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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Kidney Int. 2014 Jun 11;86(6):1150–1160. doi: 10.1038/ki.2014.196

Figure 2.

Figure 2

SA induces COX-2, pro-inflammatory and stress genes in cultured podocytes. A) Serum-starved podocytes were exposed to 40 mg/ml BSA for 4 h and 24 h, and relative mRNA levels of COX-2, pro-inflammatory and stress response genes were measured by qRT-PCR and normalized to β-actin (*P<0.05, **P<0.01 and ***P<0.001 versus time matched control, determined by t test). B) Podocytes were maintained in culture medium containing FBS or serum-starved O/N, and exposed to 40 mg/ml of BSA for 4 h and subjected to immuno-blot analysis for COX-2 and GAPDH. C) Serum-starved podocytes were exposed to 40 mg/ml BSA, human serum albumin (HSA) and Ovalbumin (OVA), and harvested at indicated time points. Protein extracts were analyzed for COX-2 and GAPDH (shown as loading control for a representative blot). D) Serum-starved podocytes were exposed for 4 h to increasing concentrations of BSA as indicated, and mRNA levels of COX-2 were measured by qRT-PCR and normalized to β-actin (***P<0.001 versus control, determined by t test).