Vascular endothelial growth factor-B-deficient mice display an atrial conduction defect

Vascular endothelial growth factors (VEGFs) and their receptors are essential regulators of vasculogenesis and angiogenesis in both embryos and adults. One of the factors with a still unknown physiological function is VEGF-B, which is expressed in many tissues, including the heart. Mice carrying a t...

Full description

Saved in:
Bibliographic Details
Published inCirculation (New York, N.Y.) Vol. 104; no. 3; pp. 358 - 364
Main Authors AASE, Karin, VON EULER, Gabriel, ALITALO, Kari, BETSHOLTZ, Christer, ERIKSSON, Ulf, XURI LI, PONTEN, Annica, THOREN, Peter, RENHAI CAO, YIHAI CAO, OLOFSSON, Birgitta, GEBRE-MEDHIN, Samuel, PEKNY, Milos
Format Journal Article
LanguageEnglish
Published Hagerstown, MD Lippincott Williams & Wilkins 17.07.2001
American Heart Association, Inc
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Vascular endothelial growth factors (VEGFs) and their receptors are essential regulators of vasculogenesis and angiogenesis in both embryos and adults. One of the factors with a still unknown physiological function is VEGF-B, which is expressed in many tissues, including the heart. Mice carrying a targeted deletion in the VEGF-B gene were developed. In VEGF-B(-/-) animals, no gross abnormalities were observed in organs that normally show high expression of VEGF-B, such as the heart, muscle, and kidney. Analysis of heart function by ECG showed that adult VEGF-B(-/-) mice have an atrial conduction abnormality characterized by a prolonged PQ interval. VEGF- or basic fibroblast growth factor-induced corneal angiogenesis was similar in normal and VEGF-B(-/-) mice. VEGF-B seems to be required for normal heart function in adult animals but is not required for proper development of the cardiovascular system either during development or for angiogenesis in adults.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0009-7322
1524-4539
1524-4539
DOI:10.1161/01.cir.104.3.358