Monensin-induced inhibition of cell spreading in normal and dystrophic human fibroblasts.

AUTOR(ES)

Pizzey, J

RESUMO

Cultured skin fibroblasts from normal individuals and from patients with Duchenne muscular dystrophy spread equally rapidly when seeded on a glass substratum. Exposure to the ionophore monensin substantially suppresses normal and dystrophic fibroblast spreading in serum-free media for up to at least 100 min. Preincubation of normal fibroblasts with monensin causes a further reduction in cell spreading. Dystrophic fibroblasts fail to spread as well as normal cells after monensin preincubation. Such findings indicate that there is a delay in the secretion of functional adhesive surface proteins in monensin-preincubated normal fibroblasts and that this lag period is significantly longer in dystrophic fibroblasts. These data are consistent with findings of altered adhesive and secretory properties of fibroblasts from patients with Duchenne muscular dystrophy.

Documentos Relacionados

• Mechanism of monensin-induced hyperpolarization of neuroblastoma-glioma hybrid NG108-15.
• Effect of cell spreading on cytoplasmic pH in normal and transformed fibroblasts.
• Confluence-induced alterations in CpG island methylation in cultured normal human fibroblasts.
• Anchorage-independent growth of normal human fibroblasts.
• n-Butyrate inhibition of hyaluronate synthesis in cultured human fibroblasts.