TY - JOUR
T1 - Receptor-mediated stimulation and inhibition of nerve growth factor secretion by vascular smooth muscle
AU - Tuttle, Jeremy B.
AU - Etheridge, Regina
AU - Creedon, Douglas J.
PY - 1993/10
Y1 - 1993/10
N2 - Nerve growth factor (NGF) is a potent neurotrophin signaling protein, the best-known member of a family of similar neurotrophins. Specific neuronal populations depend upon the neurotrophins for normal function and disturbances in NGF and neurotrophin supply have been implicated in neurodegenerative disease, diabetes, and hypertension. This report details experiments in which the hourly pattern of NGF secretion by cultured vascular smooth muscle cells is examined. Vascular smooth muscle cells are major innervation targets of the neuronal population first discovered to be NGF-dependent: the sympathetic principal neurons. The results show that arginine vasopressin (AVP), angiotensin II (AngH), and α-adrenergic receptor activation, all contractile stimuli, elevate NGF secretion. However, AVP dependably does so alone while AngH requires coactivation of adenosine receptors. Adenosine alone inhibits secretion mid the α-adrenergic increase in NGF output can be antagonized by activation of β-adrenergic receptors. A change to fresh culture medium is also a potent stimulus to increased NGF output.
AB - Nerve growth factor (NGF) is a potent neurotrophin signaling protein, the best-known member of a family of similar neurotrophins. Specific neuronal populations depend upon the neurotrophins for normal function and disturbances in NGF and neurotrophin supply have been implicated in neurodegenerative disease, diabetes, and hypertension. This report details experiments in which the hourly pattern of NGF secretion by cultured vascular smooth muscle cells is examined. Vascular smooth muscle cells are major innervation targets of the neuronal population first discovered to be NGF-dependent: the sympathetic principal neurons. The results show that arginine vasopressin (AVP), angiotensin II (AngH), and α-adrenergic receptor activation, all contractile stimuli, elevate NGF secretion. However, AVP dependably does so alone while AngH requires coactivation of adenosine receptors. Adenosine alone inhibits secretion mid the α-adrenergic increase in NGF output can be antagonized by activation of β-adrenergic receptors. A change to fresh culture medium is also a potent stimulus to increased NGF output.
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U2 - 10.1006/excr.1993.1256
DO - 10.1006/excr.1993.1256
M3 - Article
C2 - 8397098
AN - SCOPUS:0027442194
SN - 0014-4827
VL - 208
SP - 350
EP - 361
JO - Experimental Cell Research
JF - Experimental Cell Research
IS - 2
ER -