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Dopamine in vivo inhibits VEGF-induced phosphorylation of VEGFR-2, MAPK, and focal adhesion kinase in endothelial cells

¹Signal Transduction and Biogenic Amines Laboratory and ²Department of Medical Oncology, Chittaranjan National Cancer Institute, Calcutta 700026; ³Department of Pathology, Institute of Postgraduate Medical Education and Research, Calcutta 700020, India; and ⁴Mayo Clinic Cancer Center and Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905

Submitted 18 March 2004 ; accepted in final form 26 May 2004

Vascular permeability factor (VPF)/VEGF is a potent multifunctional cytokine and growth factor that has critical roles in vasculogenesis and in both physiological and pathological angiogenesis. Because it has been recently shown that the neurotransmitter dopamine at pharmacological dose can inhibit VEGF/VPF-mediated microvascular permeability, proliferation, and migration of endothelial cells in vitro, we therefore hypothesized that endogenous dopamine may regulate the actions of VPF/VEGF in vivo. We report that VPF/VEGF-induced phosphorylation of VEGF receptor 2, focal adhesion kinase, and MAPK in the endothelial cells is strikingly increased in both dopamine-depleted and dopamine D₂ receptor knockout mice compared with normal controls, thereby indicating that endogenous dopamine regulate these critical signaling cascades required for the in vivo endothelial functions of VPF/VEGF. Together, these observations provide new mechanistic insight into the dopamine-mediated inhibition of the activities of VPF/VEGF and suggest that endogenous neurotransmitter dopamine might be an important physiological regulator of VPF/VEGF activities in vivo.

signaling; vascular endothelial growth factor receptor-2; mitogen-activated protein kinase

P. S. Dasgupta, Signal Transduction and Biogenic Amines Laboratory, Chittaranjan National Cancer Institute, 37 S. P. Mukherjee Rd., Calcutta 700026, India (E-mail: partha2{at}vsnl.com)

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