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Overexpression of miR-27b-3p Targeting Wnt3a Regulates the Signaling Pathway of Wntβ-Catenin and Attenuates Atrial Fibrosis in Rats with Atrial Fibrillation
المؤلفون المشاركون
Li, Jin-yi
Zhong, Guo-qiang
Lv, Xiangwei
Hu, Yisen
Wang, Shirong
Yang, Chengye
Li, Chengxuan
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-04-17
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
MicroRNAs (miRNAs) are regarded as a potential method for the treatment of atrial fibrillation (AF) although its molecular mechanism remains unknown.
We found in our previous study that the level of peripheral blood miR-27b-3p and the expression of atrial tissue CX43 were both significantly downregulated in AF patients.
In the present study, we propose and test this hypothesis that overexpression of miR-27b-3p attenuates atrial fibrosis, increases CX43 expression, and regulates the signaling pathway of Wnt/β-Catenin by targeting Wnt3a.
miR-27b-3p overexpression was induced by rat tail vein injection of adeno-associated virus.
Two weeks after transfection of adeno-associated virus, the rat AF model was established by tail vein injection of acetylcholine- (ACh-) CaCl2 for 7 days, and 1 ml/kg was injected daily.
The incidence and duration of AF were recorded with an electrocardiogram.
Cardiac function was monitored by cardiac ultrasound.
Serum cardiac enzyme was detected by ELISA.
The expression of atrial miR-27b-3 and Wnt3a was assayed by quantitative RT-PCR.
Atrial fibrosis was determined by Masson’s trichrome staining.
Expression of atrial Collagen-I and Collagen-III was tested by the immunohistochemical method.
Expression of CX43 was measured by immunofluorescence.
The expression of Collagen-I, a-SMA, Collagen-III, TGF-β1, CX43, Wnt3a, β-Catenin, and p-β-Catenin was assayed by western blot.
Our results showed that miR-27b-3p overexpression could reduce the incidence and duration of AF, alleviate atrial fibrosis, increase atrial CX43 expression, and decrease the expression of Collagen-I, a-SMA, Collagen-III, TGF-β1, Wnt3a, and p-β-Catenin.
In addition, the results of luciferase activity assay showed that Wnt3a is a validated miR-27b-3p target in HEK 293T cells.
Our results provide a new evidence that miR-27b-3p regulates the signaling pathway of Wnt/β-Catenin by targeting Wnt3a, which may play an important role in the development of atrial fibrosis and AF.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Lv, Xiangwei& Li, Jin-yi& Hu, Yisen& Wang, Shirong& Yang, Chengye& Li, Chengxuan…[et al.]. 2019. Overexpression of miR-27b-3p Targeting Wnt3a Regulates the Signaling Pathway of Wntβ-Catenin and Attenuates Atrial Fibrosis in Rats with Atrial Fibrillation. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1204234
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Lv, Xiangwei…[et al.]. Overexpression of miR-27b-3p Targeting Wnt3a Regulates the Signaling Pathway of Wntβ-Catenin and Attenuates Atrial Fibrosis in Rats with Atrial Fibrillation. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-13.
https://search.emarefa.net/detail/BIM-1204234
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Lv, Xiangwei& Li, Jin-yi& Hu, Yisen& Wang, Shirong& Yang, Chengye& Li, Chengxuan…[et al.]. Overexpression of miR-27b-3p Targeting Wnt3a Regulates the Signaling Pathway of Wntβ-Catenin and Attenuates Atrial Fibrosis in Rats with Atrial Fibrillation. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1204234
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204234
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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