Genetic deletion of p66shc and/or cyclophilin D results in decreased pulmonary vascular tone.

ABSTRACT:

Aims

The pulmonary vascular tone and hypoxia-induced alterations of the pulmonary vasculature may be regulated by the mitochondrial membrane permeability transition pore (mPTP) that controls mitochondrial calcium load and apoptosis. We thus investigated, if the mitochondrial proteins p66shc and cyclophilin D (CypD) that regulate mPTP opening affect the pulmonary vascular tone.

Methods and results

Mice deficient for p66shc (p66shc-/-), CypD (CypD-/-), or both proteins (p66shc/CypD-/-) exhibited decreased pulmonary vascular resistance (PVR) compared to wild-type mice determined in isolated lungs and in vivo. In contrast, systemic arterial pressure was only lower in CypD-/- mice. As cardiac function and pulmonary vascular remodelling did not differ between genotypes, we determi

SUBMITTER: Gierhardt M 

PROVIDER: S-EPMC8752355 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature