Figure 3
Minocycline prevents inflammasome activation in glucose challenged podocytes and glomerular endothelial cells (GEnC) in vitro.
(a,b) High glucose (25 mM, 24 h), but not mannitol (25 mM, 24 h), induces the inflammasome markers Nlrp3 and cleaved IL1β in podocytes and glomerular endothelial cells in vitro. Minocycline (10 μM, 24 h) abrogates glucose-induced inflammasome activation. (c) Following transfection of human podocytes with a human Nlrp3 mutant (Q705K), resulting in constitutive active Nlrp3, minocycline (10 μM, 24 h) fails to suppress IL1β cleavage. (d,e) Minocycline prevents glucose-induced glomerular filtration barrier disruption in vitro; scheme reflecting the in vitro model used to mimic the glomerular filtration barrier (e) and bar graph summarizing results for albumin concentration in the lower chamber 3 hours after the addition of FITC-BSA to the upper chamber. Mean values ± SEM (a–c,e); *P < 0.05, ns: non-significant (a–c: Mann-Whitney-test; e: t-test); (a–c) representative cropped images without further modification are shown; exemplary uncropped images are provided in Supplementary Fig. 6.
