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Laminin‐like proteins are differentially regulated during cerebellar development and stimulate granule cell neurite outgrowth in vitro
Author(s) -
Powell S.K.,
Williams C.C.,
Nomizu M.,
Yamada Y.,
Kleinman H.K.
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19981015)54:2<233::aid-jnr11>3.0.co;2-5
Subject(s) - laminin , neurite , microbiology and biotechnology , biology , granule cell , basement membrane , cerebellum , glycoprotein , in vitro , extracellular matrix , biochemistry , neuroscience , central nervous system , dentate gyrus
Abstract The basement membrane glycoprotein laminin‐1 is a potent stimulator of neurite outgrowth. Although a variety of laminin isoforms have been described in recent years, the role of alternative laminin isoforms in neural development remains largely uncharacterized. We found that a polyclonal antibody raised against the α1, β1, and γ1 chains of laminin‐1 and a monoclonal antibody raised against the α2 chain of laminin‐2 detect immunoreactive material in neuronal cell bodies in the developing mouse cerebellum. In addition, laminin‐1‐like immunoreactivity was found in cell types throughout the cerebellum, but laminin‐α2‐like immunoreactivity was restricted to the Purkinje cells. Purified laminin‐1 and laminin‐2 stimulated neurite outgrowth in primary cultures of mouse cerebellar granule neurons to a similar extent, whereas the synthetic peptides tested appeared to be active only for cell adhesion and not for stimulation of neurite outgrowth. The E8 proteolytic fragment of laminin‐1 contained full neurite outgrowth activity. The identity of laminins expressed in granule neurons was also examined by Western blotting; laminin‐like complexes were associated with the cell and appeared to have novel compositions. These results suggest that laminin‐like complexes play important roles in cerebellar development. J. Neurosci. Res. 54:233–247, 1998. © 1998 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.