ArticleThe Journal of biological chemistry2010
Cardiac restricted overexpression of membrane type-1 matrix metalloproteinase causes adverse myocardial remodeling following myocardial infarction.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 65 citations in OpenAlex.
- Cardioprotective Effects of a Selective c-Jun N-terminal Kinase Inhibitor in a Rat Model of Myocardial Infarction.Biomedicines · 2023Article
- Matrix Metalloproteinase-Targeted SPECT/CT Imaging for Evaluation of Therapeutic Hydrogels for the Early Modulation of Post-Infarct Myocardial Remodeling.Journal of cardiovascular translational research · 2023Article
- Connecting different heart diseases through intercellular communication.Biology open · 2021Review
- Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Genetic ablation of fibroblast activation protein alpha attenuates left ventricular dilation after myocardial infarction.PloS one · 2021Article
- Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/TGFβ1 after myocardial infarction.eLife · 2020Article
- Increased macrophage-derived SPARC precedes collagen deposition in myocardial fibrosis.American journal of physiology. Heart and circulatory physiology · 2018Article
- Matrix metalloproteinase-14 is a biomarker of angiogenic activity in proliferative diabetic retinopathy.Molecular vision · 2018Article
- Collagenolytic Activity Is Associated with Scar Resolution in Zebrafish Hearts after Cryoinjury.Journal of cardiovascular development and disease · 2017Article
- Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage Polarization.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016Article
- Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling.Journal of molecular and cellular cardiology · 2016Review
- Downregulation of RACK1 is associated with cardiomyocyte apoptosis after myocardial ischemia/reperfusion injury in adult rats.In vitro cellular & developmental biology. Animal · 2016Article
- Development of Radiolabeled Membrane Type-1 Matrix Metalloproteinase Activatable Cell Penetrating Peptide Imaging Probes.Molecules (Basel, Switzerland) · 2015Article
- PGE2 reduces MMP-14 and increases plasminogen activator inhibitor-1 in cardiac fibroblasts.Prostaglandins & other lipid mediators · 2014Article
- Targeting matrix metalloproteinases in heart disease: lessons from endogenous inhibitors.Biochemical pharmacology · 2014Review
- Mechanistic relationship between membrane type-1 matrix metalloproteinase and the myocardial response to pressure overload.Circulation. Heart failure · 2014Article
- Translating Koch's postulates to identify matrix metalloproteinase roles in postmyocardial infarction remodeling: cardiac metalloproteinase actions (CarMA) postulates.Circulation research · 2014Review
- Alcohol modulation of cardiac matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs favors collagen accumulation.Alcoholism, clinical and experimental research · 2014Article
- Cyclosporin A in left ventricular remodeling after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2014Article
- Cellular mechanisms of tissue fibrosis. 2. Contributory pathways leading to myocardial fibrosis: moving beyond collagen expression.American journal of physiology. Cell physiology · 2013Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The membrane type-1 matrix metalloproteinase (MT1-MMP) is a unique member of the MMP family, but induction patterns and consequences of MT1-MMP overexpression (MT1-MMPexp), in a left ventricular (LV) remodeling process such as myocardial infarction (MI), have not been explored. MT1-MMP promoter activity (murine luciferase reporter) increased 20-fold at 3 days and 50-fold at 14 days post-MI. MI was then induced in mice with cardiac restricted MT1-MMPexp (n = 58) and wild type (WT, n = 60). Post-MI survival was reduced (67% versus 46%, p < 0.05), and LV ejection fraction was lower in the post-MI MT1-MMPexp mice compared with WT (41 ± 2 versus 32 ± 2%,p < 0.05). In the post-MI MT1-MMPexp mice, LV myocardial MMP activity, as assessed by radiotracer uptake, and MT1-MMP-specific proteolytic activity using a specific fluorogenic assay were both increased by 2-fold. LV collagen content was increased by nearly 2-fold in the post-MI MT1-MMPexp compared with WT. Using a validated fluorogenic construct, it was discovered that MT1-MMP proteolytically processed the pro-fibrotic molecule, latency-associated transforming growth factor-1 binding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activity was increased by 4-fold in the post-MI MT1-MMPexp group. Early and persistent MT1-MMP promoter activity occurred post-MI, and increased myocardial MT1-MMP levels resulted in poor survival, worsening of LV function, and significant fibrosis. A molecular mechanism for the adverse LV matrix remodeling with MT1-MMP induction is increased processing of pro-fibrotic signaling molecules. Thus, a proteolytically diverse portfolio exists for MT1-MMP within the myocardium and likely plays a mechanistic role in adverse LV remodeling.
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Registered trials
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