Difference between revisions of "Zhou 2007 Biochem Biophys Res Comm"
(Created page with "{{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...") |
|||
| Line 1: | Line 1: | ||
{{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 | |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: 189-195. | ||
|info=http://www.sciencedirect.com/science/article/pii/S0006291X07008261 | |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 | ||
|year=2007 | |year=2007 | ||
|journal=Biochem | |journal=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. | |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 | |keywords=Matrix metalloproteinase-2; Ischemia; Reperfusion; Mitochondria; Preconditioning; Latent mitochondrial dysfunction | ||
}} | }} | ||
| Line 13: | Line 11: | ||
|injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress | |injuries=Ischemia-Reperfusion; Preservation, RONS; Oxidative Stress | ||
|organism=Mouse | |organism=Mouse | ||
|tissues=Cardiac | |tissues=Cardiac muscle | ||
|preparations=Isolated Mitochondria | |preparations=Isolated Mitochondria | ||
|topics=Respiration; OXPHOS; ETS Capacity | |topics=Respiration; OXPHOS; ETS Capacity | ||
|additional=Latent mitochondrial dysfunction | |additional=Latent mitochondrial dysfunction | ||
}} | }} | ||
Revision as of 07:27, 5 April 2012
| 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: 189-195. |
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., RONS; Oxidative Stress"RONS; Oxidative Stress" 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. Organism: Mouse Tissue;cell: Cardiac muscle"Cardiac muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
Latent mitochondrial dysfunction
