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MicroRNA-216a Promotes Endothelial Inflammation by Smad7IκBα Pathway in Atherosclerosis
المؤلفون المشاركون
Yang, Shujun
Chen, Yu
Mi, Xuenan
Zhang, Shuyuan
Yang, Yunyun
Hui, Rutai
Zhang, Weili
المصدر
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-9، 9ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-11-18
دولة النشر
مصر
عدد الصفحات
9
التخصصات الرئيسية
الملخص EN
Background.
The endothelium is the first line of defence against harmful microenvironment risks, and microRNAs (miRNAs) involved in vascular inflammation may be promising therapeutic targets to modulate atherosclerosis progression.
In this study, we aimed to investigate the mechanism by which microRNA-216a (miR-216a) modulated inflammation activation of endothelial cells.
Methods.
A replicative senescence model of human umbilical vein endothelial cells (HUVECs) was established, and population-doubling levels (PDLs) were defined during passages.
PDL8 HUVECs were transfected with miR-216a mimics/inhibitor or small interfering RNA (siRNA) of SMAD family member 7 (Smad7).
Real-time PCR and Western blot assays were performed to detect the regulatory role of miR-216a on Smad7 and NF-κB inhibitor alpha (IκBα) expression.
The effect of miR-216a on adhesive capability of HUVECs to THP-1 cells was examined.
MiR-216a and Smad7 expression in vivo were measured using human carotid atherosclerotic plaques of the patients who underwent carotid endarterectomy (n=41).
Results.
Luciferase assays showed that Smad7 was a direct target of miR-216a.
Smad7 mRNA expression, negatively correlated with miR-216a during endothelial aging, was downregulated in senescent PDL44 cells, compared with young PDL8 HUVECs.
MiR-216a markedly increased endothelial inflammation and adhesive capability to monocytes in PDL8 cells by promoting the phosphorylation and degradation of IκBα and then activating NF-κB signalling pathway.
The effect of miR-216a on endothelial cells was consistent with that blocked Smad7 by siRNAs.
When inhibiting endogenous miR-216a, the Smad7/IκBα expression was rescued, which led to decreased endothelial inflammation and monocytes recruitment.
In human carotid atherosclerotic plaques, Smad7 level was remarkably decreased in high miR-216a group compared with low miR-216a group.
Moreover, miR-216a was negatively correlated with Smad7 and IκBα levels and positively correlated with interleukin 1 beta (IL1β) expression in vivo.
Conclusion.
In summary, our findings suggest a new mechanism of vascular endothelial inflammation involving Smad7/IκBα signalling pathway in atherosclerosis.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Yang, Shujun& Chen, Yu& Mi, Xuenan& Zhang, Shuyuan& Yang, Yunyun& Hui, Rutai…[et al.]. 2020. MicroRNA-216a Promotes Endothelial Inflammation by Smad7IκBα Pathway in Atherosclerosis. Disease Markers،Vol. 2020, no. 2020, pp.1-9.
https://search.emarefa.net/detail/BIM-1154148
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Yang, Shujun…[et al.]. MicroRNA-216a Promotes Endothelial Inflammation by Smad7IκBα Pathway in Atherosclerosis. Disease Markers No. 2020 (2020), pp.1-9.
https://search.emarefa.net/detail/BIM-1154148
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Yang, Shujun& Chen, Yu& Mi, Xuenan& Zhang, Shuyuan& Yang, Yunyun& Hui, Rutai…[et al.]. MicroRNA-216a Promotes Endothelial Inflammation by Smad7IκBα Pathway in Atherosclerosis. Disease Markers. 2020. Vol. 2020, no. 2020, pp.1-9.
https://search.emarefa.net/detail/BIM-1154148
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1154148
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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