E-Cadherin enhances neuregulin signaling and promotes Schwann cell myelination

Sayantani Basak, Darshan Desai, Esther H. Rho, Roselle Ramos, Patrice Maurel, Haesun A. Kim

Research output: Contribution to journalArticle

  • 8 Citations

Abstract

In myelinating Schwann cells, E-cadherin is a component of the adherens junctions that stabilize the architecture of the noncompact myelin region. In other cell types, E-cadherin has been considered as a signaling receptor that modulates intracellular signal transduction and cellular responses. To determine whether E-cadherin plays a regulatory role during Schwann cell myelination, we investigated the effects of E-cadherin deletion and over-expression in Schwann cells. In vivo, Schwann cell-specific E-cadherin ablation results in an early myelination delay. In Schwann cell-dorsal root ganglia neuron co-cultures, E-cadherin deletion attenuates myelin formation and shortens the myelin segment length. When over-expressed in Schwann cells, E-cadherin improves myelination on Nrg1 type III+/- neurons and induces myelination on normally non-myelinated axons of sympathetic neurons. The pro-myelinating effect of E-cadherin is associated with an enhanced Nrg1-erbB receptor signaling, including activation of the downstream Akt and Rac. Accordingly, in the absence of E-cadherin, Nrg1-signaling is diminished in Schwann cells. Our data also show that E-cadherin expression in Schwann cell is induced by axonal Nrg1 type III, indicating a reciprocal interaction between E-cadherin and the Nrg1 signaling. Altogether, our data suggest a regulatory function of E-cadherin that modulates Nrg1 signaling and promotes Schwann cell myelin formation.

LanguageEnglish (US)
Pages1522-1536
Number of pages15
JournalGlia
Volume63
Issue number9
DOIs
StatePublished - Jan 1 2015
Externally publishedYes

Fingerprint

Neuregulins
Schwann Cells
Cadherins
Myelin Sheath
Neurons
Adherens Junctions
Spinal Ganglia
Coculture Techniques

All Science Journal Classification (ASJC) codes

  • Neurology
  • Cellular and Molecular Neuroscience

Cite this

Basak, Sayantani ; Desai, Darshan ; Rho, Esther H. ; Ramos, Roselle ; Maurel, Patrice ; Kim, Haesun A. / E-Cadherin enhances neuregulin signaling and promotes Schwann cell myelination. In: Glia. 2015 ; Vol. 63, No. 9. pp. 1522-1536.
@article{c623bb9aaf404f60b9522bfe511c6cca,
title = "E-Cadherin enhances neuregulin signaling and promotes Schwann cell myelination",
abstract = "In myelinating Schwann cells, E-cadherin is a component of the adherens junctions that stabilize the architecture of the noncompact myelin region. In other cell types, E-cadherin has been considered as a signaling receptor that modulates intracellular signal transduction and cellular responses. To determine whether E-cadherin plays a regulatory role during Schwann cell myelination, we investigated the effects of E-cadherin deletion and over-expression in Schwann cells. In vivo, Schwann cell-specific E-cadherin ablation results in an early myelination delay. In Schwann cell-dorsal root ganglia neuron co-cultures, E-cadherin deletion attenuates myelin formation and shortens the myelin segment length. When over-expressed in Schwann cells, E-cadherin improves myelination on Nrg1 type III+/- neurons and induces myelination on normally non-myelinated axons of sympathetic neurons. The pro-myelinating effect of E-cadherin is associated with an enhanced Nrg1-erbB receptor signaling, including activation of the downstream Akt and Rac. Accordingly, in the absence of E-cadherin, Nrg1-signaling is diminished in Schwann cells. Our data also show that E-cadherin expression in Schwann cell is induced by axonal Nrg1 type III, indicating a reciprocal interaction between E-cadherin and the Nrg1 signaling. Altogether, our data suggest a regulatory function of E-cadherin that modulates Nrg1 signaling and promotes Schwann cell myelin formation.",
author = "Sayantani Basak and Darshan Desai and Rho, {Esther H.} and Roselle Ramos and Patrice Maurel and Kim, {Haesun A.}",
year = "2015",
month = "1",
day = "1",
doi = "https://doi.org/10.1002/glia.22822",
language = "English (US)",
volume = "63",
pages = "1522--1536",
journal = "GLIA",
issn = "0894-1491",
publisher = "John Wiley and Sons Inc.",
number = "9",

}

E-Cadherin enhances neuregulin signaling and promotes Schwann cell myelination. / Basak, Sayantani; Desai, Darshan; Rho, Esther H.; Ramos, Roselle; Maurel, Patrice; Kim, Haesun A.

In: Glia, Vol. 63, No. 9, 01.01.2015, p. 1522-1536.

Research output: Contribution to journalArticle

TY - JOUR

T1 - E-Cadherin enhances neuregulin signaling and promotes Schwann cell myelination

AU - Basak, Sayantani

AU - Desai, Darshan

AU - Rho, Esther H.

AU - Ramos, Roselle

AU - Maurel, Patrice

AU - Kim, Haesun A.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - In myelinating Schwann cells, E-cadherin is a component of the adherens junctions that stabilize the architecture of the noncompact myelin region. In other cell types, E-cadherin has been considered as a signaling receptor that modulates intracellular signal transduction and cellular responses. To determine whether E-cadherin plays a regulatory role during Schwann cell myelination, we investigated the effects of E-cadherin deletion and over-expression in Schwann cells. In vivo, Schwann cell-specific E-cadherin ablation results in an early myelination delay. In Schwann cell-dorsal root ganglia neuron co-cultures, E-cadherin deletion attenuates myelin formation and shortens the myelin segment length. When over-expressed in Schwann cells, E-cadherin improves myelination on Nrg1 type III+/- neurons and induces myelination on normally non-myelinated axons of sympathetic neurons. The pro-myelinating effect of E-cadherin is associated with an enhanced Nrg1-erbB receptor signaling, including activation of the downstream Akt and Rac. Accordingly, in the absence of E-cadherin, Nrg1-signaling is diminished in Schwann cells. Our data also show that E-cadherin expression in Schwann cell is induced by axonal Nrg1 type III, indicating a reciprocal interaction between E-cadherin and the Nrg1 signaling. Altogether, our data suggest a regulatory function of E-cadherin that modulates Nrg1 signaling and promotes Schwann cell myelin formation.

AB - In myelinating Schwann cells, E-cadherin is a component of the adherens junctions that stabilize the architecture of the noncompact myelin region. In other cell types, E-cadherin has been considered as a signaling receptor that modulates intracellular signal transduction and cellular responses. To determine whether E-cadherin plays a regulatory role during Schwann cell myelination, we investigated the effects of E-cadherin deletion and over-expression in Schwann cells. In vivo, Schwann cell-specific E-cadherin ablation results in an early myelination delay. In Schwann cell-dorsal root ganglia neuron co-cultures, E-cadherin deletion attenuates myelin formation and shortens the myelin segment length. When over-expressed in Schwann cells, E-cadherin improves myelination on Nrg1 type III+/- neurons and induces myelination on normally non-myelinated axons of sympathetic neurons. The pro-myelinating effect of E-cadherin is associated with an enhanced Nrg1-erbB receptor signaling, including activation of the downstream Akt and Rac. Accordingly, in the absence of E-cadherin, Nrg1-signaling is diminished in Schwann cells. Our data also show that E-cadherin expression in Schwann cell is induced by axonal Nrg1 type III, indicating a reciprocal interaction between E-cadherin and the Nrg1 signaling. Altogether, our data suggest a regulatory function of E-cadherin that modulates Nrg1 signaling and promotes Schwann cell myelin formation.

UR - http://www.scopus.com/inward/record.url?scp=84949100234&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84949100234&partnerID=8YFLogxK

U2 - https://doi.org/10.1002/glia.22822

DO - https://doi.org/10.1002/glia.22822

M3 - Article

VL - 63

SP - 1522

EP - 1536

JO - GLIA

T2 - GLIA

JF - GLIA

SN - 0894-1491

IS - 9

ER -