Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction
Background: Platelets are major players of thrombosis and inflammation after acute myocardial infarction (AMI). The impact of thrombocytopenia on platelet-induced cellular processes post AMI is not well defined. Methods: The left anterior descending artery was ligated in C57/Bl6 mice and in two thro...
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| Format: | Article |
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MDPI AG
2022-11-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/11/21/3500 |
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| author | Friedrich Reusswig Amin Polzin Meike Klier Matthias Achim Dille Aysel Ayhan Marcel Benkhoff Celina Lersch Anika Prinz Simone Gorressen Jens Walter Fischer Malte Kelm Margitta Elvers |
| author_facet | Friedrich Reusswig Amin Polzin Meike Klier Matthias Achim Dille Aysel Ayhan Marcel Benkhoff Celina Lersch Anika Prinz Simone Gorressen Jens Walter Fischer Malte Kelm Margitta Elvers |
| author_sort | Friedrich Reusswig |
| collection | DOAJ |
| description | Background: Platelets are major players of thrombosis and inflammation after acute myocardial infarction (AMI). The impact of thrombocytopenia on platelet-induced cellular processes post AMI is not well defined. Methods: The left anterior descending artery was ligated in C57/Bl6 mice and in two thrombocytopenic mouse models to induce AMI. Results: Platelets from STEMI patients and from C57/Bl6 mice displayed enhanced platelet activation after AMI. This allows platelets to migrate into the infarct but not into the remote zone of the left ventricle. Acute thrombocytopenia by antibody-induced platelet depletion resulted in reduced infarct size and improved cardiac function 24 h and 21 days post AMI. This was due to reduced platelet-mediated inflammation after 24 h and reduced scar formation after 21 days post AMI. The collagen composition and interstitial collagen content in the left ventricle were altered due to platelet interaction with cardiac fibroblasts. Acute inflammation was also significantly reduced in <i>Mpl<sup>−/−</sup></i> mice with chronic thrombocytopenia, but cardiac remodeling was unaltered. Consequently, left ventricular function, infarct size and scar formation in <i>Mpl<sup>−/−</sup></i> mice were comparable to controls. Conclusion: This study discovers a novel role for platelets in cardiac remodeling and reveals that acute but not chronic thrombocytopenia protects left ventricular function post AMI. |
| first_indexed | 2024-03-09T19:11:14Z |
| format | Article |
| id | doaj.art-447c91b559a04920aae20fe22b44659d |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T19:11:14Z |
| publishDate | 2022-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-447c91b559a04920aae20fe22b44659d2023-11-24T04:09:47ZengMDPI AGCells2073-44092022-11-011121350010.3390/cells11213500Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial InfarctionFriedrich Reusswig0Amin Polzin1Meike Klier2Matthias Achim Dille3Aysel Ayhan4Marcel Benkhoff5Celina Lersch6Anika Prinz7Simone Gorressen8Jens Walter Fischer9Malte Kelm10Margitta Elvers11Heinrich-Heine University Medical Center, Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Cardiology, Pulmonology and Angiology, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Cardiology, Pulmonology and Angiology, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Cardiology, Pulmonology and Angiology, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, 40225 Düsseldorf, GermanyInstitute for Pharmacology and Clinical Pharmacology, Heinrich-Heine University, 40225 Düsseldorf, GermanyInstitute for Pharmacology and Clinical Pharmacology, Heinrich-Heine University, 40225 Düsseldorf, GermanyInstitute for Pharmacology and Clinical Pharmacology, Heinrich-Heine University, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Cardiology, Pulmonology and Angiology, 40225 Düsseldorf, GermanyHeinrich-Heine University Medical Center, Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, 40225 Düsseldorf, GermanyBackground: Platelets are major players of thrombosis and inflammation after acute myocardial infarction (AMI). The impact of thrombocytopenia on platelet-induced cellular processes post AMI is not well defined. Methods: The left anterior descending artery was ligated in C57/Bl6 mice and in two thrombocytopenic mouse models to induce AMI. Results: Platelets from STEMI patients and from C57/Bl6 mice displayed enhanced platelet activation after AMI. This allows platelets to migrate into the infarct but not into the remote zone of the left ventricle. Acute thrombocytopenia by antibody-induced platelet depletion resulted in reduced infarct size and improved cardiac function 24 h and 21 days post AMI. This was due to reduced platelet-mediated inflammation after 24 h and reduced scar formation after 21 days post AMI. The collagen composition and interstitial collagen content in the left ventricle were altered due to platelet interaction with cardiac fibroblasts. Acute inflammation was also significantly reduced in <i>Mpl<sup>−/−</sup></i> mice with chronic thrombocytopenia, but cardiac remodeling was unaltered. Consequently, left ventricular function, infarct size and scar formation in <i>Mpl<sup>−/−</sup></i> mice were comparable to controls. Conclusion: This study discovers a novel role for platelets in cardiac remodeling and reveals that acute but not chronic thrombocytopenia protects left ventricular function post AMI.https://www.mdpi.com/2073-4409/11/21/3500plateletsmyocardial infarctioninflammationremodelingscar formation |
| spellingShingle | Friedrich Reusswig Amin Polzin Meike Klier Matthias Achim Dille Aysel Ayhan Marcel Benkhoff Celina Lersch Anika Prinz Simone Gorressen Jens Walter Fischer Malte Kelm Margitta Elvers Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction Cells platelets myocardial infarction inflammation remodeling scar formation |
| title | Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction |
| title_full | Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction |
| title_fullStr | Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction |
| title_full_unstemmed | Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction |
| title_short | Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction |
| title_sort | only acute but not chronic thrombocytopenia protects mice against left ventricular dysfunction after acute myocardial infarction |
| topic | platelets myocardial infarction inflammation remodeling scar formation |
| url | https://www.mdpi.com/2073-4409/11/21/3500 |
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