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. 2011 Apr;162(8):1716–1730. doi: 10.1111/j.1476-5381.2010.01189.x

Figure 3.

Figure 3

Decrease of nuclear factor of activated T-lymphocyte-3 (NFAT3) activation, its related signalling pathways, and NFAT-driven luciferase activity induced by carboplatin (Cbpt) in renal tubular cells (RTC) overexpressing haem oxygenase (HO)-1 and their increase in RTC with HO-1 knockdown. (A) Cell variants were treated with 200 µM carboplatin to examine activation of the extracellular signal regulated kinase (ERK)/Jun N-terminal kinase (JNK)/protein kinase C (PKC) pathways involved in NFAT3 activation by Western blot analysis. (B) carboplatin-treated RTC variants were partitioned into nuclear-cytosolic fractions for the Western blot analysis of NFAT3 activation. (C) Cell variants were transiently transfected with the NFAT3-reported vector and pRL-TK for 24 h, followed by a 200 µM carboplatin treatment for 4 h. Results show the mean ± SEM of four independent experiments (*P < 0.05, significantly different from pGL3 alone and #P < 0.05, significantly different from pGL3 with additional carboplatin treatment). Ctrl, control.