ArticleMedicine2017
Expression of matrix metalloproteinases-12 in ST-segment elevation myocardial infarction: A case-control study.
Article in Medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Matrix metalloproteinases and risk of cardiovascular mortality and morbidity in the United Kingdom: A prospective cohort study with machine learning analysis.Preventive medicine reports · 2026Article
- Matrix metalloproteinases in coronary artery disease and myocardial infarction.Basic research in cardiology · 2023Review
- Immunohistochemical characteristics of coronary thrombi in ST-elevation myocardial infarction.American heart journal plus : cardiology research and practice · 2022Article
- Matrix Metalloproteinases as Biomarkers of Atherosclerotic Plaque Instability.International journal of molecular sciences · 2020Review
- Immune-Mediated Inflammation in Vulnerable Atherosclerotic Plaques.Molecules (Basel, Switzerland) · 2019Review
- Matrix metalloproteinase-12 as an endogenous resolution promoting factor following myocardial infarction.Pharmacological research · 2018Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinases-12 (MMP12) can lead to degradation of elastin resulting in plaque destabilization and rupture. MMP12 also facilitates platelet aggregation, adhesion, and granule secretion. However, evidence in the literature related to the function of MMP12 in ST-segment elevation myocardial infarction (STEMI) is little. This study investigated the expression of MMP12 in human coronary thrombus and examined the relationship between plasma MMP12 and STEMI.Arterial plasma was obtained from 46 STEMI patients and 52 stable angina pectoris (SAP) patients and 30 controls with angiographically normal coronary arteries. Coronary thrombi were obtained from 26 STEMI patients with a large thrombus burden (LTB). The expression levels of MMP12 in coronary thrombus were analyzed by immunohistochemistry and immunofluorescence, reverse transcription-polymerase chain reaction (RT-PCR), Western blotting (WB) and casein zymography. In addition, MMP12 concentration measured by enzyme-linked immunosorbent assay (ELISA) and activity measured by fluorescence resonance energy transfer (FRET) were used to assess the levels in plasma.We confirmed the expression of MMP12 in human coronary thrombus. MMP12 was secreted mainly in active form of 45 kDa in coronary thrombus. In plasma samples of the STEMI group, MMP12 concentrations were found to be higher than the SAP group (5.030 ± 2.24 pg/mL vs 3.010 ± 1.99 pg/mL, P < .05) but with lower MMP12 activity (332 ± 77 RFU vs 458 ± 91 RFU, P < .05). Also, the STEMI group demonstrated much higher MMP12 concentrations than the normal coronary artery control group (5.030 ± 2.24 pg/mL vs 1.720 ± 0.51 pg/mL, P < .05) and with lower MMP12 activity (332 ± 77 RFU vs 549 ± 112 RFU, P < .05). In addition, the STEMI group had significantly higher tissue inhibitor of metalloproteinases-1 (TIMP1) concentration (573.40 ± 270.60 pg/mL) than SAP group (384.50 ± 147.70 pg/mL) and control group (219.90 ± 154.80 pg/mL, P < .05). The imbalance in MMP12/TIMP ratio was observed in the STEMI group compared with SAP and control group (P < .05).This study demonstrated that MMP12 exists in human coronary thrombus. Patients with STEMI have elevated plasma level of MMP12 and the imbalance of MMP12/TIMP1. These data supported that MMP12 might be of potential relevance in STEMI.
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Registered trials
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