2002Journal of Neuroscience ResearchRequires access

Neural cell adhesion molecule‐mediated neurite outgrowth is repressed by overexpression of HES‐1

Ulla Jessen, Vera Novitskaya, Peter S. Walmod, Vladimir Berezin, Elisabeth Bock

Open publisher page 12 citations

Abstract

The neural cell adhesion molecule (NCAM) stimulates neurite outgrowth by activating intracellular signaling cascades. We investigated the role of the transcriptional repressor HES-1 in NCAM-dependent neurite outgrowth by estimating neurite extension from PC12-E2 cells grown in coculture with NCAM-negative or NCAM-positive fibroblasts. PC12-E2 cells were transiently transfected with an expression plasmid encoding HES-1. We found that expression of HES-1 inhibited NCAM-dependent neurite outgrowth. Treatment with arachidonic acid (an important messenger in NCAM-dependent signaling) restored NCAM-induced neurite outgrowth inhibited by HES-1. These results suggest that HES-1 is a regulator of intracellular signal transduction stimulated by cell adhesion molecules involved in neurite outgrowth.

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What this paper is about

The neural cell adhesion molecule (NCAM) stimulates neurite outgrowth by activating intracellular signaling cascades. We investigated the role of the transcriptional repressor HES-1 in NCAM-dependent neurite outgrowth by estimating neurite extension from PC12-E2 cells grown in coculture with NCAM-negative or NCAM-positive fibroblasts. PC12-E2 cells were transiently transfected with an expression plasmid encoding HES-1. We found that expression of HES-1 inhibited NCAM-dependent neurite outgrowth. Treatment with arachidonic acid (an important messenger in NCAM-dependent signaling) restored NCAM-induced neurite outgrowth inhibited by HES-1. These results suggest that HES-1 is a regulator of intracellular signal transduction stimulated by cell adhesion molecules involved in neurite outgrowth.

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Available abstract

The neural cell adhesion molecule (NCAM) stimulates neurite outgrowth by activating intracellular signaling cascades. We investigated the role of the transcriptional repressor HES-1 in NCAM-dependent neurite outgrowth by estimating neurite extension from PC12-E2 cells grown in coculture with NCAM-negative or NCAM-positive fibroblasts. PC12-E2 cells were transiently transfected with an expression plasmid encoding HES-1. We found that expression of HES-1 inhibited NCAM-dependent neurite outgrowth. Treatment with arachidonic acid (an important messenger in NCAM-dependent signaling) restored NCAM-induced neurite outgrowth inhibited by HES-1. These results suggest that HES-1 is a regulator of intracellular signal transduction stimulated by cell adhesion molecules involved in neurite outgrowth.

Key concepts: Neurite, Neural cell adhesion molecule, Cell biology, Cell adhesion, Cell adhesion molecule, Transfection, Intracellular, Signal transduction

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