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Expression of CD44 and its isoforms in the fetal neuroblasts

Kaya, Gurkan; Laurini, Ricardo LU ; Chaubert, Pascal and Gross, Nicole (2001) In Applied Immunohistochemistry & Molecular Morphology 9(2). p.180-184
Abstract
CD44 is a polymorphic transmembrane glycoprotein that exists as multiple isoforms resulting from alternative splicing and posttranslational modifications. Enhanced expression of CD44 has been correlated to the tumorigenicity and metastatic behavior in different malignant tumors. In contrast, human neuroblastomas exhibit an inverse correlation between CD44 expression and tumor malignancy. To determine whether there is a CD44 silencing in sympatho-adrenal precursors as a possible explanation for the down-regulation of CD44 in neuroblastomas, the expression of standard CD44H and v6, v7, v7v8, or v10 isoforms was analyzed by immunohistochemistry in human adrenal glands of 14- to 20-week-old gestational age fetuses. All of the fetal neuroblasts... (More)
CD44 is a polymorphic transmembrane glycoprotein that exists as multiple isoforms resulting from alternative splicing and posttranslational modifications. Enhanced expression of CD44 has been correlated to the tumorigenicity and metastatic behavior in different malignant tumors. In contrast, human neuroblastomas exhibit an inverse correlation between CD44 expression and tumor malignancy. To determine whether there is a CD44 silencing in sympatho-adrenal precursors as a possible explanation for the down-regulation of CD44 in neuroblastomas, the expression of standard CD44H and v6, v7, v7v8, or v10 isoforms was analyzed by immunohistochemistry in human adrenal glands of 14- to 20-week-old gestational age fetuses. All of the fetal neuroblasts localized in the adrenal gland parenchyma and migrating from the sympathetic nerve chain into the fetal adrenal cortex strongly expressed CD44H but none of the CD44 isoforms could be detected in these cells. In contrast, a strong expression of CD44v7 and v6 was detected in the fetal adrenal cells. These results indicate that, as for many other cell types, the CD44H expressed by fetal neuroblasts may contribute to controlling their migration into the adrenal medulla and that the down-regulation of CD44H in neuroblastoma cells should be explained by mechanisms other than the fetal suppression of CD44H expression in their normal counterparts. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Applied Immunohistochemistry & Molecular Morphology
volume
9
issue
2
pages
180 - 184
publisher
Lippincott Williams & Wilkins
external identifiers
  • pmid:11396637
  • scopus:0035009785
ISSN
1533-4058
language
English
LU publication?
yes
id
dc912603-0e16-44af-9f93-3cec185d721e (old id 1122994)
date added to LUP
2008-07-01 13:10:22
date last changed
2018-05-29 12:28:23
@article{dc912603-0e16-44af-9f93-3cec185d721e,
  abstract     = {CD44 is a polymorphic transmembrane glycoprotein that exists as multiple isoforms resulting from alternative splicing and posttranslational modifications. Enhanced expression of CD44 has been correlated to the tumorigenicity and metastatic behavior in different malignant tumors. In contrast, human neuroblastomas exhibit an inverse correlation between CD44 expression and tumor malignancy. To determine whether there is a CD44 silencing in sympatho-adrenal precursors as a possible explanation for the down-regulation of CD44 in neuroblastomas, the expression of standard CD44H and v6, v7, v7v8, or v10 isoforms was analyzed by immunohistochemistry in human adrenal glands of 14- to 20-week-old gestational age fetuses. All of the fetal neuroblasts localized in the adrenal gland parenchyma and migrating from the sympathetic nerve chain into the fetal adrenal cortex strongly expressed CD44H but none of the CD44 isoforms could be detected in these cells. In contrast, a strong expression of CD44v7 and v6 was detected in the fetal adrenal cells. These results indicate that, as for many other cell types, the CD44H expressed by fetal neuroblasts may contribute to controlling their migration into the adrenal medulla and that the down-regulation of CD44H in neuroblastoma cells should be explained by mechanisms other than the fetal suppression of CD44H expression in their normal counterparts.},
  author       = {Kaya, Gurkan and Laurini, Ricardo and Chaubert, Pascal and Gross, Nicole},
  issn         = {1533-4058},
  language     = {eng},
  number       = {2},
  pages        = {180--184},
  publisher    = {Lippincott Williams & Wilkins},
  series       = {Applied Immunohistochemistry & Molecular Morphology},
  title        = {Expression of CD44 and its isoforms in the fetal neuroblasts},
  volume       = {9},
  year         = {2001},
}