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. 2013 Jan 16;83(4):635–646. doi: 10.1038/ki.2012.447

Figure 7.

Figure 7

Melanocortin 1 receptor (MC1R) mediates the anti-apoptotic effect of adrenocorticotropic hormone (ACTH) in renal tubular epithelial cells. (a) ACTH reinstates the viability of tumor necrosis factor (TNF)–injured IRPTC cells in a dose-dependent manner. IRPTC cells were treated with vehicle, TNF (10 ng/ml), ACTH (10−8M), or TNF in combination with ACTH (10−10M, 10−9M, 10−8M, 10−7M) for 6 h before cellular viability was estimated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay; *P<0.05 versus other groups. (b) After MC1R silencing, ACTH fails to prevent TNF-induced PARP cleavage. IRPTC cells were transfected with scrambled (si-Control) or MC1R-specific (si-MC1R) siRNA for RNA interference. Cells were then treated with vehicle, TNF (10 ng/ml), and/or ACTH (10−8M) for 6 h. (b) Cell lysates were subjected to immunoblot analysis for MC1R, PARP, and actin; cellular viability assessed by MTT assay (c); *P<0.05 versus other groups in si-Control. (d) Fixed cells were prepared for TdT-mediated dUTP nick-end labeling (TUNEL) staining (green), fluorescent immunocytochemistry staining for MC1R (green), and counterstaining of DAPI (blue); bar=30 μm. (e) Absolute counts of TUNEL-positive cells in cell cultures; *P<0.05 versus other groups in si-Control.