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. 2015 Jan 13;19(3):608–619. doi: 10.1111/jcmm.12445

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© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fig 5 — The STAT3/c-Myc pathway mediates miR-16 down-regulation during cardiac hypertrophy. (A) Activation of STAT3 and c-Myc in myocardial hypertrophy in rats receiving AAC treatment for 2 weeks (n + 5–7). (B) Activation of STAT3 and c-Myc in PE-treated NRVCs (n + 3). (C) miR-16 and ANP mRNA expressions were assessed by qRT-PCR assay in PE-treated NRVCs without and with the presence of STAT3 inhibitor cryptotanshinone (10 μM) and c-Myc inhibitor 10058-F4 (30 μM), respectively (n + 3). Data are shown as mean ± SD; *P < 0.05, **P < 0.01, ***P < 0.001.