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. 2020 Jan 23;19(3):2229–2235. doi: 10.3892/etm.2020.8470

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Copyright: © Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — miR-489 inhibited the isoproterenol-induced cardiac fibrosis induced via HDAC2. (A) RT-qPCR was used to determine the expression level of HDAC2 in CFs transfected with pcDNA3.1 and pcDNA3.1-HDAC2. (B) HDAC2, and (C) Col1A1 and α-SMA expression levels in CFs transfected with NC, miR-489 mimic or miR-489 mimic plus HDAC2 were determined by RT-qPCR. (D) An MTT assay was used to assess the viability of CFs transfected with NC, miR-489 mimic or miR-489 mimic plus HDAC2. The data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01. miR, microRNA; HDAC2, histone deacetylase 2; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; CFs, cardiac fibroblasts; Col1A1, collagen I; α-SMA, α-smooth muscle actin; NC negative control.