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. Author manuscript; available in PMC: 2023 Apr 29.
Published in final edited form as: Circ Res. 2022 Apr 28;130(9):1466–1486. doi: 10.1161/CIRCRESAHA.121.319971

Figure 2. Plexogenic arteriopathy and severe PAH in mice lacking both Sirt3 and Ucp2.

Figure 2.

(A) Representative histology (Hematoxylin-Eosin staining) of a lung from a Sirt3−/−;Ucp2−/− mouse shows numerous plexogenic lesions (back arrows). (B) Representative photomicrograph of confocal fluorescence immunohistochemistry of small pulmonary arteries from wild-type WT and Sirt3−/−;Ucp2−/− mice shows smooth muscle cells (green) and endothelial cells (magenta) in plexogenic lesions. (C) Representative tracings of RV and PA pressures from WT and Sirt3−/−;Ucp2−/− mice by close-chest right heart catheterization through the jugular vein shows that Sirt3−/−;Ucp2−/− mice have a significant increase in RV and PA pressure. SMA: smooth muscle actin, vWF: von Willebrand Factor (marking endothelial cells), DAPI (marking nuclei). (Images courtesy of Dr Gopinath Sutendra.)