Nerve growth factor activates aorta endothelial cells causing PI3K/Akt- and ERK-dependent migration.
Nerve growth factor (NGF) is a well-known neurotrophin. We determined whether NGF can activate endothelial cell migration and signalling that underlie angiogenic processes. We showed that aorta endothelial cells express mRNA for both the receptor tyrosine kinase TrkA and the p75 neurotrophin receptor (p75NTR) that associates with TrkA when signalling occurs. Pig aortic endothelial cells migrated when exposed to an NGF gradient, due to the simultaneous activation of the phosphatidylinositol 3-kinase and extracellular signal-regulated kinase signalling pathways. Furthermore, morphological changes were found in migrating cells: they appear with elongated structures with a smaller cell volume than control cells. Our data show that NGF is an activator of endothelial cells and suggest that NGF plays a role in mediating angiogenesis.
Rahbek
Ulrik L
UL
Department of Medical Physiology, The Panum Institute, University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen N, Denmark.
Dissing
Steen
S
Thomassen
Camilla
C
Hansen
Anker J
AJ
Tritsaris
Katerina
K
D000818:Animals; D001011:Aorta / Q000166:cytology; D002465:Cell Movement / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000502:physiology*; D020932:Nerve Growth Factor / Q000494:pharmacology*; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology*; D020917:Receptor, trkA / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D013552:Swine
D020932:Nerve Growth Factor; D019869:Phosphatidylinositol 3-Kinases; D020917:Receptor, trkA; D048049:Extracellular Signal-Regulated MAP Kinases