C27 LET'S PRETEND WE'RE MARRIED: THE RIGHT VENTRICLE AND THE PULMONARY VASCULATURE: Pharmacological Inhibition Of Mtor Kinase Selectively Suppresses Rv-Specific Activation Of Mtorc1 Signaling, Reverses Rv Remodeling And Improves Rv Morphology And Function In Rats With Established Ph

Mechanistic target of rapamycin (mTOR) promotes smooth muscle cell proliferation, survival and pulmonary vascular remodeling via two functionally distinct complexes, mTORC1 (supports cell growth) and mTORC2 (promotes cell survival). Results: We found that, in contrast to activation of both, mTORC1 a...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2017-01, Vol.195
Main Authors: Pena, A, Kobir, A, Goncharov, D, Goda, A, Delgado-Montero, A, Tayal, B, Vanderpool, R, Baust, J, Chang, B, Mora, A L, Gorcsan, J, Goncharova, E A
Format: Article
Language:English
Subjects:
Cardiomyocytes
Cell growth
Circulatory system
Morphology
Pulmonary arteries
Rodents
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Summary:Mechanistic target of rapamycin (mTOR) promotes smooth muscle cell proliferation, survival and pulmonary vascular remodeling via two functionally distinct complexes, mTORC1 (supports cell growth) and mTORC2 (promotes cell survival). Results: We found that, in contrast to activation of both, mTORC1 and mTORC2 pathways in small remodeled PAs at five weeks post-PH induction, RV tissues had predominant up-regulation of mTORC1 signaling accompanied by cardiomyocyte and RV hypertrophy, increased RV wall thickness (RV WT), RV/LV end-diastolic area (EDA) ratio, RV contractility (max dP/dT) and afterload (Ea), shorter RV acceleration time (RV-AT) and decreased tricuspid annular plane systolic excursion (TAPSE) compared to controls.
ISSN:1073-449X
1535-4970