Monensin does not consistently inhibit the spreading of normal or Duchenne fibroblasts on glass.
The spreading on glass of monensin-treated normal and Duchenne fibroblasts has been investigated with the intention of extending this approach to a study of the comparative spreading of these cells on differing substrata. Untreated normal and Duchenne fibroblasts varied considerably in their ability to spread on glass. The spreading properties of normal and DMD fibroblasts treated in four different ways were compared: (1) pre-incubated and plated without monensin; (2) pre-incubated with, but plated without monensin; (3) pre-incubated without, but plated with monensin; (4) pre-incubated and plated with monensin. The response to plating with monensin (and pre-incubation/plating with monensin) also varied from patient to patient, but no statistically significant differences in the degree of spreading between the four treatment groups were observed in pooled data for either normal or dystrophic fibroblasts. Our data thus do not substantiate the previous finding of Pizzey et al. (1984) that Duchenne fibroblasts spread less well than normal fibroblasts after pre-incubation or plating with monensin, and possible explanations for this are discussed. The observations made are, however, consistent with the recent report that dystrophin is effectively not expressed in fibroblasts, and with the idea that the abnormal behaviour of endomysial fibroblasts in Duchenne dystrophy is a secondary consequence of their proximity to degenerating muscle.
Brown
S C
SC
Department of Biochemistry and Chemistry, Royal Free Hospital School of Medicine, University of London, UK.
Fisher
D
D
Lucy
J A
JA
D002448:Cell Adhesion / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects*; D005898:Glass; D006801:Humans; D066298:In Vitro Techniques; D008985:Monensin / Q000494:pharmacology*; D009136:Muscular Dystrophies / Q000473:pathology*
D008985:Monensin