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. Author manuscript; available in PMC: 2015 Aug 1.
Published in final edited form as: Transplantation. 2010 Jul 27;90(2):142–149. doi: 10.1097/TP.0b013e3181e228db

Figure 3. Simvastatin preserves the endothelial anti-inflammatory phenotype upon cold storage through a KLF2-dependent mechanism.

Figure 3

A) E-Selectin (top) and VCAM-1 (bottom) mRNA expression determined in EC expose to vasoprotective flow for 24h and statically cold preserved for 0h or 6h with simvastatin or its vehicle, and afterwards stimulated for 4h with IL-1β (0.1U/mL) in warm culture conditions (n=3). B) Top, representative flow cytometry histogram of E-Selectin and VCAM-1 cell surface expression determined in EC described above. Bottom, flow cytometry quantitative analysis of four independent experiments (*p<0.05 vs. 0h; #p<0.05 vs. 6h vehicle+IL1β). C) Expression of KLF2 and inflammatory genes VCAM-1 and E-Selectin in EC transfected with specific siRNA against KLF2 or control, cultured for 24h under vasoprotective flow, preserved at 4°C for 6h in University of Wisconsin Solution supplemented with simvastatin (1μM) or its vehicle, and stimulated for 4h with IL1β (0.1U/mL) in warm culture conditions (*p<0.05 vs. ctrl siRNA 6h vehicle. n=3).