Induction of VMAT-1 and TPH-1 Expression Induces Vesicular Accumulation of Serotonin and Protects Cells and Tissue from Cooling/Rewarming Injury
Figure 3
Co-expression of rat vesicular monoamine transporter-1 (VMAT-1) and tryptophan hydroxylase-1 (TPH-1) in kidney slices (VTkidney) and treatment of kidney slices with NaHS (0.3 mM) protect tissue against static hypothermic storage (3°C, 24h) by induction of cystathionine beta synthase (CBS) and H2S production.
A, VTkidney show increased expression of VMAT-1. B, VTkidney shows increased expression of CBS, with main presence in tubular cells. C, VTkidney and NaHS treated slices show absence of hypothermia induced loss of fatty acid binding protein (FABP1). FABP1 staining (green) was predominantly in the cytoplasmic region of the proximal tubule. D, VTkidney and NaHS treated slices lack hypothermia induced increased expression of caspase 3/7 activity. E, VTkidney shows increased production of H2S. Data are means ± SEM. * denotes difference from non-cooled tissue (Controls 37°C), # denotes difference from empty vector hypothermic tissue (3°C), ANOVA tests, p<0.05. Gray bars represent controls and black bars hypothermia treated tissue. Experiments consist of n ≥3. All magnifications are 40x.