Title | Functional identification of integrin laminin receptors that mediate process outgrowth by human SY5Y neuroblastoma cells |
Publication Type | Journal Article |
Year of Publication | 1994 |
Authors | Choi ES, Rettig WJ, Wayner EA, Srour ML, Clegg DO |
Journal | Journal of Neuroscience Research |
Volume | 37 |
Issue | 4 |
Pagination | 475-88 |
Date Published | 1994 Mar 1 |
ISSN | 0360-4012 |
Keywords | Antibodies, Monoclonal, Cell Differentiation, Extracellular Matrix, Humans, Integrins, Laminin, Neoplasm Proteins, Neoplastic Stem Cells, Nerve Growth Factors, Neurites, Neuroblastoma, Receptors, Laminin, Tumor Cells, Cultured |
Abstract | Treatment of the human neuroblastoma cell line SY5Y with nerve growth factor (NGF) induces terminal neuronal differentiation of a subpopulation of cells which can be selected by treatment with a DNA synthesis inhibitor. We have examined the interactions of naive (untreated) and NGF-differentiated SY5Y cells with laminin, and identified integrin receptors that mediate laminin-induced process outgrowth. Differentiated cells displayed a greater capacity for process extension, which correlated with increased expression of integrin laminin receptors. Both naive and differentiated cells expressed integrins alpha 1/beta 1, alpha 2/beta 1, and alpha 3/beta 1 but the differentiated population expressed about 5-fold higher levels of alpha 1/beta 1 and about 2-fold more alpha 2/beta 1 and alpha 3/beta 1 on their surface. Function blocking monoclonal antibodies were used to identify integrin receptors mediating process outgrowth. The anti-alpha 1 monoclonal antibody SR84 was shown to block alpha 1 function and inhibit process outgrowth on laminin. Despite the presence of multiple integrins which have been shown to bind laminin in other cell types, alpha 1/beta 1 mediated the majority of process outgrowth in both naive and differentiated cells, with a minor role played by alpha 3/beta 1. These data indicate that alpha 1/beta 1 function is required for process outgrowth on laminin by SY5Y cells and suggest that increased expression may be a crucial aspect of neuronal differentiation. |
DOI | 10.1002/jnr.490370407 |
Alternate Journal | J. Neurosci. Res. |
PubMed ID | 8021971 |
Grant List | NS27356 / NS / NINDS NIH HHS / United States |