Acute myocardial infarction (AMI) is characterized by a rapid increase in circulating platelet size but the mechanism for this is unclear. Large platelets are hyperactive and associated with adverse clinical outcomes. We determined mean platelet volume (MPV) and platelet–monocyte conjugation (PMC) using blood samples from patients, and blood and the spleen from mice with AMI. We further measured changes in platelet size, PMC, cardiac and splenic contents of platelets and leucocyte infiltration into the mouse heart. In AMI patients, circulating MPV and PMC increased at 1–3 h post-MI and MPV returned to reference levels within 24 h after admission. In mice with MI, increases in platelet size and PMC became evident within 12 h and were sustained up to 72 h. Splenic platelets are bigger than circulating platelets in normal or infarct mice. At 24 h post-MI, splenic platelet storage was halved whereas cardiac platelets increased by 4-fold. Splenectomy attenuated all changes observed in the blood, reduced leucocyte and platelet accumulation in the infarct myocardium, limited infarct size and alleviated cardiac dilatation and dysfunction. AMI-induced elevated circulating levels of adenosine diphosphate and catecholamines in both human and the mouse, which may trigger splenic platelet release. Pharmacological inhibition of angiotensin-converting enzyme, β1-adrenergic receptor or platelet P2Y12 receptor reduced platelet abundance in the murine infarct myocardium albeit having diverse effects on platelet size and PMC. In conclusion, AMI evokes release of splenic platelets, which contributes to the increase in platelet size and PMC and facilitates myocardial accumulation of platelets and leucocytes, thereby promoting post-infarct inflammation.
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July 2016
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Sagittal section through the retina of a hypertensive dTGR rat: staining in blue (DAPI) of cell nuclei and in red GFAP (glial fibrillary acidic protein). The GFAP staining shows activated astrocytes in the ganglion cell layer of the retina. See pp. 1075–1088 for further details. Image kindly provided by Olaf Strauß.
Research Article|
May 23 2016
Splenic release of platelets contributes to increased circulating platelet size and inflammation after myocardial infarction
Xiao-Ming Gao;
Xiao-Ming Gao
1
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
†Central Clinical School, Monash University, Melbourne, VIC 3004, Australia
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Xiao-Lei Moore;
Xiao-Lei Moore
1
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
‡Alfred Heart Centre, Alfred Hospital, Melbourne, VIC 3004, Australia
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Yang Liu;
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Xin-Yu Wang;
Xin-Yu Wang
§Department of Cardiology, Third Hospital of Peking University, Beijing 100191, China
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Li-Ping Han;
Li-Ping Han
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Yidan Su;
Yidan Su
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Alan Tsai;
Alan Tsai
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Qi Xu;
Qi Xu
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Ming Zhang;
Ming Zhang
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Gavin W. Lambert;
Gavin W. Lambert
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
†Central Clinical School, Monash University, Melbourne, VIC 3004, Australia
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Helen Kiriazis;
Helen Kiriazis
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
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Wei Gao;
Wei Gao
§Department of Cardiology, Third Hospital of Peking University, Beijing 100191, China
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Anthony M. Dart;
Anthony M. Dart
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
†Central Clinical School, Monash University, Melbourne, VIC 3004, Australia
‡Alfred Heart Centre, Alfred Hospital, Melbourne, VIC 3004, Australia
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Xiao-Jun Du
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
†Central Clinical School, Monash University, Melbourne, VIC 3004, Australia
Correspondence: Xiao-Jun Du (email [email protected]).
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Publisher: Portland Press Ltd
Received:
January 22 2016
Revision Received:
March 31 2016
Accepted:
April 01 2016
Accepted Manuscript online:
April 05 2016
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2016
Clin Sci (Lond) (2016) 130 (13): 1089–1104.
Article history
Received:
January 22 2016
Revision Received:
March 31 2016
Accepted:
April 01 2016
Accepted Manuscript online:
April 05 2016
Citation
Xiao-Ming Gao, Xiao-Lei Moore, Yang Liu, Xin-Yu Wang, Li-Ping Han, Yidan Su, Alan Tsai, Qi Xu, Ming Zhang, Gavin W. Lambert, Helen Kiriazis, Wei Gao, Anthony M. Dart, Xiao-Jun Du; Splenic release of platelets contributes to increased circulating platelet size and inflammation after myocardial infarction. Clin Sci (Lond) 1 July 2016; 130 (13): 1089–1104. doi: https://doi.org/10.1042/CS20160234
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