Laminin‐induced PC‐12 cell differentiation is inhibited following laser inactivation of cellular prion protein

FEBS Letters

Jay, Daniel G.²  Martins, Vilma R.¹  Brentani, Ricardo R.³  Mercadante, Adriana F.³  Graner, Edgard³  Zanata, Sı́lvio M.³ 

[1] Centro de Tratamento e Pesquisa Hospital do Câncer, Rua Prof. Antônio Prudente 109/4A, 01509-010 São Paulo, SP, Brazil;Department of Physiology, Tufts University, School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA;Ludwig Institute for Cancer Research, São Paulo Branch, Rua Prof. Antônio Prudente 109/4A, 01509-010 São Paulo, SP, Brazil

关键词: Cellular prion protein;    Laminin;    Extracellular matrix;    Neurite outgrowth;    PC-12 cell;    Cell differentiation;   

DOI  :  10.1016/S0014-5793(00)02070-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Prions, the etiological agents for infectious degenerative encephalopathies, act by inducing structural modifications in the cellular prion protein (PrPc). Recently, we demonstrated that PrPc binds laminin (LN) and that this interaction is important for the neuritogenesis of cultured hippocampal neurons. Here we have used the PC-12 cell model to explore the biological role of LN–PrPc interaction. Antibodies against PrPc inhibit cell adhesion to LN-coated culture plaques. Furthermore, chromophore-assisted laser inactivation of cell surface PrPc perturbs LN-induced differentiation and promotes retraction of mature neurites. These results point out to the importance of PrPc as a cell surface ligand for LN.

【 授权许可】

Unknown