التفاصيل البيبلوغرافية
| العنوان: |
miR-455-5p promotes pathological cardiac remodeling via suppression of PRMT1-mediated Notch signaling pathway |
| المؤلفون: |
Cai, Sidong, Chang, Junlei, Su, Mengqi, Wei, Yinxia, Sun, Haoran, Chen, Cong, Yiu, Kai-Hang |
| المساهمون: |
Basic and Applied Basic Research Foundation of Guangdong Province, National Natural Science Foundation of China, Program of the Shenzhen Municipal Science and Technology Commission, Sanming Project of Medicine in Shenzhen, HKU-SZH Fund for Shenzhen Key Medical Discipline |
| المصدر: |
Cellular and Molecular Life Sciences ; volume 80, issue 12 ; ISSN 1420-682X 1420-9071 |
| بيانات النشر: |
Springer Science and Business Media LLC |
| سنة النشر: |
2023 |
| مصطلحات موضوعية: |
Cell Biology, Cellular and Molecular Neuroscience, Pharmacology, Molecular Biology, Molecular Medicine |
| الوصف: |
Pathological cardiac remodeling plays an essential role in the progression of cardiovascular diseases, and numerous microRNAs have been reported to participate in pathological cardiac remodeling. However, the potential role of microRNA-455-5p (miR-455-5p) in this process remains to be elucidated. In the present study, we focused on clarifying the function and searching the direct target of miR-455-5p, as well as exploring its underlying mechanisms in pathological cardiac remodeling. We found that overexpression of miR-455-5p by transfection of miR-455-5p mimic in vitro or tail vain injection of miR-455-5p agomir in vivo provoked cardiac remodeling, whereas genetic knockdown of miR-455-5p attenuated the isoprenaline-induced cardiac remodeling. Besides, miR-455-5p directly targeted to 3’-untranslated region of protein arginine methyltransferase 1 (PRMT1) and subsequently downregulated PRMT1 level. Furthermore, we found that PRMT1 protected against cardiac hypertrophy and fibrosis in vitro. Mechanistically, miR-455-5p induced cardiac remodeling by downregulating PRMT1-induced asymmetric di-methylation on R1748, R1750, R1751 and R1752 of Notch1, resulting in suppression of recruitment of Presenilin, Notch1 cleavage, NICD releasing and Notch signaling pathway. Finally, circulating miR-455-5p was positively correlated with parameters of left ventricular wall thickening. Taken together, miR-455-5p plays a provocative role in cardiac remodeling via inactivation of the PRMT1-mediated Notch signaling pathway, suggesting miR-455-5p/PRMT1/Notch1 signaling axis as potential therapeutic targets for pathological cardiac remodeling. |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
English |
| DOI: |
10.1007/s00018-023-04987-2 |
| DOI: |
10.1007/s00018-023-04987-2.pdf |
| DOI: |
10.1007/s00018-023-04987-2/fulltext.html |
| الإتاحة: |
https://doi.org/10.1007/s00018-023-04987-2Test |
| حقوق: |
https://creativecommons.org/licenses/by/4.0Test ; https://creativecommons.org/licenses/by/4.0Test |
| رقم الانضمام: |
edsbas.24D843FA |
| قاعدة البيانات: |
BASE |
