2006
DOI: 10.1038/nm1428
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VEGF modulates erythropoiesis through regulation of adult hepatic erythropoietin synthesis

Abstract: Vascular endothelial growth factor (VEGF) exerts crucial functions during pathological angiogenesis and normal physiology. We observed increased hematocrit (60-75%) after high-grade inhibition of VEGF by diverse methods, including adenoviral expression of soluble VEGF receptor (VEGFR) ectodomains, recombinant VEGF Trap protein and the VEGFR2-selective antibody DC101. Increased production of red blood cells (erythrocytosis) occurred in both mouse and primate models, and was associated with near-complete neutral… Show more

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Cited by 153 publications
(111 citation statements)
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“…However, the unexpectedly high rates of VEGF production in non-tumor-bearing adult mice and humans is consistent with the recent realization that VEGF likely plays an ongoing role in the ''quiescent'' vasculature of normal adults (23). For example, treating normal adult mice and monkeys with VEGF antagonists can increase hematocrit (a measure of the proportion of the blood volume occupied by red blood cells) (24). Similarly, VEGF antagonists can also increase blood pressure (25), indicating that VEGF is involved in regulating VEGF Trap Complex provides guidance on when optimal VEGF blockade is achieved for antitumor purposes.…”
Section: Discussionsupporting
confidence: 75%
“…However, the unexpectedly high rates of VEGF production in non-tumor-bearing adult mice and humans is consistent with the recent realization that VEGF likely plays an ongoing role in the ''quiescent'' vasculature of normal adults (23). For example, treating normal adult mice and monkeys with VEGF antagonists can increase hematocrit (a measure of the proportion of the blood volume occupied by red blood cells) (24). Similarly, VEGF antagonists can also increase blood pressure (25), indicating that VEGF is involved in regulating VEGF Trap Complex provides guidance on when optimal VEGF blockade is achieved for antitumor purposes.…”
Section: Discussionsupporting
confidence: 75%
“…[32][33][34] Regulation of EPO through an HIF-1a-independent mechanism also has been recently reported. 35 In our study, we determined that treatment with EPO reduced the number of activated lung endothelial cells 6-fold in animals treated with bleomycin, as evidenced by changes in morphology. When activation of the endothelial cells occurs, these cells frequently assume a more round shape, cell-tocell junctions are destroyed and the endothelium becomes interrupted and leaky.…”
Section: Discussionmentioning
confidence: 77%
“…VEGF inhibition may also increase risk of thrombosis by increasing haematocrit and blood viscosity via overproduction of erythropoietin. 47,48 Moreover, VEGFR-TKIs may increase the release of procoagulant from the tumor into the blood stream due to an enhanced cytotoxic effect. VEGF inhibition may also increase expression of proinflammatory cytokines causing damage and in situ thrombus formation.…”
Section: Discussionmentioning
confidence: 99%