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. 2014 Nov 21;308(2):L208–L220. doi: 10.1152/ajplung.00242.2014

Fig. 6.

Fig. 6.

Upregulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in PTEN-transgenic (TG) mice attenuates the development and progression of hypoxia-induced pulmonary hypertension. A: representative Western blots (left) and quantifications (means ± SE, n = 3–5, right) of the PTEN expression in lungs from WT and PTEN-TG mice exposed to normoxia or chronic hypoxia. B and C: representative record of RVP (B) and summarized data (means ± SE, C) showing RVSP in PTEN-TG mice and WT littermates during Nor and Hyp conditions. D: summarized data (means ± SE) showing Fulton index [RV/(LV+S)] in PTEN-TG mice and WT littermates during Nor and Hyp conditions. E: representative H and E image of distal PAs from PTEN-TG mice and WT littermates during Nor and Hyp conditions. F: summarized data (means ± SE) showing quantification of PA wall thickness, as measured by ratio of wall area to total vessel area, for both medium-sized (50 μm < diameter <100 μM) and small (diameter <50 μM) PAs in PTEN-TG mice and WT littermates in Nor and Hyp. *P < 0.05; **P < 0.01 vs. WT mice in Hyp.