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. 2000 Sep 15;106(6):733–738. doi: 10.1172/JCI11144

Figure 3.

Figure 3

Lungs from chronically hypoxic rats treated with the VEGF-R2 inhibitor SU5416 for 3 weeks. (a) Intimal obliteration of precapillary pulmonary artery (arrows), resulting in almost-complete disappearance of vascular lumen; (b) the intimal obliteration is due to expansion of Factor VIII–related antigen–positive cells (arrow). (c) The intraluminal cluster of endothelial cells shows expression of the key apoptosis effector active caspase 3 (arrowhead), while endothelial cells in the center of the cluster (arrow) show evidence of proliferation with expression of proliferating cell nuclear antigen (inset, arrowheads). (d) Caspase inhibition with the broad spectrum caspase inhibitor Z-Asp-CH2, administered at the beginning of the chronic hypoxia and SU5416 treatment, results in a marked decrease in pulmonary artery pressures. The pulmonary arteries are lined by a monolayer of Factor VIII–related antigen–positive endothelial cells, with preservation of vascular lumen. (a: pentachrome staining, ×320; b: Factor VIII–related antigen immunostaining, ×300; c: active caspase 3 immunostaining, ×400; d: Factor VIII–related antigen immunostaining, ×200.)