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Platelets Induce Cell Apoptosis of Cardiac Cells via FasL after Acute Myocardial Infarction.
Krott, Kim J; Reusswig, Friedrich; Dille, Matthias; Krüger, Evelyn; Gorressen, Simone; Karray, Saoussen; Polzin, Amin; Kelm, Malte; Fischer, Jens W; Elvers, Margitta.
Affiliation
  • Krott KJ; Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, Medical Center, Heinrich-Heine-University, 40225 Düsseldorf, Germany.
  • Reusswig F; Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, Medical Center, Heinrich-Heine-University, 40225 Düsseldorf, Germany.
  • Dille M; Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, Medical Center, Heinrich-Heine-University, 40225 Düsseldorf, Germany.
  • Krüger E; Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, Medical Center, Heinrich-Heine-University, 40225 Düsseldorf, Germany.
  • Gorressen S; Institute for Pharmacology and Clinical Pharmacology, Heinrich-Heine University, 40225 Düsseldorf, Germany.
  • Karray S; INSERM U976, Université de Paris, F-7510 Paris, France.
  • Polzin A; Department of Cardiology, Pulmonology and Angiology, Medical Center, Heinrich-Heine University, 40225 Düsseldorf, Germany.
  • Kelm M; Department of Cardiology, Pulmonology and Angiology, Medical Center, Heinrich-Heine University, 40225 Düsseldorf, Germany.
  • Fischer JW; Institute for Pharmacology and Clinical Pharmacology, Heinrich-Heine University, 40225 Düsseldorf, Germany.
  • Elvers M; Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, Medical Center, Heinrich-Heine-University, 40225 Düsseldorf, Germany.
Biomedicines ; 12(5)2024 May 13.
Article in En | MEDLINE | ID: mdl-38791039
ABSTRACT
Acute myocardial infarction (AMI) is one of the leading causes of death worldwide. Cell apoptosis in the myocardium plays an important role in ischemia and reperfusion (I/R) injury, leading to cardiac damage and dysfunction. Platelets are major players in hemostasis and play a crucial role in vessel occlusion, inflammation, and cardiac remodeling after I/R. Here, we studied the impact of platelets on cell apoptosis in the myocardium using a close-chest mouse model of AMI. We found caspase-3-positive resident cardiac cells, while leukocytes were negative for caspase-3. Using two different mouse models of thrombocytopenia, we detected a significant reduction in caspase-3 positive cells in the infarct border zone after I/R injury. Further, we identified platelet FasL to induce cell apoptosis via the extrinsic pathway of Fas receptor activation of target cells. Mechanistically, hypoxia triggers platelet adhesion to FasR, suggesting that platelet-induced apoptosis is elevated after I/R. Platelet-specific FasL knock-out mice showed reduced Bax and Bcl2 expression, suggesting that platelets modulate the intrinsic and extrinsic pathways of apoptosis, leading to reduced infarct size after myocardial I/R injury. Thus, a new mechanism for how platelets contribute to tissue homeostasis after AMI was identified that should be validated in patients soon.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Biomedicines Year: 2024 Document type: Article Affiliation country: Germany Country of publication: Switzerland

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Biomedicines Year: 2024 Document type: Article Affiliation country: Germany Country of publication: Switzerland