1. Fig. 7. Role of PDE5 up-regulation in lung cancer–associated PH.
Role of PDE5 up-regulation in lung cancer–associated PH. Expression of PDE5 mRNA in (A) PASMCs and (B) PAAFs that were stimulated with basal medium (BM) or indicated cytokines for 24 hours (n = 4). (C) Representative photomicrographs of PDE5 (green), α-SMA (red), and DAPI (nuclei, blue) in pulmonary vessels from human lung tissue without (Donor) or with lung cancer. Scale bars, 100 μm. (D) Migration and (E) apoptosis of human PASMCs and PAAFs that had been stimulated with BM or indicated cytokines in the absence or presence of the PDE5 inhibitor sildenafil; n = 3. *P < 0.05, **P < 0.01, ***P < compared with BM; §P < 0.05, §§P < 0.01 compared with cytokine stimulation in the absence of sildenafil. C57BL/6 mice were treated with sildenafil or vehicle and intratracheally instilled with LLC1 cells. (F) Echocardiographic measurements. (G) Physiological measurements. For WT, n = 5; for LLC1 treated with vehicle or sildenafil, n = 8 each. (H) Representative photomicrographs of elastica van Gieson–stained tissues (bottom), followed by quantification of medial wall thickness of pulmonary vessels (top). Scale bars, 20 μm; n = 4. §P < 0.05, §§P < 0.01 compared with vehicle-treated LLC1 mice.
Soni Savai Pullamsetti et al., Sci Transl Med 2017;9:eaai9048
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