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N‐acetylglucosaminyltranferase VB expression enhances β1 integrin‐ dependent PC12 neurite outgrowth on laminin and collagen
Author(s) -
Lee Intaek,
Guo HuaBei,
Kamar Maria,
Abbott Karen,
Troupe Karolyn,
Lee JinKyu,
AlvarezManilla Gerardo,
Pierce Michael
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.03785.x
Subject(s) - neurite , integrin , laminin , microbiology and biotechnology , nerve growth factor , cell adhesion , extracellular matrix , chemistry , cell culture , adhesion , cell , biology , receptor , in vitro , biochemistry , organic chemistry , genetics
N‐acetylglucosaminyltransferase VB (GnT‐VB, ‐IX) is a newly discovered glycosyltransferase expressed exclusively in high levels in neuronal tissue during early development. Its homolog, GnT‐V, is expressed in many tissues and modulates cell–cell and cell–matrix adhesion. The ability of GnT‐VB to regulate cell–matrix interactions was initially investigated using the rat pheochromocytoma PC12 neurite outgrowth model. PC12 cells stably transfected with GnT‐VB consistently showed an enhanced rate of nerve growth factor (NGF)‐induced neurite outgrowth on collagen and laminin substrates. Levels of TrkA receptor phosphorylation and downstream ERK activation induced by NGF were not influenced by GnT‐VB expression. No significant difference was observed in the rate of neurite outgrowth when cells were cultured on non‐coated culture dishes, indicating that integrin–ECM interaction is required for the stimulatory effects. Neurite outgrowth induced by manganese‐dependent activation of β1 integrin on collagen and laminin substrates, however, showed a significant increase in neurite length for the PC12/GnT‐VB cells, compared with control cells, suggesting that the enhancement is most likely mediated by alteration of β1 integrin–ECM interaction by GnT‐VB. These results demonstrate that GnT‐VB expression can modulate the rate of neurite outgrowth by affecting β1 integrin–ECM interaction.