A67 BREAKDOWN: THE CELLULAR CONTRIBUTION TO PULMONARY HYPERTENSION: Targeted Inhibition Of Mitochondrial Hsp90 Improves Pulmonary Arterial Hypertension

The molecular chaperone heat shock protein 90 (Hsp90), by interacting with its client proteins, is directly associated with malignant growth and proliferation. Whereas cytosolic Hsp90 inhibition displays a lack of absolute specificity for PAH-PASMCs, selective inhibition of mtHsp90 activity using Ga...

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Published inAmerican journal of respiratory and critical care medicine Vol. 195
Main Authors Boucherat, O, Breuils-Bonnet, S, Chabot, S, Meloche, J, Vitry, G, Lambert, C, Nadeau, V, Tremblay, E, Zervopoulos, S, Sutendra, G, Michelakis, E D, Chae, Y C, Altieri, D, Paulin, R, Provencher, S, Bonnet, S
Format Journal Article
LanguageEnglish
Published New York American Thoracic Society 01.01.2017
Subjects
Apoptosis
Hypertension
Medical prognosis
Mitochondrial DNA
Pulmonary arteries
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Summary:The molecular chaperone heat shock protein 90 (Hsp90), by interacting with its client proteins, is directly associated with malignant growth and proliferation. Whereas cytosolic Hsp90 inhibition displays a lack of absolute specificity for PAH-PASMCs, selective inhibition of mtHsp90 activity using Gamitrinib decreased PAH-PASMC proliferation (Ki67 labeling) and resistance to apoptosis (Annexin V assay) without affecting control cells.
ISSN:1073-449X
1535-4970