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40
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Text
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Pages
81–91
Issue
1
Volume
74
Dublin Core
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Title
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Rat alpha1-macroglobulin enhances nerve growth factor-promoted neurite outgrowth, TrkA phosphorylation, and gene expression of pheochromocytoma PC12 cells.
Publisher
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Journal of neurochemistry
Date
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2000
2000-01
Subject
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Animals; Phosphorylation/drug effects; Rats; Transcription Factors/genetics; Gene Expression/*drug effects; Nerve Growth Factor/*pharmacology; *Immediate-Early Proteins; alpha-Macroglobulins/drug effects/metabolism/*pharmacology; Carrier Proteins; DNA-Binding Proteins/genetics; Early Growth Response Protein 1; Matrix Metalloproteinase 3/metabolism; Membrane Proteins; Nerve Growth Factors/genetics; Neurites/drug effects/*physiology; PC12 Cells/drug effects/metabolism/*physiology; Proto-Oncogene Proteins c-jun/genetics; Serotonin/pharmacology; Sprague-Dawley; Receptor; trkA/*metabolism
Creator
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Lee P G; Koo P H
Description
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Monoamine-activated human alpha2-macroglobulin (alpha2M) has been previously demonstrated to inhibit TrkA-, TrkB-, and TrkC-mediated signal transduction. Rat alpha1-macroglobulin (alpha1M) and alpha2M are structural homologues of human alpha2M, but rat alpha1M is distinctly different from rat alpha2M in many ways and its role in the mammalian nervous system is unknown. In this report, monoamine-activated rat alpha1M was demonstrated to enhance in a dose-dependent manner nerve growth factor (NGF)-promoted neurite outgrowth in pheochromocytoma PC12 cells. Monoamine-activated alpha1M by itself, however, was neither neurotrophic nor mitogenic to PC12 cells. To investigate further its possible mode of action, the ability of monoamine-activated alpha1M and normal alpha1M to bind and to activate the NGF receptor (TrkA) was investigated. Monoamine-activated alpha1M formed a more stable complex with TrkA than normal alpha1 M, but the binding of monoamine-activated alpha1M to TrkA was adversely affected by prior stimulation of TrkA with NGF. In addition, monoamine-activated alpha1M enhanced the NGF-promoted TrkA phosphorylation and up-regulated the expression of NGF-inducible immediate-early genes (c-jun and NGFI-A) and delayed-response genes (SCG10 and transin) in PC12 cells; normal alpha1M, in contrast, produced little or no effect. This study demonstrates that alpha1M, the constitutive form of alpha-macroglobulin in the rat, possesses the ability to promote NGF-mediated differentiation in PC12 cells, possibly via its direct action on TrkA receptors and TrkA-mediated signal transduction and gene expression.
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Immediate-Early Proteins
2000
alpha-Macroglobulins/drug effects/metabolism/*pharmacology
Animals
Carrier Proteins
DNA-Binding Proteins/genetics
Early Growth Response Protein 1
Gene Expression/*drug effects
Journal of neurochemistry
Koo P H
Lee P G
Matrix Metalloproteinase 3/metabolism
Membrane Proteins
Nerve Growth Factor/*pharmacology
Nerve Growth Factors/genetics
Neurites/drug effects/*physiology
PC12 Cells/drug effects/metabolism/*physiology
Phosphorylation/drug effects
Proto-Oncogene Proteins c-jun/genetics
Rats
Receptor
Serotonin/pharmacology
Sprague-Dawley
Transcription Factors/genetics
trkA/*metabolism