scholarly journals Direct activation of second messenger pathways mimics cell adhesion molecule-dependent neurite outgrowth.

1992 ◽  
Vol 118 (3) ◽  
pp. 663-670 ◽  
Author(s):  
J L Saffell ◽  
F S Walsh ◽  
P Doherty
Keyword(s):  
Cell Adhesion ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Calcium Channel Antagonists ◽  
3T3 Cells ◽  
Second Messenger Pathways

We present evidence that direct activation of neuronal second messenger pathways in PC12 cells by opening voltage-dependent calcium channels mimics cell adhesion molecule (CAM)-induced differentiation of these cells. PC12 cells were cultured on monolayers of control 3T3 cells or 3T3 cells expressing transfected N-cadherin in the presence of KCl or a calcium channel agonist Bay K 8644. Both potassium depolarization and agonist-induced activation of calcium channels promoted substantial neurite outgrowth from PC12 cells cultured on control 3T3 monolayers and increased neurite outgrowth from those cultured on N-cadherin-expressing 3T3 monolayers. The potassium-induced response could be inhibited by L- and N-type calcium channel antagonists and by kinase inhibitor K-252b but was unaffected by pertussis toxin. In contrast activators of protein kinase C did not stimulate neurite outgrowth, and the neurite outgrowth response induced by activation of protein kinase A was not inhibited by calcium channel antagonists or pertussis toxin. These studies support the postulate that CAM-induced neuronal differentiation involves a specific transmembrane signaling pathway and suggest that activation of this pathway after CAM binding may be more important for the neurite outgrowth response than CAM-dependent adhesion per se.

scholarly journals Ganglioside modulation of neural cell adhesion molecule and N-cadherin-dependent neurite outgrowth

1992 ◽  
Vol 117 (5) ◽  
pp. 1093-1099 ◽  
Author(s):  
P Doherty ◽  
SV Ashton ◽  
SD Skaper ◽  
A Leon ◽  
FS Walsh
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Calcium Influx ◽  
Neural Cell ◽  
3T3 Cells ◽  
Neural Cell Adhesion

We have used monolayers of control 3T3 cells and 3T3 cells expressing transfected human neural cell adhesion molecule (NCAM) or chick N-cadherin as a culture substrate for PC12 cells. NCAM and N-cadherin in the monolayer directly promote neurite outgrowth from PC12 cells via a G-protein-dependent activation of neuronal calcium channels. In the present study we show that ganglioside GM1 does not directly activate this pathway in PC12 cells. However, the presence of GM1 (12.5-100 micrograms/ml) in the co-culture was associated with a potentiation of NCAM and N-cadherin-dependent neurite outgrowth. Treatment of PC12 cells with GM1 (100 micrograms/ml) for 90 min led to trypsin-stable increases in both beta-cholera toxin binding to PC12 cells and an enhanced neurite outgrowth response to N-cadherin. The ganglioside response could be fully inhibited by treatment with pertussis toxin. These data are consistent with exogenous gangliosides enhancing neuritic growth by promoting cell adhesion molecule-induced calcium influx into neurons.

scholarly journals Thy-1 antibody-triggered neurite outgrowth requires an influx of calcium into neurons via N- and L-type calcium channels

1993 ◽  
Vol 122 (1) ◽  
pp. 181-189 ◽  
Author(s):  
P Doherty ◽  
A Singh ◽  
G Rimon ◽  
SR Bolsover ◽  
FS Walsh
Keyword(s):  
Cell Adhesion ◽  
Calcium Channels ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Pertussis Toxin ◽  
Cell Adhesion Molecule ◽  
Calcium Influx ◽  
Present Evidence ◽  
Cells Cultured

We present evidence that the neurite out-growth stimulated by the binding of Thy-1 antibodies to PC12 cells is mediated by calcium influx through both N- and L-type calcium channels. PC12 cells cultured on a noncellular substratum in the presence of NGF, or on a cellular substratum in the absence of NGF, responded to soluble Thy-1 antibody by extending longer neurites. The response required bivalent antibody and could be blocked by removing Thy-1 from the surface of PC12 cells with phosphatidylinositol specific phospholipase C. The response could also be blocked by reducing extracellular calcium to 0.25 mM, or by antagonists of L- and N-type calcium channels. Additionally, the response could be fully inhibited by preloading PC12 cells with BAPTA/AM which buffers changes in intracellular calcium. A heterotrimeric G-protein is also implicated in the pathway as the response could be fully inhibited by pertussis toxin. These data suggest that antibody-induced clustering of Thy-1 stimulates neurite outgrowth by activating a second messenger pathway that has previously been shown to underlie cell adhesion molecule (NCAM, N-cadherin, and L1), but not integrin or NGF-dependent neurite outgrowth.

Computational Analysis of Isoform-Specific Signal Regulation by CEACAM1-A Cell Adhesion Molecule Expressed in PC12 Cells

2002 ◽  
Vol 971 (1) ◽  
pp. 597-607 ◽  
Author(s):  
BJÖRN ÖBRINK ◽  
HIROKI SAWA ◽  
INKA SCHEFFRAHN ◽  
BERNHARD B. SINGER ◽  
KRISTMUNDUR SIGMUNDSSON ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Pc12 Cells ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Computational Analysis ◽  
Specific Signal ◽  
A Cell ◽  
Signal Regulation

scholarly journals A soluble form of the F3 neuronal cell adhesion molecule promotes neurite outgrowth

1992 ◽  
Vol 117 (4) ◽  
pp. 877-887 ◽  
Author(s):  
P Durbec ◽  
G Gennarini ◽  
C Goridis ◽  
G Rougon
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Dorsal Root Ganglion Neurons ◽  
Soluble Form ◽  
Dependent Manner ◽  
Neurite Initiation ◽  
Ganglion Neurons ◽  
Adhesive Proteins

The F3 molecule is a member of the immunoglobulin superfamily anchored to membranes by a glycane-phosphatidylinositol, and is predominantly expressed on subsets of axons of the central and peripheral nervous system. In a previous paper (Gennarini, G., P. Durbec, A. Boned, G. Rougon, and C. Goridis. 1991. Neuron. 6:595-606), we have established that F3 fulfills the operational definition of a cell adhesion molecule and that it stimulates neurite outgrowth when presented to sensory neurons as a surface component of transfected CHO cells. In the present study the question as to whether soluble forms of F3 would be functionally active was addressed in vitro on cultures of mouse dorsal root ganglion neurons. We observed that preparations enriched in soluble F3 had no effect on neuron attachment but enhanced neurite initiation and neurite outgrowth in a dose-dependent manner. By contrast, soluble NCAM-120 does not have any measurable effect on these phenomena. Addition of anti-F3 monovalent antibodies reduced the number of process-bearing neurons and the neuritic output per neuron to control values. Addition of cerebrospinal fluid, a natural source of soluble F3, also stimulated neurite extension, and this effect was partially blocked by anti-F3 antibodies. Our results suggest that the soluble forms of adhesive proteins with neurite outgrowth-promoting properties could act at a distance from their site of release in a way reminiscent of growth and trophic factors.

The cell adhesion molecule L1 regulates the expression of FGF21 and enhances neurite outgrowth

2013 ◽  
Vol 1530 ◽  
pp. 13-21 ◽  
Author(s):  
Xiaohua Huang ◽  
Jiliang Hu ◽  
Ying Li ◽  
Zara Zhuyun Yang ◽  
Hongmei Zhu ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Cell Adhesion Molecule L1
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