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. 2016 Oct 22;7(51):84907–84923. doi: 10.18632/oncotarget.12823

Figure 9. Interaction of occludin, p38 with MKP-1.

Figure 9

TM4 Mkp-1 silencing cells and TM4 control cells were either not stimulated or stimulated with LPS (100 ng/ml). Cells were harvested for protein after 0, 15, 30, 60 and 120 minutes (short timepoint, A.) or 24 hours (long timepoint, B.). Cell lysates were subjected to western blot analysis for MKP-1, phospho-IκBα (p-IκBα), total-IκBα (IκBα), phospho-p38 (p-p38), total-p38 (p38), and β-actin (short timepoint, A) or MKP-1, occludin, and β-actin (long timepoint, B). Immunoblots were scanned, and the intensity of bands was quantified by the image program. Data were normalized to the control and expressed as the percentage of maximum activation or fold change of stimulation (a1-a3, b1-b2). C. Mkp-1 siRNA or control siRNA TM4 Sertoli cells were either not stimulated or stimulated with LPS (100 ng/ml). Cells were harvested for RNA after 1, 2 and 6 hours. Cells were harvested for RNA, and realtime PCR was carried out using primers specific to Mkp-1 (c1), occludin (c2) and β-actin. Data were normalized to the control and the ratio was expressed as fold change relative to the control sample. D. TM4 Sertoli cells were either not stimulated or stimulated with LPS. Cells were harvested for protein after 30, 60 and 120 minutes, and MKP-1 was immunoprecipitated (IP) from cell lysates and analyzed by western blotting for presence of p38, occludin and MKP-1. *p<0.05.