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E‐cadherin expression in postnatal Schwann cells is regulated by the cAMP‐dependent protein kinase a pathway
Author(s) -
Crawford Audrita T.,
Desai Darshan,
Gokina Pradeepa,
Basak Sayantani,
Kim Haesun A.
Publication year - 2008
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20716
Subject(s) - biology , cadherin , microbiology and biotechnology , protein kinase a , kinase , schwann cell , neuroscience , genetics , cell
Expression of E‐cadherin in the peripheral nervous system is a highly regulated process that appears postnatally in concert with the development of myelinating Schwann cell lineage. As a major component of autotypic junctions, E‐cadherin plays an important role in maintaining the structural integrity of noncompact myelin regions. In vivo , the appearance of E‐cadherin in postnatal Schwann cell is accompanied by the disappearance of N‐cadherin, suggesting reciprocal regulation of the two cadherins during Schwann cell development. The molecular signal that regulates the cadherin switch in Schwann cell is unclear. Using a neuron‐Schwann cell co‐culture system, here we show that E‐cadherin expression is induced by components on the axonal membrane. We also show that the axonal effect is mediated through cAMP‐dependent protein kinase A (cAMP‐PKA) activation in the Schwann cell: (1) inhibition of cAMP‐PKA blocks axon‐induced E‐cadherin expression and (2) cAMP elevation in the Schwann cell is sufficient to induce E‐cadherin expression. In addition, cAMP‐dependent E‐cadherin expression is promoted by contact between adjacent Schwann cell membranes, suggesting its role in autotypic junction formation during myelination. Furthermore, cAMP‐induced E‐cadherin expression is accompanied by suppression of N‐cadherin expression. Therefore, we propose that axon‐dependent activation of cAMP‐PKA serves as a signal that promotes cadherin switch during postnatal development of Schwann cells. © 2008 Wiley‐Liss, Inc.