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JCR 2016
جستجوی مقالات
شنبه 18 بهمن 1404
Iranian Journal of Public Health
، جلد ۵۳، شماره ۱۰، صفحات ۲۲۶۰-۲۲۷۰
عنوان فارسی
چکیده فارسی مقاله
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عنوان انگلیسی
MiR-21-5p Promotes Osteogenic Differentiation and Calcification of Valvular Interstitial Cells by Targeting TGFBI in Calcific Aortic Valve Disease
چکیده انگلیسی مقاله
Background: Calcific aortic valve disease (CAVD) is the most common heart relating disease with high morbidity and mortality, especially in elderly population. While extensive investigations have been devoted to the study of mechanistic pathways related to CAVD, the key factors and mechanisms mediating valve mineralization remain unclear. The aim of this study is to investigate the role of mirnas and their downstream targets in CAVD disease progression. A previous recent multi-omics study suggested a novel CAVD molecular interaction network contained miR-21-5p. Methods: CAV and their pair-matched adjacent normal tissues were obtained from 15 patients pathologically diagnosed as CAVD and admitted in Yancheng Third People's Hospital (The Sixth Affiliated Hospital of Nantong University) from 2019-2021. RT-qPCR was utilized for detection of miR-21-5p and related protein expression levels to confirm the related factors in CAVD progression. Western blotting was applied to strengthen the results of RT-qPCR and confirm osteogenic differentiation of VICs via biomarker detection. The staining of alkaline phosphatase (ALP) and alizarin red was performed to assess the degree of VIC mineralization. Results: We found that miR-21-5p was remarkably increased (P<0.0001) in calcified aortic valves (AVs) whereas TGFBI was diminished (P<0.01) in CAVD samples compared to the paired normal tissues from CAVD patients. Additionally, TGFBI was targeted by miR-21-5p. Furthermore, overexpressing TGFBI could block VIC osteogenic differentiation mediated by miR-21-5p. To sum up, miR-21-5p promotes VIC osteogenic differentiation and calcification via TGFBI in CAVD progression. Conclusion: Our work might bring a sight on underlying mechanisms of CAVD progression and provide a possible therapeutic target for diagnosis and treatment.
کلیدواژههای انگلیسی مقاله
نویسندگان مقاله
| Yan Gu
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Rongjin Chen
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Jianxiang Song
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Zhan Shi
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Jixiang Wu
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Huiwen Chang
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Conghu Yuan
Department of Anesthesiology, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yan-cheng, Jiangsu 224000, China
| Woda Shi
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
| Yajun Zhang
Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hos-pital, Yancheng, Jiangsu 224000, China
نشانی اینترنتی
https://ijph.tums.ac.ir/index.php/ijph/article/view/33840
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