FIGURE 7.

PIO reverses alcohol-mediated pathways that upregulate Nox isoform expression in hAM. hAM were collected from control subjects (Con; n = 17) and from subjects with an AUD (Alc; n = 17). hAM were then treated ± PIO (10 μM) ex vivo for 1 d. (A) mRNA levels of C/EBPβ were measured in hAM by quantitative RT-PCR (qRT-PCR; in duplicate), normalized to 9s mRNA, and expressed as mean ± SEM, relative to control. (B) Cytosolic and nuclear protein expression of C/EBPβ was determined in hAM (10 fields per condition) using confocal fluorescence microscopy. Fluorescence was normalized to DAPI nuclear stain and expressed as mean RFU per cell ± SEM, relative to control. miR levels of Nox1-related miR-1264 and miR-1982 (C), and Nox2-related miR-103 and miR-107 (D) were measured in hAM by qRT-PCR (in duplicate), normalized to 5U ribosomal mRNA, and expressed as mean ± SEM, relative to control. *p < 0.05 versus Con, ^Φp < 0.05 versus Alc.