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. 2012 Apr 23;109(19):7529–7534. doi: 10.1073/pnas.1200650109

Fig. 2.

Fig. 2.

STAT5b negatively regulates 20α-HSD in human myometrial cells. Binding of endogenous STAT5b to response elements in the 20α-HSD/AKR1C18 promoter declines in pregnant mouse myometrium at term. (A–C) hTERT-HM cells were transfected with a pCMV–STAT5b expression plasmid or with an empty vector (control). Levels of STAT5b mRNA (A) and protein (B) were increased after 24 h. Up-regulation of STAT5b was associated with a significant suppression of 20α-HSD mRNA levels (C). (D–F) hTERT-HM cells were transfected with STAT5b siRNA or with a scrambled siRNA (control). Levels of STAT5b mRNA (D) and protein (E) were significantly reduced after 72 h. (F) The decline in STAT5b expression was associated with a significant induction of 20α-HSD mRNA levels. Data shown in A, C, D, and F are the mean ± SD of values from three independent experiments, each conducted in triplicate. *Significantly (P < 0.05) different from control. (G) Binding of endogenous STAT5b to the AKR1C18 promoter is significantly decreased in pregnant mouse myometrium between 15.5 dpc and just before labor. ChIP using antibodies to STAT5b was used to assess binding of endogenous STAT5b to the region of the AKR1C18 promoter that contains putative STAT5b response elements. STAT5b binding was quantified by PCR, normalized to input and expressed as fold-increase over binding using nonimmune IgG. Data are the mean ± SEM (*P < 0.05; n = 5 mice per group).