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- Title
miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease.
- Authors
Rong, Xing; Ge, Donghui; Shen, Danping; Chen, Xianda; Wang, Xuliang; Jia, Chang; Zeng, Jingjing; He, Yue’e; Qiu, Huixian; Su, Xiaoping; Chu, Maoping; Zhang, Lu
- Abstract
<bold>Background/Aims:</bold> Increasing evidence indicates that microRNAs (miRNAs) play important roles in Kawasaki disease (KD). Our previous study demonstrated that hsa-miR-27b-3p (miR-27b) was up-regulated in KD serum. However, the specific role of miR-27b in KD remains unclear. We aimed to investigate that miR-27b could be a biomarker and therapeutic target for KD treatment. As well, the specific mechanism of miR-27b effecting endothelial cell functions was studied. <bold>Methods:</bold> The expression of miR-27b and Smad7 was measured by qRT-PCR. Gain-of-function strategy was used to observe the effect of miR-27b on human umbilical vein endothelial cells (HUVECs) proliferation and migration. Bioinformatics analyses were applied to predict miR-27b targets and then we verified Smad7 by a luciferase reporter assay. Western blot was performed to detect the protein expression of Smad7, PCNA, MMP9, MMP12 and TGF-β-related genes. <bold>Results:</bold> We confirmed that miR-27b was shown to be dramatically up-regulated in KD serum and KD serum-treated HUVECs and that elevated expression of miR-27b suppressed the proliferation and migration of HUVECs. Furthermore, our results verified that miR-27b mediated cell functions by affecting the TGF-β via targeting Smad7 in HUVECs. <bold>Conclusion:</bold> These results suggested that up-regulated miR-27b had a protective role in HUVECs proliferation and migration via targeting Smad7 and affecting TGF-β pathway. Therefore, miR-27b represented a potential biomarker for KD and may serve as a promising therapeutic target for KD treatment.
- Subjects
MICRORNA genetics; ENDOTHELIAL cells; GENE silencing; CELL proliferation; CELL migration; MUCOCUTANEOUS lymph node syndrome; BIOMARKERS; GENETICS
- Publication
Cellular Physiology & Biochemistry (Karger AG), 2018, Vol 48, Issue 4, p1804
- ISSN
1015-8987
- Publication type
Article
- DOI
10.1159/000492354