Zhou 2007 Biochem Biophys Res Comm: Difference between revisions
(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...") |
No edit summary |
||
| (6 intermediate revisions by 4 users not shown) | |||
| 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 358:189-95. | ||
|info= | |info=[https://www.ncbi.nlm.nih.gov/pubmed/17475219 PMID: 17475219 Open Access] | ||
|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 | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|injuries=Ischemia- | |injuries=Ischemia-reperfusion, Oxidative stress;RONS | ||
|organism=Mouse | |organism=Mouse | ||
|tissues= | |tissues=Heart | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
| | |couplingstates=OXPHOS | ||
|additional=Latent mitochondrial dysfunction | |additional=Latent mitochondrial dysfunction | ||
}} | }} | ||
Latest revision as of 15:51, 12 March 2019
| 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, Oxidative stress;RONS Organism: Mouse Tissue;cell: Heart Preparation: Isolated mitochondria
Coupling state: OXPHOS
Latent mitochondrial dysfunction
