ArticleMolecular and cellular biochemistry2005
Reduction of myocardial infarct size by doxycycline: a role for plasmin inhibition.
Article in Molecular and cellular biochemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Distinguishing Plasmin-Generating Microvesicles: Tiny Messengers Involved in Fibrinolysis and Proteolysis.International journal of molecular sciences · 2023Review
- Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms.Current cardiology reviews · 2022Review
- Cardioprotective Effect of Novel Matrix Metalloproteinase Inhibitors.International journal of molecular sciences · 2020Article
- Doxycycline attenuates cisplatin-induced acute kidney injury through pleiotropic effects.American journal of physiology. Renal physiology · 2018Article
- ModulatingJournal of materials chemistry. B · 2016Article
- Effect of tetracyclines on the development of vascular disease in veterans with acne or rosacea: a retrospective cohort study.The Journal of investigative dermatology · 2014Article
- Targeting matrix metalloproteinases in heart disease: lessons from endogenous inhibitors.Biochemical pharmacology · 2014Review
- Urokinase plasminogen activator induces pro-fibrotic/m2 phenotype in murine cardiac macrophages.PloS one · 2013Article
- Proof of Concept: Matrix metalloproteinase inhibitor decreases inflammation and improves muscle insulin sensitivity in people with type 2 diabetes.Journal of inflammation (London, England) · 2012Article
- Serum proteomic signature of human chagasic patients for the identification of novel potential protein biomarkers of disease.Molecular & cellular proteomics : MCP · 2012Article
- Effects of (-)-epicatechin on myocardial infarct size and left ventricular remodeling after permanent coronary occlusion.Journal of the American College of Cardiology · 2010Article
- Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6.Cell stem cell · 2009Article
- Protective effects of doxycycline in ischemia/reperfusion injury on kidney.Journal of physiology and biochemistry · 2009Article
- 2008 Landis Award lecture. Inflammation and the autodigestion hypothesis.Microcirculation (New York, N.Y. : 1994) · 2009Article
- Cardiac uptake of minocycline and mechanisms for in vivo cardioprotection.Journal of the American College of Cardiology · 2008Article
- Proteinase activity and receptor cleavage: mechanism for insulin resistance in the spontaneously hypertensive rat.Hypertension (Dallas, Tex. : 1979) · 2008Article
- Short- and long-term effects of (-)-epicatechin on myocardial ischemia-reperfusion injury.American journal of physiology. Heart and circulatory physiology · 2008Article
- Zinc-binding groups modulate selective inhibition of MMPs.ChemMedChem · 2008Article
- A role for non-antimicrobial actions of tetracyclines in combating oxidative stress in periodontal and metabolic diseases: a literature review.The open dentistry journal · 2008Article
- Effects of timed administration of doxycycline or methylprednisolone on post-myocardial infarction inflammation and left ventricular remodeling in the rat heart.Molecular and cellular biochemistry · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial ischemia-reperfusion (I/R) is associated with the activation of matrix metalloproteinases (MMPs) and serine proteases. We hypothesized that activation of MMPs and the serine protease plasmin contribute to early cardiac myocyte death following I/R and that broad-spectrum protease inhibition with doxycycline (DOX) preserves myocyte viability. Rats treated daily with or without DOX beginning 48 h prior to experimentation were subjected to 30 min of coronary occlusion and 2 days of reperfusion. DOX pre-treatment reduced infarct size by 37%. DOX attenuated increases in MMP-9 and plasmin levels as determined by gelatin zymography and immunoblot, respectively. Neutrophil extravasation was unaltered by DOX as assessed by myeloperoxidase (MPO) activity. To examine the contribution of MMP-9 and plasmin to myocyte injury, cultures of neonatal rat ventricular myocytes (NRVMs) were treated for 48 h with 83 kDa MMP-9 or plasminogen in the presence or absence of DOX. MMP-9 treatment did not affect myocyte viability. Plasminogen treatment led to increased plasmin activity, resulting in loss of beta1-integrin, NRVM detachment and apoptosis. DOX co-treatment inhibited plasmin activity and preserved NRVM attachment, whereas co-treatment with the broad-spectrum MMP inhibitor GM6001 had no effect. These results indicate that plasmin causes disruption of myocyte attachment and viability independently of MMP activation in vitro and that inhibition of plasmin by DOX may reduce I/R-induced myocyte death in vivo through the inhibition of plasmin.
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Registered trials
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