Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation.
<h4>Background</h4>Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are upregulated after myocardial infarction (MI) in both humans and mice. They modulate inflammation and the extracellular matrix, and could there...
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2013
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oai:doaj.org-article:8a57fd2f9da348b0bd8047d22b88e1b22021-11-18T08:47:29ZExogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation.1932-620310.1371/journal.pone.0078938https://doaj.org/article/8a57fd2f9da348b0bd8047d22b88e1b22013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24244389/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 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.<h4>Methods and results</h4>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.<h4>Conclusion</h4>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.Christina PachelDenise MathesBarbara BayerCharlotte DieneschGaby WangorschWolfram HeitzmannIsabell LangHossein ArdehaliGeorg ErtlThomas DandekarHarald WajantStefan FrantzPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 11, p e78938 (2013) |
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Medicine R Science Q Christina Pachel Denise Mathes Barbara Bayer Charlotte Dienesch Gaby Wangorsch Wolfram Heitzmann Isabell Lang Hossein Ardehali Georg Ertl Thomas Dandekar Harald Wajant Stefan Frantz Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation. |
| description |
<h4>Background</h4>Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 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.<h4>Methods and results</h4>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.<h4>Conclusion</h4>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. |
| format |
article |
| author |
Christina Pachel Denise Mathes Barbara Bayer Charlotte Dienesch Gaby Wangorsch Wolfram Heitzmann Isabell Lang Hossein Ardehali Georg Ertl Thomas Dandekar Harald Wajant Stefan Frantz |
| author_facet |
Christina Pachel Denise Mathes Barbara Bayer Charlotte Dienesch Gaby Wangorsch Wolfram Heitzmann Isabell Lang Hossein Ardehali Georg Ertl Thomas Dandekar Harald Wajant Stefan Frantz |
| author_sort |
Christina Pachel |
| title |
Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation. |
| title_short |
Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation. |
| title_full |
Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation. |
| title_fullStr |
Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation. |
| title_full_unstemmed |
Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation. |
| title_sort |
exogenous administration of a recombinant variant of tweak impairs healing after myocardial infarction by aggravation of inflammation. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2013 |
| url |
https://doaj.org/article/8a57fd2f9da348b0bd8047d22b88e1b2 |
| work_keys_str_mv |
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