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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Pediatr Res. 2015 Sep 2;78(6):650–656. doi: 10.1038/pr.2015.168

Figure 5.

Figure 5

Fluticasone phosphorylates serine 211 (P-GR211) but not serine 226 (P-GR226) of the glucocorticoid receptor in fetal airway smooth muscle (ASM). Fluticasone treatment of fetal ASM significantly increased phosphorylation of glucocorticoid receptors (GR) at Serine 211 (panel a) but had no effect on phosphorylation of the Ser 226 residue (panel b). Cotreatment of fetal ASM cells with Fluticasone and TNF-α resulted in a significant increase in P-GR Ser 211 (panel a) and P-GR Ser 211 (panel b). Quiescent fetal ASM cells were treated with fluticasone (1 and 100 nmol/l, FP) and TNF-α (20 ng/ml) or vehicle (control). Scanning densitometry of three representative immunoblots normalized over the area density of the corresponding glyceraldehyde 3-phosphate dehydrogenase content. The results are expressed as the fold increase over basal values. *P < 0.05, **P < 0.01.