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. Author manuscript; available in PMC: 2011 Feb 2.
Published in final edited form as: Circulation. 2010 Jan 18;121(4):529–536. doi: 10.1161/CIRCULATIONAHA.109.862946

Figure 2. Validation of PGT targeting by loss of protein expression and transport function.

Figure 2

(a) Lung tissue from PGT Neo/Neo mice shows absence of PGT protein, whereas PGT +/+ mice express PGT (brown reaction product) in type II cells (see Supplemental Data Figure 1S for birefringence of granules of these cells in our PGT +/+ mice).

(b) PGE2 uptake by mouse embryonic fibroblasts (MEFs) derived from PGT wild type (+/+) versus PGT null (−/−) mice. 3H-PGE2 uptake was determined alone (this represents PGT-mediated uptake plus simple diffusion) and also in the presence of excess unlabeled PGE2 (this blocks PGT-mediated tracer uptake and reveals uptake due to simple diffusion alone). For each set of paired uptake data, we calculated the percent increase in PGE2 uptake attributable to PGT: (uptaketracer) ÷ (uptaketracer + unlabeled) × 100. MEFs from PGT +/+ mice (n = 7) had a PGT-mediated change in uptake of +30.3% ± 8.38% (n = 7), whereas MEFs derived from PGT −/− animals had a PGT-mediated change in uptake of −1.29% ± 3.38% (n = 7). The difference was highly statistically significant (p = 0.008 by unpaired t-test; p = 0.007 by Wilcoxon two-sample test).