Fig. 1
From: PPAR-γ promotes p38 MAP kinase-mediated endothelial cell permeability through activating Sirt3
Sirt3 attenuates endothelial cell permeability in p38 dependent manner. a, Protein levels of Sirt3 and p38 during early post-reperfusion stages (6 h–24 h) of HBMECs I/R injury model, as compared to control groups with no reperfusion treatment (0 h). B & C, TEER measurement (b) and dextran permeability testing (c) in HBMEC cells either from normal HBMECs with or without SIRT3 inhibited by Sirtuin inhibitor 3-TYP (BLANK and 3-TYP), or from HBMECs at 24 h of reperfusion of I/R injury with Sirt3 overexpression, together with or without treatment of a specific p38 MAP kinase the activator U-46619 (Control, Vector, Sirt3 and Sirt3 + U-46619). The column graph are representative data of an n = 3 performed in quadruplicate. ***, p < 0.001 as compared to the normal HBMECs model (BLANK). ###, p < 0.001 as compared to the non-overexpression control group (Control) and!!! as compared to the Sirt3 overexpression group (Sirt3). TEER: Transepithelial/endothelial Electrical Resistance