Fig. 4: Inhibition of Panx1 channels attenuates AAA formation in the Ang-II model.

a Schematic depicting the Ang-II model of AAA in ApoE^−/− mice. Osmotic pumps with either Ang II or saline (control) were inserted into the subcutaneous tissue of mice with/without treatment with PBN. Aortic diameter was measured on day 28, and tissue was harvested for further analysis. b Ang-II mice treated with PBN demonstrated significantly decreased aortic diameter compared with angiotensin treated mice alone. *P = 0.001; n = 15 mice/group. c Representative images of aortic phenotype in all groups. d–i Comparative histology performed on day 28 demonstrates that Ang-II-treated ApoE^−/− mice administered with PBN have decreased polymorphonuclear neutrophil (PMNs), macrophage (Mac-2), CD3 + T-cell infiltration, and elastic-fiber disruption (Verhoeff–Van Gieson staining), and increase in SM-α-actin expression compared with mice treated with Ang II alone. Arrows indicate areas of immunostaining. *P = 0.007; n = 5 mice/group. Scale bar is 200 μm. j–n Aortic inflammation is mitigated by Panx1 antagonism in the Ang II model of AAA. Aortic tissue from Ang-II-treated ApoE^−/− mice after PBN administration showed a significant attenuation in pro-inflammatory cytokine/chemokine production compared with Ang-II-treated mice alone. *P = 0.007 vs. respective Ang-II controls; **P = 0.01; n = 5 mice/group. o A significant decrease in aortic tissue ATP content was observed in PBN-treated mice compared with Ang-II-treated mice alone. *P = 0.01; n = 5 mice/group. p Expression of MMP2 in aortic tissue was significantly attenuated in PBN-treated mice compared with elastase-treated mice alone. *P = 0.02; n = 4/group. Data are represented as mean values ± SEM and comparative statistical analyses were done by two-tailed t-test.