Reevaluation of the role of VEGF-B suggests a restricted role in the revascularization of the ischemic myocardium.

نویسندگان

  • Xuri Li
  • Marc Tjwa
  • Inge Van Hove
  • Berndt Enholm
  • Elke Neven
  • Karri Paavonen
  • Michael Jeltsch
  • Toni Diez Juan
  • Richard E Sievers
  • Emmanuel Chorianopoulos
  • Hiromichi Wada
  • Maarten Vanwildemeersch
  • Agnes Noel
  • Jean-Michel Foidart
  • Matthew L Springer
  • Georges von Degenfeld
  • Mieke Dewerchin
  • Helen M Blau
  • Kari Alitalo
  • Ulf Eriksson
  • Peter Carmeliet
  • Lieve Moons
چکیده

OBJECTIVE The endogenous role of the VEGF family member vascular endothelial growth factor-B (VEGF-B) in pathological angiogenesis remains unclear. METHODS AND RESULTS We studied the role of VEGF-B in various models of pathological angiogenesis using mice lacking VEGF-B (VEGF-B(-/-)) or overexpressing VEGF-B(167). After occlusion of the left coronary artery, VEGF-B deficiency impaired vessel growth in the ischemic myocardium whereas, in wild-type mice, VEGF-B(167) overexpression enhanced revascularization of the infarct and ischemic border zone. By contrast, VEGF-B deficiency did not affect vessel growth in the wounded skin, hypoxic lung, ischemic retina, or ischemic limb. Moreover, VEGF-B(167) overexpression failed to enhance vascular growth in the skin or ischemic limb. CONCLUSIONS VEGF-B appears to have a relatively restricted angiogenic activity in the ischemic heart. These insights might offer novel therapeutic opportunities.

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عنوان ژورنال:
  • Arteriosclerosis, thrombosis, and vascular biology

دوره 28 9  شماره 

صفحات  -

تاریخ انتشار 2008