| Literature DB >> 19666009 |
Rongsong Li1, Tyler Beebe, Jeffrey Cui, Mahsa Rouhanizadeh, Lisong Ai, Pin Wang, Martin Gundersen, Wakako Takabe, Tzung K Hsiai.
Abstract
Mitochondrial dysfunction is intimately involved in cardiovascular diseases. Mitochondrial membrane potential (DeltaPsi(m)) is coupled with oxidative phosphorylation to drive ATP synthesis. In this study, we examined the effect of physiological pulsatile shear stress (PSS) on DeltaPsi(m) and the role of Mn-SOD expression on DeltaPsi(m). Confluent human aortic endothelial cells (HAEC) were exposed to PSS, and DeltaPsi(m) was monitored using tetramethylrhodamine methyl ester (TMRM(+)), a mitochondrial membrane potential probe. PSS significantly increased DeltaPsi(m) and the change in DeltaPsi(m) was a dynamic process. DeltaPsi(m) returned to baseline level after PSS for 2h followed by static state for 4h. Mitochondrial Mn-SOD expression and activities were also significantly up-regulated in response to PSS. Silencing Mn-SOD attenuated PSS-mediated DeltaPsi(m) increase while adding Mn-SOD mimetic, MnTMPyP, increased DeltaPsi(m) to the similar extent as induced by PSS. Our findings suggest that PSS-increased mitochondrial DeltaPsi(m), in part, via Mn-SOD up-regulation.Entities:
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Year: 2009 PMID： 19666009 PMCID： PMC2746082 DOI： 10.1016/j.bbrc.2009.08.022
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575