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. Author manuscript; available in PMC: 2018 Apr 17.
Published in final edited form as: Sci Signal. 2017 Oct 17;10(501):eaaj1784. doi: 10.1126/scisignal.aaj1784

Fig. 6. Potential clinical relevance of Nox1-mediated endothelial senescence in human pulmonary vascular tissue.

Fig. 6

Data points for human tissue are shown in green; data for cell experiments are shown in red; data in gray are the corresponding controls. Data for (A) to (E) are plotted as linear regression (n = 8 samples); equation, r2, and P values are indicated in the corresponding graph. (A and B) Correlation between NADPH-driven O2•− production, as measured by cytochrome c reduction (A), or H2O2 production, as measured by Amplex Red fluorescence (B), and age in human lung homogenates. (C and D) Abundance of Nox1 (C) and p53 and p21cip (D), as measured by Western blot of total homogenates of aging human lung. (E) Intimal immunofluorescence for Nox1 (top, green) and p21cip (bottom, red) in aged human lung sections. Scale bar, 50 μm. Graphs show linear regression analyses. (F) HPAEC senescence induced by TSP1 in the presence or absence of NoxA1ds, as measured by SA-β-Gal staining. Graphical data are means ± SEM (n = 3 biological replicates per treatment). Scale bar, 40 μm. *P < 0.05 for TSP1 challenge compared to scrambled vehicle control by Student’s t test.

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