Zhou 2007 Biochem Biophys Res Comm: Difference between revisions
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{{Publication | {{Publication | ||
|title=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- | |title=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. | ||
|info=[http://www.sciencedirect.com/science/article/pii/S0006291X07008261 sciencedirect] | |info=[http://www.sciencedirect.com/science/article/pii/S0006291X07008261 sciencedirect] | ||
|authors=Zhou H-Z, Ma X, Gray MO, Zhu B, Nguyen AP, Bakera AJ, Simonis U, Cecchini G, Lovett DH, Karliner JS | |authors=Zhou H-Z, Ma X, Gray MO, Zhu B, Nguyen AP, Bakera AJ, Simonis U, Cecchini G, Lovett DH, Karliner JS | ||
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{{Labeling | {{Labeling | ||
|organism=Mouse | |organism=Mouse | ||
|tissues=Heart | |tissues=Heart | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|injuries=Ischemia-reperfusion;preservation, Oxidative stress;RONS | |||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|additional=Latent mitochondrial dysfunction | |additional=Latent mitochondrial dysfunction | ||
}} | }} | ||
Revision as of 13:27, 13 February 2015
| 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
