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. 2019 Aug 23;42(5):1781–1792. doi: 10.3892/or.2019.7293

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Copyright: © Zhuang 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 5. — Co-culturing with MSCs^Hypoxia functionally targets Smads downstream of TGF-β1 to reduce fibroblast proliferation and FMT. Fibroblasts were transfected with siRNA against Smad7, or with siRNA-NT as a control, followed by co-culture with MSCs^Hypoxia in the presence of radiation. In parallel experiments, fibroblasts were treated with radiation, or co-cultured with MSCs^Hypoxia in the presence of radiation. Fibroblasts under normal culture conditions were used as the control. (A) Proliferation growth curves as determined using an MTT assay. (B and C) Col1 and α-SMA mRNA levels as analyzed by RT-qPCR. (D) Expression of α-SMA as measured by immunofluorescence staining. Each column represents the mean ± SD from three independent experiments; ^*P<0.05 vs. the Control; ^▲P<0.05 vs. Radiation; ^○P<0.05 vs. Radiation + MSCs^Hypoxia + siRNA-Smad7. MSCs, mesenchymal stem cells; FMT, fibroblast-to-myofibroblast transition; Col1, type I collagen; α-SMA, α-smooth muscle actin.