• search hit 8 of 8
Back to Result List

Exogenous Administration of a Recombinant Variant of TWEAK Impairs Healing after Myocardial Infarction by Aggravation of Inflammation

Please always quote using this URN: urn:nbn:de:bvb:20-opus-129889
  • Background: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factorinducible 14 (Fn14) are upregulated after myocardial infarction (MI) in both humans and mice. They modulate inflammation and the extracellular matrix, and could therefore be important for healing and remodeling after MI. However, the function of TWEAK after MI remains poorly defined. Methods and results: Following ligation of the left coronary artery, mice were injected twice per week with a recombinant human serum albuminBackground: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factorinducible 14 (Fn14) are upregulated after myocardial infarction (MI) in both humans and mice. They modulate inflammation and the extracellular matrix, and could therefore be important for healing and remodeling after MI. However, the function of TWEAK after MI remains poorly defined. Methods and results: Following ligation of the left coronary artery, mice were injected twice per week with a recombinant human serum albumin conjugated variant of TWEAK (HSA-Flag-TWEAK), mimicking the activity of soluble TWEAK. Treatment with HSA-Flag-TWEAK resulted in significantly increased mortality in comparison to the placebo group due to myocardial rupture. Infarct size, extracellular matrix remodeling, and apoptosis rates were not different after MI. However, HSA-Flag-TWEAK treatment increased infiltration of proinflammatory cells into the myocardium. Accordingly, depletion of neutrophils prevented cardiac ruptures without modulating all-cause mortality. Conclusion: Treatment of mice with HSA-Flag-TWEAK induces myocardial healing defects after experimental MI. This is mediated by an exaggerated neutrophil infiltration into the myocardium.show moreshow less

Download full text files

Export metadata

Additional Services

Share in Twitter Search Google Scholar Statistics
Metadaten
Author: Christina Pachel, Denise Mathes, Barbara Bayer, Charlotte Dienesch, Gaby Wangorsch, Wolfram Heitzmann, Isabell Lang, Hossein Ardehali, Georg Ertl, Thomas DandekarORCiD, Harald Wajant, Stefan Frantz
URN:urn:nbn:de:bvb:20-opus-129889
Document Type:Journal article
Faculties:Medizinische Fakultät / Medizinische Klinik und Poliklinik I
Language:English
Parent Title (English):PLoS ONE
Year of Completion:2013
Volume:8
Issue:11
Pagenumber:e78938
Source:PLoS ONE 8(11): e78938. doi:10.1371/journal.pone.0078938
DOI:https://doi.org/10.1371/journal.pone.0078938
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:apoptosis; cytokines; extracellular matrix; heart; inflammation; myocardial infarction; myocardium; neutrophils
Release Date:2016/07/04
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung