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Figure 5 | Clinical Epigenetics

Figure 5

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

Figure 5

Hypoxia induces STAT3 and H2A.Zac and H3K9ac turnover at the NOS3 promoter region. (A) Predicted STAT3 binding site in the NOS3 promoter region based on the STAT3 consensus motifs are shown. During normoxia in human umbilical artery endothelial cells (HUAEC), only one region 1554 bp upstream of the transcription start site (TSS) was enriched in immune precipitates using STAT3 specific antibodies. Enrichment significantly increased during hypoxia with additional sequences being amplified 1,260 and 620 bp upstream of the TSS. (B) NOS3 and STAT3, particularly STAT3α expression, is upregulated in HUAEC in response to hypoxia. (C) Enrichment of the promoter sequence 1554 upstream of the TSS in STAT3 immune precipitates is upregulated during hypoxia in HUAECs. (D) Hypoxia induces a substantial increase in H2A.Zac and H3K9ac turnover at the NOS3 promoter region in HUAECs.

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