NDLI: Phosphorylation and IGF-1-mediated dephosphorylation pathways control the activity and the pharmacological properties of skeletal muscle chloride channels

Content Provider	PubMed Central
Author	Luca, Annamaria De Sabata, Pierno Liantonio, Antonella Camerino, Claudia Camerino, Diana Conte
Copyright Year	1998
Abstract	In the present study we tested the hypothesis that insulin-like growth factor-1 (IGF-1) modulates resting chloride conductance (GCl) of rat skeletal muscle by activating a phosphatase and that the chloride channel, based on the activity of phosphorylating-dephosphorylating pathways, has different sensitivity to specific ligands, such as the enantiomers of 2-(p-chlorophenoxy) propionic acid (CPP). For this purpose GCl in EDL muscle isolated from adult rat was first lowered by treatment with 5 nM 4-β-phorbol 12,13 dibutyrate (4-β-PDB), presumably activating protein kinase C (PKC). The effects of IGF-1 and of the enantiomers of CPP on GCl were then tested. IGF-1 (3.3 nM) had no effect of GCl on EDL muscle fibres in normal physiological solution, whereas it completely counteracted the 30% decrease of GCl induced by 4-β-PDB. No effects of IGF-1 were observed on GCl lowered by the phosphatase inhibitor okadaic acid (0.25 μM). Ceramide, reported to activate on okadaic acid-sensitive phosphatase, mimicked the effects of IGF-1. In fact, N-acetyl-sphingosine (2.5–5 μM), not very effective in control conditions, increased the GCl lowered by the phorbol ester, but not the GCl lowered by okadaic acid. In the presence of 4-β-PDB, GCl was differently affected by the enantiomers of CPP. The S(−)-CPP was remarkably less potent in producing the concentration-dependent reduction of GCl, whereas the R(+)-CPP caused an increase of GCl at all the concentrations tested. In conclusion, the PKC-induced lowering of GCl is counteracted by IGF-1 through an okadaic acid sensitive phosphatase, and this effect can have therapeutic relevance in situations characterized by excessive channel phosphorylation. In turn the phosphorylation state of the channel can modulate the effects and the therapeutic potential of direct channel ligands.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0702107
Ending Page	482
Page Count	6
Starting Page	477
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	3
Volume Number	125
Language	English
Publisher Date	1998-10-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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