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9 results on '"Wilmes, Verena"'

1. From rare events to systematic data collection: the RESCUED registry for sudden cardiac death in the young in Germany

Author

Barkauskas, Renaldas, Jenewein, Tina, Scheiper-Welling, Stefanie, Wilmes, Verena, Niess, Constanze, Petzel-Witt, Silvana, Reitz, Alexandra, Gradhand, Elise, Falagkari, Anastasia, Papathanasiou, Maria, Wakili, Reza, Leistner, David M., Vasseur, Jessica, Göbel, Jens, Storf, Holger, Toennes, Stefan W., Kettner, Matthias, Verhoff, Marcel A., Beckmann, Britt-Maria, Kauferstein, Silke, and Corvest, Eva

Published
2024
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6. The Role of Inducible Nitric Oxide Synthase (iNOS) in Human Myocardial Infarction

Author

Wilmes, Verena and Wilmes, Verena

Abstract

Cardiovascular diseases (CVDs), which include disorders of the heart and its blood vessels, such as myocardial infarction (MI), are the leading cause of death globally. During MI necrosis of myocardial cells leads to inflammation and fibrosis. Cardiac scarring and subsequently adverse remodeling, negatively impact myocardial healing and may lead to further disease states after MI, such as hypertension, heart failure, and death. While elevated levels of cardiac-specific troponins (cTnT and cTnI), as well as cardiac specific creatine kinase (CK-MB) are central biomarkers for the diagnosis of MI, interleukins, natriuretic peptides, matrix metallopeptidases (MMPs) and noncoding RNAs are currently discussed as biomarkers for adverse cardiac remodeling after MI. Nevertheless, a thorough understanding of the molecular processes during MI may lead to further biomarkers or improved therapy options. Inducible nitric oxide synthase (iNOS) is one of the three NOS isoforms that produce nitric oxide (NO). It is induced by stimuli such as inflammation and hypoxia and has been described in patients with end-stage heart failure, cardiomyopathy and ischemic heart disease. In murine and rabbit models of MI increased iNOS expression is suggested to contribute to left ventricular dysfunction, heart failure progression, myocardial injury and extent of infarct size, even late after ischemia and reperfusion. These detrimental effects are due to the reaction of iNOS derived NO with superoxide anion (O2-), which leads to reactive intermediates that can nitrate, nitrosate or oxidize their biological environment. This oxidative nitrosative stress promotes DNA damage, suppresion of DNA-repair enzymes and post-translational modifications of proteins. Specifically, peroxynitrite (ONOO-) is formed by the reaction of NO with O2- and is a strong oxidant causing nitrosylation of proteins and the formation of nitrotyrosine. Further peroxynitrite inactivates anti-proteases and activates MMPs, that are

Published
2023

9. Influence of microRNAs on iNOS expression in postmortem human infarction hearts.

Author

Wilmes, Verena, Mildeberger, Luise, Verhoff, Marcel A., and Kauferstein, Silke

Subjects
*MICRORNA, *GENE expression, *AUTOPSY, *CARDIOVASCULAR diseases, *POLYMERASE chain reaction
Abstract

MicroRNAs (miRNAs) are important post-transcriptional regulators in several diseases, including cancer, immunologic and cardiovascular diseases. A growing list of miRNAs are dysregulated in cardiac arrhythmias, contractility diseases, myocardial infarction (MI), sudden cardiac death (SCD), chronic heart failure and hypertrophy. However, the exact regulatory pathways, through which miRNAs exert their effects are often unclear. In this study, we measured the expression patterns of miR-21, miR-939 and miR-30e in postmortem human MI. The aim of the study was to examine the influence of these miRNAs on cardiac inducible nitric oxide synthase (iNOS) mRNA levels. We measured iNOS mRNA and miRNA expression patterns by means of qPCR. Further we used correlation analyses to determine causality between miRNA expression and cardiac iNOS levels. iNOS mRNA, miR-21, miR-939 and miR-30e were significantly upregulated in infarcted and non-infarcted regions of postmortem human MI hearts in comparison to healthy controls. While miR-21 and miR-939 showed their strongest expression in infarcted regions, miR-30e peaked in the non-infarcted myocardium. Further, we found a significant correlation between miR-939 and iNOS expression levels in controls and infarcted regions. The results indicate, that miR-939 is a regulator of cardiac iNOS expression. However, a massive iNOS activation might exceed the capability of miR-939 to keep its expression in balance. miR-21 and miR-30e do not seem to influence cardiac iNOS levels in MI. Further studies are needed to evaluate downstream targets of these miRNAs and their signaling pathways to clarify their role in human MI. • iNOS mRNA expression is significantly increased in human MI hearts. • miR-21 and miR-939 are strongly increased in infarcted regions of human MI hearts. • miR-30e is strongly increased in non-infarcted regions of human MI hearts. • miR-939 expression significantly correlates with iNOS mRNA expression. • miR-939 might regulate iNOS expression in the heart. [ABSTRACT FROM AUTHOR]

Published
2024
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