The transport of high amounts of vascular endothelial growth factor by blood platelets underlines their potential contribution in systemic sclerosis angiogenesis
Solanilla A et al. – Study demonstrates that platelets transport high levels of VEGF in systemic sclerosis (SSc); may contribute to circulating VEGF because of ongoing activation in the course of the disease. If activated at the contact of injured endothelium, platelets may be important in the altered angiogenesis.Methods- An investigation of platelet activation and the role of platelets as a source of VEGF and other angiogenic mediators in SSc
- 40 patients with SSc; age- and sex-matched healthy subjects and subjects presenting a primary RP as controls
- Platelets were isolated, activated with thrombin and the secretion of VEGF, PDGF, homodimeric form BB (PDGF-BB), TGF-β1 and angiopoietins-1 and -2 measured
- Plasma concns of these mediators and the functionality of platelet-derived VEGF were also studied
- Platelet activation was assayed by measuring plasma β-thromboglobulin and expression of P-selectin on platelets
- The effect of iloprost on VEGF secretion by platelets was studied
Results- Platelets from SSc pts, vs controls, secreted large amounts of VEGF when activated, but not PDGF-BB, TGF-β1 or angiopoietins
- Increased expression of membrane P-selectin confirmed platelet activation in the pts
- Iloprost inhibited VEGF secretion by platelets both in vivo and in vitro, through inhibition of platelet activation
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