Fig. 1: HDAC1 inhibition promotes the expression of antifibrotic miRNAs targeting TGFBRI mRNA.

A left, RT-PCR showing the expression of TGFBRI mRNA in MCs from PD patients treated with MS-275 (250 nM for, 24, 48 and 72 h). Quantitative RT-PCR was performed on total RNA. L34 mRNA levels were used for normalization. Bars represent the mean ± SEM of triplicate determinations in four independent experiments. middle, WB showing the expression of TGFBRI from the same experiment. GAPDH was used as a loading control. Data are representative of three independent experiments. right, RT-PCR showing TGFBRI mRNA expression upon HDAC1 genetic silencing using a specific siRNA. L34 mRNA levels were used for normalization. Bars represent the mean ± SEM of duplicate determinations in four independent experiments. B top, RT-PCR showing the expression of miR-769-5p, miR3607-3p, miR5195-3p, miR-98-5p, miR-490-3p and miR-27b-3p upon exposure to MS-275 at the same conditions as in A miR-16 was used for normalization. Bars represent the mean ± SEM of duplicate determinations in five independent experiments. Bottom, the expression of the same miRNAs was analyzed upon HDAC1 genetic silencing. miR-16 was used for normalization. Bars represent the mean ± SEM of duplicate determinations in four independent experiments. C RT-PCR showing the expression of miR-769-5p, miR3607-3p and miR5195-3p upon treatment with TGFβ1 (2 ng/ml for 72 h) (top), or upon treatment with anti-TGF-β1 monoclonal antibody 1D11.16 (100 μg/ml). (bottom). Bars represent the mean ± SEM of duplicate determinations in three to five independent experiments.