Zhou 2007 Biochem Biophys Res Comm
| Zhou H-Z, Ma X, Gray MO, Zhu B, Nguyen AP, Bakera AJ, Simonis U, Cecchini G, Lovett DH, Karliner JS (2007) Transgenic MMP-2 expression induces latent cardiac mitochondrial dysfunction. Biochem Biophys Res Comm 358:189-95. |
Zhou H-Z, Ma X, Gray MO, Zhu B, Nguyen AP, Bakera AJ, Simonis U, Cecchini G, Lovett DH, Karliner JS (2007) Biochem Biophys Res Comm
Abstract: Matrix metalloproteinases (MMPs) are central to the development and progression of dysfunctional ventricular remodeling after tissue injury. We studied 6 month old heterozygous mice with cardiac-specific transgenic expression of active MMP-2 (MMP-2 Tg). MMP-2 Tg hearts showed no substantial gross alteration of cardiac phenotype compared to age-matched wild-type littermates. However, buffer perfused MMP-2 Tg hearts subjected to 30 min of global ischemia followed by 30 min of reperfusion had a larger infarct size and greater depression in contractile performance compared to wild-type hearts. Importantly, cardioprotection mediated by ischemic preconditioning (IPC) was completely abolished in MMP-2 Tg hearts, as shown by abnormalities in mitochondrial ultrastructure and impaired respiration, increased lipid peroxidation, cell necrosis and persistently reduced recovery of contractile performance during post-ischemic reperfusion. We conclude that MMP-2 functions not only as a proteolytic enzyme but also as a previously unrecognized active negative regulator of mitochondrial function during superimposed oxidative stress. • Keywords: Matrix metalloproteinase-2; Ischemia; Reperfusion; Mitochondria; Preconditioning; Latent mitochondrial dysfunction
Labels:
Stress:Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Oxidative stress;RONS Organism: Mouse Tissue;cell: Heart Preparation: Isolated mitochondria
Coupling state: OXPHOS
Latent mitochondrial dysfunction
