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α V integrins in Schwann cells promote attachment to axons, but are dispensable in vivo
Author(s) -
Catignas Kathleen K.,
Frick Luciana R.,
Pellegatta Marta,
Hurley Edward,
Kolb Zachary,
Addabbo Kathryn,
McCarty Joseph H.,
Hynes Richard O.,
Flier Arjan,
Poitelon Yannick,
Wrabetz Lawrence,
Feltri Maria Laura
Publication year - 2021
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.23886
Subject(s) - integrin , biology , microbiology and biotechnology , protein subunit , gene knockdown , schwann cell , neuroscience , neurite , growth cone , in vitro , axon , receptor , cell culture , biochemistry , genetics , gene
In the developing peripheral nervous system, Schwann cells (SCs) extend their processes to contact, sort, and myelinate axons. The mechanisms that contribute to the interaction between SCs and axons are just beginning to be elucidated. Using a SC‐neuron coculture system, we demonstrate that Arg‐Gly‐Asp (RGD) peptides that inhibit α V ‐containing integrins delay the extension of SCs elongating on axons. α V integrins in SC localize to sites of contact with axons and are expressed early in development during radial sorting and myelination. Short interfering RNA‐mediated knockdown of the α V integrin subunit also delays SC extension along axons in vitro, suggesting that α V ‐containing integrins participate in axo‐glial interactions. However, mice lacking the α V subunit in SCs, alone or in combination with the potentially compensating α 5 subunit, or the α V partners β 3 or β 8 , myelinate normally during development and remyelinate normally after nerve crush, indicating that overlapping or compensatory mechanisms may hide the in vivo role of RGD‐binding integrins.