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Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice
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نویسنده
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stieger p. ,daniel j.-m. ,thölen c. ,dutzmann j. ,knöpp k. ,gündüz d. ,aslam m. ,kampschulte m. ,langheinrich a. ,fischer s. ,cabrera-fuentes h. ,wang y. ,wollert k.c. ,bauersachs j. ,braun-dullaeus r. ,preissner k.t. ,sedding d.g.
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منبع
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journal of the american heart association - 2017 - دوره : 6 - شماره : 6
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چکیده
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Background: following myocardial infarction (mi),peri-infarct myocardial edema formation further impairs cardiac function. extracellular rna (erna) released from injured cells strongly increases vascular permeability. this study aimed to assess the role of erna in mi-induced cardiac edema formation,infarct size,cardiac function,and survival after acute mi and to evaluate the therapeutic potential of ribonuclease 1 (rnase-1) treatment as an erna-degrading intervention.methods and results: c57bl/6j mice were subjected to mi by permanent ligation of the left anterior descending coronary artery. plasma erna levels were significantly increased compared with those in controls starting from 30 minutes after ligation. systemic application of rnase-1,but not dnase,significantly reduced myocardial edema formation 24 hours after ligation compared with controls. consequently,erna degradation by rnase-1 significantly improved the perfusion of collateral arteries in the border zone of the infarcted myocardium 24 hours after ligation of the left anterior descending coronary artery,as detected by micro-computed tomography imaging. although there was no significant difference in the area at risk,the area of vital myocardium was markedly larger in mice treated with rnase-1 compared with controls,as detected by evans blue and 2,3,5-triphenyltetrazolium chloride staining. the increase in viable myocardium was associated with significantly preserved left ventricular function,as assessed by echocardiography. moreover,rnase-1 significantly improved 8-week survival following mi.conclusions: erna is an unrecognized permeability factor in vivo,associated with myocardial edema formation after acute mi. rnase-1 counteracts erna-induced edema formation and preserves perfusion of the infarction border zone,reducing infarct size and protecting cardiac function after mi. © 2017 the authors. published on behalf of the american heart association,inc.,by wiley.
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کلیدواژه
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edema; extracellular RNA; myocardial infarction; RNase‐1
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آدرس
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department of cardiology and angiology,otto-von-guericke university magdeburg,magdeburg, Germany, department of cardiology and angiology,hannover medical school,hannover, Germany, department of cardiology and angiology,university hospital giessen and marburg,giessen, Germany, department of cardiology and angiology,hannover medical school,hannover, Germany, department of cardiology and angiology,hannover medical school,hannover, Germany, department of cardiology and angiology,university hospital giessen and marburg,giessen, Germany, department of cardiology and angiology,university hospital giessen and marburg,giessen, Germany, department of radiology,university hospital giessen and marburg,giessen, Germany, department of radiology,university hospital giessen and marburg,giessen, Germany, institute of biochemistry,medical school,justus-liebig-university,giessen, Germany, institute of biochemistry,medical school,justus-liebig-university,giessen,germany,national heart research institute,singapore,national heart research institute singapore,national heart centre singapore,singapore,department of microbiology,kazan federal university,kazan, Russian Federation, department of cardiology and angiology,hannover medical school,hannover,germany,division of molecular and translational cardiology,hannover medical school,hannover, Germany, department of cardiology and angiology,hannover medical school,hannover,germany,division of molecular and translational cardiology,hannover medical school,hannover, Germany, department of cardiology and angiology,hannover medical school,hannover, Germany, department of cardiology and angiology,otto-von-guericke university magdeburg,magdeburg, Germany, institute of biochemistry,medical school,justus-liebig-university,giessen, Germany, department of cardiology and angiology,hannover medical school,hannover,germany,institute of biochemistry,medical school,justus-liebig-university,giessen, Germany
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Authors
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