Pathogenic Role of mTORC1 and mTORC2 in Pulmonary Hypertension
Haiyang Tang, Kang Wu, Jian Wang, Sujana Vinjamuri, Yali Gu, Shanshan Song, Ziyi Wang, Qian Zhang, Angela Balistrieri, Ramon J. Ayon, Franz Rischard, Rebecca Vanderpool, Jiwang Chen, Guofei Zhou, Ankit A. Desai, Stephen M. Black, Joe G.N. Garcia, Jason X.-J. Yuan and Ayako Makino
Rictor Deletion in Endothelial Cells Fails to Cause Spontaneous Pulmonary Hypertension
Endothelial-specific conditional and inducible KO of Rictor fails to attenuates hypoxia-induced pulmonary hypertension in RictorEC−/− mice. (A) Schematic strategy for the generation of EC-specific Rictor-KO mice (RictorEC−/−) and the timeline indicating the time for Tam injection and experimental measurements. (B) Representative record of RVP (a) and summarized data (mean ± SE) showing the peak value of RVSP (b) (Kruskal-Wallis test, p < 0.001) and the Fulton index (RV/[LV + S]) ratio (c) (Kruskal-Wallis test, p < 0.001) in WT and RictorEC−/− mice exposed to normoxia and hypoxia (for 3 weeks). Dunn test, **p < 0.01, ***p < 0.001 versus Normoxia-WT. (C) Representative hematoxylin and eosin images of the cross-section of small PA (a) and summarized data (mean ± SE) showing the PA wall thickness in WT and RictorEC−/− mice under normoxic and hypoxic conditions (b). The numbers of experiments or samples (n) for each group are indicated in each bar. Abbreviations as in Figure 1.