@article{CDT33332,
author = {Jinsong Tao and Jingyi Wang and Chunyu Li and Weiwei Wang and Hao Yu and Jinhui Liu and Xiangqing Kong and Yan Chen},
title = {MiR-216a accelerates proliferation and fibrogenesis via targeting PTEN and SMAD7 in human cardiac fibroblasts},
journal = {Cardiovascular Diagnosis and Therapy},
volume = {9},
number = {6},
year = {2019},
keywords = {},
abstract = {Background: Heart failure (HF) is a progressive disease with relatively poor prognosis and lacks effective therapy, and the discovery of dysregulated microRNAs (miRNAs) and their role in cardiac fibroblasts have provided a new avenue for elucidating the mechanism involved in HF.
Methods: Two datasets of GSE53080 and GSE57338 were used to screen the miRNAs profiling and analysis the differentially expressed genes (DEGs) in HF. QRT-PCR was used to detect miR-216a between HF and healthy controls (HC). Cell counting kit-8 (CCK-8) assay and clonogenic assay were used to analyze the effect of proliferation and fibrogenesis. Then dual-luciferase activity assay and western blotting were used to confirm the key mechanism.
Results: In this study, the results showed that miR-216a was significantly up-regulated in HF and over- expression of miR-216a promoted proliferation and enhanced the fibrogenesis in the human cardiac fibroblasts (HCF) cells. Phosphatase and tensin homolog (PTEN) and mothers against decapentaplegic homolog 7 (SMAD7) were both validated as the direct target genes of miR-216a, which were confirmed by the dual-luciferase reporter assay. MiR-216a decreased the expression of PTEN and SMAD7 leading to the activation of Akt/mTOR and TGF-βRI/Smad2 in the HCF cells, which might act as a promoter of cardiac fibrosis.
Conclusions: Our study might provide a promising approach for the treatment of HF in the future.},
issn = {2223-3660}, url = {https://cdt.amegroups.org/article/view/33332}
}