoptosis induced by IGF2R signaling under hypoxic conditions.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
Relation: http://www.mdpi.com/1422-0067/16/11/26067; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms161126067
URL الوصول: https://doaj.org/article/66c282a58b8c4b6981a3487f0483ff78
رقم الأكسشن: edsdoj.66c282a58b8c4b6981a3487f0483ff78
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
DOI:10.3390/ijms161126067