Elevated platelet–leukocyte complexes are associated with, but dispensable for myocardial ischemia–reperfusion injury
Abstract: Aims
P-selectin is an activatable adhesion molecule on platelets promoting platelet aggregation, and platelet–leukocyte complex (PLC) formation. Increased numbers of PLC are circulating in the blood of patients shortly after acute myocardial infarction and predict adverse outcomes. These correlations led to speculations about whether PLC may represent novel therapeutic targets. We therefore set out to elucidate the pathomechanistic relevance of PLC in myocardial ischemia and reperfusion injury.
Methods and results
By generating P-selectin deficient bone marrow chimeric mice, the post-myocardial infarction surge in PLC numbers in blood was prevented. Yet, intravital microscopy, flow cytometry and immunohistochemical staining, echocardiography, and gene expression profiling showed unequivocally that leukocyte adhesion to the vessel wall, leukocyte infiltration, and myocardial damage post-infarction were not altered in response to the lack in PLC.
Conclusion
We conclude that myocardial infarction associated sterile inflammation triggers PLC formation, reminiscent of conserved immunothrombotic responses, but without PLC influencing myocardial ischemia and reperfusion injury in return. Our experimental data do not support a therapeutic concept of selectively targeting PLC formation in myocardial infarction
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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Online-Ressource
- Sprache
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Englisch
- Anmerkungen
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Basic research in cardiology. - 117, 1 (2022) , 61, ISSN: 1435-1803
- Ereignis
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Veröffentlichung
- (wo)
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Freiburg
- (wer)
-
Universität
- (wann)
-
2022
- Urheber
-
Starz, Christopher
Härdtner, Carmen
Mauler, Maximilian
Dufner, Bianca
Hoppe, Natalie
Krebs, Katja
Ehlert, Carolin A.
Merz, Julian
Heidt, Timo
Stachon, Peter
Wolf, Dennis
Bode, Christoph
Zur Mühlen, Constantin von
Rottbauer, Wolfgang
Gawaz, Meinrad Paul
Dürschmied, Daniel
Leuschner, Florian
Borst, Oliver
Westermann, Dirk
Hilgendorf, Ingo
- DOI
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10.1007/s00395-022-00970-3
- URN
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urn:nbn:de:bsz:25-freidok-2311972
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
15.08.2025, 07:34 MESZ
Datenpartner
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Starz, Christopher
- Härdtner, Carmen
- Mauler, Maximilian
- Dufner, Bianca
- Hoppe, Natalie
- Krebs, Katja
- Ehlert, Carolin A.
- Merz, Julian
- Heidt, Timo
- Stachon, Peter
- Wolf, Dennis
- Bode, Christoph
- Zur Mühlen, Constantin von
- Rottbauer, Wolfgang
- Gawaz, Meinrad Paul
- Dürschmied, Daniel
- Leuschner, Florian
- Borst, Oliver
- Westermann, Dirk
- Hilgendorf, Ingo
- Universität
Entstanden
- 2022
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