| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1933060 | Biochemical and Biophysical Research Communications | 2009 | 7 Pages |
Mitochondrial dysfunction is intimately involved in cardiovascular diseases. Mitochondrial membrane potential (ΔΨm) is coupled with oxidative phosphorylation to drive ATP synthesis. In this study, we examined the effect of physiological pulsatile shear stress (PSS) on ΔΨm and the role of Mn-SOD expression on ΔΨm. Confluent human aortic endothelial cells (HAEC) were exposed to PSS, and ΔΨm was monitored using tetramethylrhodamine methyl ester (TMRM+), a mitochondrial membrane potential probe. PSS significantly increased ΔΨm and the change in ΔΨm was a dynamic process. ΔΨm returned to baseline level after PSS for 2 h followed by static state for 4 h. Mitochondrial Mn-SOD expression and activities were also significantly up-regulated in response to PSS. Silencing Mn-SOD attenuated PSS-mediated ΔΨm increase while adding Mn-SOD mimetic, MnTMPyP, increased ΔΨm to the similar extent as induced by PSS. Our findings suggest that PSS-increased mitochondrial ΔΨm, in part, via Mn-SOD up-regulation.
