Author + information
- Received January 24, 2006
- Revision received April 14, 2006
- Accepted April 17, 2006
- Published online December 5, 2006.
- Enrico Lupia, MD⁎,
- Ornella Bosco, PhD†,
- Serena Bergerone, MD‡,
- Anna Erna Dondi, MD†,
- Alberto Goffi, MD†,
- Elena Oliaro, MD‡,
- Marco Cordero, MD‡,
- Lorenzo Del Sorbo, MD†,
- Giampaolo Trevi, MD‡ and
- Giuseppe Montrucchio, MD†,⁎ ()
- ↵⁎Reprint requests and correspondence:
Prof. Giuseppe Montrucchio, Dipartimento di Fisiopatologia Clinica, Università degli Studi di Torino, Via Genova 3, 10126 Torino, Italy.
Objectives We sought to investigate the potential role of elevated levels of thrombopoietin (TPO) in platelet activation during unstable angina (UA).
Background Thrombopoietin is a humoral growth factor that does not induce platelet aggregation per se, but primes platelet activation in response to several agonists. No data concerning its contribution to platelet function abnormalities described in patients with UA are available.
Methods We studied 15 patients with UA and, as controls, 15 patients with stable angina (SA) and 15 healthy subjects. We measured TPO and C-reactive protein (CRP), as well as monocyte-platelet binding and the platelet expression of P-selectin and of the TPO receptor, c-Mpl. The priming activity of patient or control plasma on platelet aggregation and monocyte-platelet binding and the role of TPO in this effect also were studied.
Results Patients with UA showed higher circulating TPO levels, as well as increased monocyte-platelet binding, platelet P-selectin expression, and CRP levels, than those with SA and healthy control subjects. The UA patients also showed reduced platelet expression of the TPO receptor, c-Mpl. In vitro, the plasma from UA patients, but not from SA patients or healthy controls, primed platelet aggregation and monocyte-platelet binding, which were both reduced when an inhibitor of TPO was used.
Conclusions Thrombopoietin may enhance platelet activation in the early phases of UA, potentially participating in the pathogenesis of acute coronary syndromes.
Dr. Montrucchio was supported by Murst ex-60%, Murst Cofin 2002, FIRB 2001, and Progetto di Ricerca Sanitaria Finalizzata–Regione Piemonte 2004. Drs. Lupia and Bosco contributed equally to this work.
- Received January 24, 2006.
- Revision received April 14, 2006.
- Accepted April 17, 2006.
- American College of Cardiology Foundation