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. 2022 May 13;6(7):bvac078. doi: 10.1210/jendso/bvac078

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© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 4. — Forced expression of ZNF217 in polycystic ovary syndrome (PCOS) theca cells converts PCOS theca cells to a normal phenotype of reduced DENND1A.V2, CYP17A1, and dehydroepiandrosterone (DHEA) biosynthesis using a ZNF217 adenovirus (Adv). PCOS theca cells (N=5) were infected with either 3 pfu/cell of Null (empty) vector adenovirus (Null Adv) or ZNF217 adenovirus (ZNF217 Adv) overnight, then treated in the absence (Control) and presence of forskolin (20 μM) for 36 hours for RNA studies or 72 hours for DHEA studies. A, ZNF217 Adv infection augmented ZNF217 messenger RNA (mRNA) expression under unstimulated (control, ***P < .0001) and forskolin-stimulated conditions (**P < .001). ZNF217 Adv infection following forskolin stimulation resulted in decreased ZNF217 mRNA compared to control untreated cells (^αP < .01). B, Following ZNF217 Adv infection, PCOS theca cells were converted to a normal phenotype of diminished DENND1A.V2 mRNA accumulation, under both control (**P < .001) and forskolin-stimulated conditions (**P < .001), compared to Null Adv (control) infected cells. C, CYP17A1 mRNA accumulation was increased following forskolin-treatment (^αP < .01) in Null Adv–infected cells. In addition, ZNF217 Adv infection dramatically decreased CYP17A1 mRNA accumulation under both control (**P < .001) and forskolin-stimulated conditions (**P < .001). D, At 72 hours following infection with Null Adv, DHEA accumulation was observed to be increased by forskolin treatment (^αP < .01). ZNF217 Adv infection resulted in decreased DHEA biosynthesis under both control (**P < .001) and forskolin-stimulated cells (**P < .001). E, Forced ZNF217 overexpression with ZNF217 Adv, augmented miR-130b-3p expression under unstimulated (control, **P < .001) and forskolin-stimulated conditions (*P < .1). ZNF217 Adv infection following forskolin stimulation resulted in decreased ZNF217 mRNA compared to control untreated cells (^αP < .01).