VEGF modulates erythropoiesis through regulation of adult hepatic erythropoietin synthesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-06-25

AUTHORS

Betty Y Y Tam, Kevin Wei, John S Rudge, Jana Hoffman, Joceyln Holash, Sang-ki Park, Jenny Yuan, Colleen Hefner, Cecile Chartier, Jeng-Shin Lee, Shelly Jiang, Nihar R Nayak, Frans A Kuypers, Lisa Ma, Uma Sundram, Grace Wu, Joseph A Garcia, Stanley L Schrier, Jacquelyn J Maher, Randall S Johnson, George D Yancopoulos, Richard C Mulligan, Calvin J Kuo

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 neutralization of VEGF corneal micropocket angiogenesis. High-grade inhibition of VEGF induced hepatic synthesis of erythropoietin (Epo, encoded by Epo) >40-fold through a HIF-1α–independent mechanism, in parallel with suppression of renal Epo mRNA. Studies using hepatocyte-specific deletion of the Vegfa gene and hepatocyte–endothelial cell cocultures indicated that blockade of VEGF induced hepatic Epo by interfering with homeostatic VEGFR2-dependent paracrine signaling involving interactions between hepatocytes and endothelial cells. These data indicate that VEGF is a previously unsuspected negative regulator of hepatic Epo synthesis and erythropoiesis and suggest that levels of Epo and erythrocytosis could represent noninvasive surrogate markers for stringent blockade of VEGF in vivo.NOTE: In the version of this article initially published, the name of one of the authors, Nihar R. Nayak, was misspelled as Nihar R. Niyak. The error has been corrected in the HTML and PDF versions of the article. More... »

PAGES

793-800

Journal

TITLE

Nature Medicine

ISSUE

7

VOLUME

12

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm1428

DOI

http://dx.doi.org/10.1038/nm1428

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1015883708

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16799557


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