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Figure 4 | Clinical Epigenetics

Figure 4

From: CpG signalling, H2A.Z/H3 acetylation and microRNA-mediated deferred self-attenuation orchestrate foetal NOS3 expression

Figure 4

Histone acetylation changes underlie NOS3 expression in HUAEC in response to trichostatin A treatment and is followed by deferred self-attenuation. (A) Upon HDAC inhibition via trichostatin A (TSA) in HUAEC, there is a rapid, up to 55-fold increase prior to a steep and long-lasting decrease of NOS3 mRNA levels (A). A similar pattern is seen for STAT3 expression (A). (B) Treatment of HUAEC by a restricted TSA pulse leads to an initial boost of NOS3 expression followed by deferred, continuously decreasing amplitudes upon further TSA pulses. (C) Expression of STAT3 α not STAT3β is induced by TSA treatment. (D) Transfection of HUAEC with siRNA targeted to STAT3 or NOS3 mRNA leads to a significant reduction of NOS3 mRNA levels and vice versa. Thereby, the effect of STAT3 inhibition on NOS3 is much stronger than of NOS3 on STAT3.

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