Developmental expression of receptor for advanced glycation end products (RAGE), amphoterin and sulfoglucuronyl (HNK-1) carbohydrate in mouse cerebellum and their role in neurite outgrowth and cell migration

D K H Chou, J Zhang, F I Smith, P McCaffery, F B Jungalwala

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Abstract

Receptor for advanced glycation end products (RAGE) has been proposed as a signal transduction receptor to promote neurite outgrowth and cell migration, by its interaction with a neurite outgrowth promoting protein, Amphoterin. Amphoterin has been shown to interact with sulfoglucuronyl carbohydrate (SGC). The developmental expression of RAGE, Amphoterin and SGC was studied in pre-natal and post-natal mouse cerebellum to establish their cellular and subcellular localization and function. The amount of RAGE in the cerebellum increased with age. RAGE was expressed pre-natally in the external germinal layer and post-natally in the plasma membranes of the granule neurons of the external and internal granule cell layers and in Purkinje cells. Immunocytochemical analysis by high magnification confocal microscopy showed that RAGE was co-expressed with Amphoterin and SGC in the cell surfaces of granule neurons. This co-localization of RAGE, Amphoterin, and SGC was confirmed in isolated and cultured granule neurons and in migrating granule neurons in explant cultures. Anti-RAGE antibodies inhibited neurite outgrowth and cell migration in explant and slice cultures, similar to anti-Amphoterin and anti-SGC antibodies shown previously. The results suggest that RAGE could act as a signaling molecule for neurite outgrowth and cell migration by its interaction with Amphoterin and that of Amphoterin with SGC.

Original languageEnglish
Pages (from-to)1389-1401
Number of pages13
JournalJournal of Neurochemistry
Volume90
Issue number6
Early online date27 Jul 2004
DOIs
Publication statusPublished - Sep 2004

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HMGB1 Protein
Cerebellum
Cell Movement
Carbohydrates
Neurons
Signal transduction
Advanced Glycosylation End Product-Specific Receptor
Neuronal Outgrowth
Antibodies
Confocal microscopy
Purkinje Cells
Cell membranes
Confocal Microscopy
Signal Transduction
Cells
Cell Membrane
Molecules

Keywords

  • Amphoterin
  • cell migration
  • HNK-1
  • neurite outgrowth
  • receptor for advanced glycation end products
  • sulfoglucuronyl carbohydrate
  • embryonal carcinoma-cells
  • dveloping nervous-system
  • binding-protein SBP-1
  • L2/HNK-1 carbohydrate
  • rat cerebellum
  • adheion molecules
  • mice deficient
  • neurons
  • differentiation
  • epitope

Cite this

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title = "Developmental expression of receptor for advanced glycation end products (RAGE), amphoterin and sulfoglucuronyl (HNK-1) carbohydrate in mouse cerebellum and their role in neurite outgrowth and cell migration",
abstract = "Receptor for advanced glycation end products (RAGE) has been proposed as a signal transduction receptor to promote neurite outgrowth and cell migration, by its interaction with a neurite outgrowth promoting protein, Amphoterin. Amphoterin has been shown to interact with sulfoglucuronyl carbohydrate (SGC). The developmental expression of RAGE, Amphoterin and SGC was studied in pre-natal and post-natal mouse cerebellum to establish their cellular and subcellular localization and function. The amount of RAGE in the cerebellum increased with age. RAGE was expressed pre-natally in the external germinal layer and post-natally in the plasma membranes of the granule neurons of the external and internal granule cell layers and in Purkinje cells. Immunocytochemical analysis by high magnification confocal microscopy showed that RAGE was co-expressed with Amphoterin and SGC in the cell surfaces of granule neurons. This co-localization of RAGE, Amphoterin, and SGC was confirmed in isolated and cultured granule neurons and in migrating granule neurons in explant cultures. Anti-RAGE antibodies inhibited neurite outgrowth and cell migration in explant and slice cultures, similar to anti-Amphoterin and anti-SGC antibodies shown previously. The results suggest that RAGE could act as a signaling molecule for neurite outgrowth and cell migration by its interaction with Amphoterin and that of Amphoterin with SGC.",
keywords = "Amphoterin, cell migration, HNK-1, neurite outgrowth, receptor for advanced glycation end products, sulfoglucuronyl carbohydrate, embryonal carcinoma-cells, dveloping nervous-system, binding-protein SBP-1, L2/HNK-1 carbohydrate, rat cerebellum, adheion molecules, mice deficient, neurons, differentiation, epitope",
author = "Chou, {D K H} and J Zhang and Smith, {F I} and P McCaffery and Jungalwala, {F B}",
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TY - JOUR

T1 - Developmental expression of receptor for advanced glycation end products (RAGE), amphoterin and sulfoglucuronyl (HNK-1) carbohydrate in mouse cerebellum and their role in neurite outgrowth and cell migration

AU - Chou, D K H

AU - Zhang, J

AU - Smith, F I

AU - McCaffery, P

AU - Jungalwala, F B

PY - 2004/9

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N2 - Receptor for advanced glycation end products (RAGE) has been proposed as a signal transduction receptor to promote neurite outgrowth and cell migration, by its interaction with a neurite outgrowth promoting protein, Amphoterin. Amphoterin has been shown to interact with sulfoglucuronyl carbohydrate (SGC). The developmental expression of RAGE, Amphoterin and SGC was studied in pre-natal and post-natal mouse cerebellum to establish their cellular and subcellular localization and function. The amount of RAGE in the cerebellum increased with age. RAGE was expressed pre-natally in the external germinal layer and post-natally in the plasma membranes of the granule neurons of the external and internal granule cell layers and in Purkinje cells. Immunocytochemical analysis by high magnification confocal microscopy showed that RAGE was co-expressed with Amphoterin and SGC in the cell surfaces of granule neurons. This co-localization of RAGE, Amphoterin, and SGC was confirmed in isolated and cultured granule neurons and in migrating granule neurons in explant cultures. Anti-RAGE antibodies inhibited neurite outgrowth and cell migration in explant and slice cultures, similar to anti-Amphoterin and anti-SGC antibodies shown previously. The results suggest that RAGE could act as a signaling molecule for neurite outgrowth and cell migration by its interaction with Amphoterin and that of Amphoterin with SGC.

AB - Receptor for advanced glycation end products (RAGE) has been proposed as a signal transduction receptor to promote neurite outgrowth and cell migration, by its interaction with a neurite outgrowth promoting protein, Amphoterin. Amphoterin has been shown to interact with sulfoglucuronyl carbohydrate (SGC). The developmental expression of RAGE, Amphoterin and SGC was studied in pre-natal and post-natal mouse cerebellum to establish their cellular and subcellular localization and function. The amount of RAGE in the cerebellum increased with age. RAGE was expressed pre-natally in the external germinal layer and post-natally in the plasma membranes of the granule neurons of the external and internal granule cell layers and in Purkinje cells. Immunocytochemical analysis by high magnification confocal microscopy showed that RAGE was co-expressed with Amphoterin and SGC in the cell surfaces of granule neurons. This co-localization of RAGE, Amphoterin, and SGC was confirmed in isolated and cultured granule neurons and in migrating granule neurons in explant cultures. Anti-RAGE antibodies inhibited neurite outgrowth and cell migration in explant and slice cultures, similar to anti-Amphoterin and anti-SGC antibodies shown previously. The results suggest that RAGE could act as a signaling molecule for neurite outgrowth and cell migration by its interaction with Amphoterin and that of Amphoterin with SGC.

KW - Amphoterin

KW - cell migration

KW - HNK-1

KW - neurite outgrowth

KW - receptor for advanced glycation end products

KW - sulfoglucuronyl carbohydrate

KW - embryonal carcinoma-cells

KW - dveloping nervous-system

KW - binding-protein SBP-1

KW - L2/HNK-1 carbohydrate

KW - rat cerebellum

KW - adheion molecules

KW - mice deficient

KW - neurons

KW - differentiation

KW - epitope

U2 - 10.1111/j.1471-4159.2004.02609.x

DO - 10.1111/j.1471-4159.2004.02609.x

M3 - Article

VL - 90

SP - 1389

EP - 1401

JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 0022-3042

IS - 6

ER -