Platelet Vegf Contents In Patients With Pulmonary Hypertension Or With Chronic Hypoxemic Lung Disease

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It is now well established that VEGF is also synthetized by megacaryocytes and stored in circulating platelets, where it colocalizes with PDGF [23]. One speculative role for VEGF in platelets is promotion of vascular repair and wound healing in conjunction with PDGF. Platelet VEGF and PDGF are released during blood clotting or following platelet adhesion to the suben-dothelial basement membrane at sites of blood vessel injury. PDGF, as a potent mitogen for fibroblasts and smooth muscle cells, effectively promotes wound healing, while VEGF may initiate angiogenesis and accelerate repair of the endothelial cell lining [21]. From a physiological point of view, platelets could thus be regarded as transporters of circulating VEGF that restrict its angiogenic activity to sites of vascular injury.

VEGF released from platelets and acting specifically on endothelial cells may play a pivotal role. In systemic vessels, increasing VEGF bioavailability at sites of endothelial denudation has been shown to accelerate endothelial repair and to limit neointima formation [34]. Moreover, VEGF overexpression within the vascular wall has been shown to restore endothelium-dependent relaxation and to protect against vasoconstriction and platelet activation. The overall balance between VEGF and other platelet-derived non-specific mitogens such as PDGF may, therefore, be of importance in pulmonary vascular diseases and pulmonary hypertension.

In recent studies, we investigated serum and platelet VEGF and PDGF in a large population of patients with pulmonary arterial hypertension, either idi-opathic or associated with various diseases, as well as in patients with chronic hypoxemic lung disease. We found that platelet VEGF content was markedly elevated in patients with idiopathic or associated PH, compared with normal controls, whereas platelet PDGF content was unchanged [11]. These findings imply that sustained pulmonary artery pressure elevation, regardless of its cause, may lead to an increase in platelet VEGF content and, potentially, to an increase in platelet delivery of VEGF to the pulmonary vasculature. Intrestingly, platelet VEGF content was increased by continuous prostacyclin infusion, suggesting that continuous prostacyclin therapy results in enhanced VEGF release at sites of vascular injury. In polycythemic patients with severe chronic hypoxemic lung disease, only moderate increases in platelet VEGF and PDGF contents were observed, suggesting that hypoxemia was the main factor leading to the increases in platelet VEGF and PDGF contents. We s uggest that platelet VEGF elevation during PH may be a protective mechanism against pulmonary vascular injury and remodeling.

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