Neurotrophin actions on the endothelial cell

Neurotrophin actions on the endothelial cell. Under basal conditions, the neurotrophin receptor trkA and trkB (and, in some tissues, also trkC) are expressed by EC. Trk receptor engagement by mature NTs initiates two major signaling pathways, Erk MAPK and IP3K/Akt. Nerve growth factor (NGF) treatment of EC causes a rapid phosphorylation of trkA, determining a parallel activation of ERK1/2 and a subsequent increase in EC proliferation and migration. Activation of the PI3K/Akt signaling pathway promotes EC survival. Moreover, via the PI3K/Akt, NGF stimulates EC invasion and cord formation by augmenting MMP-2. NGF, via trkA, supports EC survival in vitro and in vivo, an action which is, at least in part, mediated by increased VEGF-A. BDNF, via trkB, also supports EC survival. Under basal conditions, the p75NTR is scarcely expressed by EC. Following p75NTR induction or transduction, the receptor triggers EC apoptosis and inhibits EC cell cycling through mechanisms that may be dependent or not from ligand (mature NT and pro-NGF) activation.

Publication

Cardiovascular Actions of Neurotrophins. () ANDREA CAPORALI, et al. Physiol Rev. ;89(1):279-308. Figure: F3. Homo sapiens

Disease mentions