Immunocytochemical expression of human muscle cell p75 neurotrophin receptor is down-regulated by cyclic adenosine 3',5'-monophosphate.
To investigate whether the immunocytochemical expression of low affinity neurotrophin receptor (p75) in human muscle is modulated by increased levels of intracellular cyclic adenosine 3',5'-monophosphate (cAMP), human cultured myogenic cells were treated with cAMP analogues dibutyryl cAMP (dbcAMP 0.5-1 mM) and 8-bromo cAMP (1 mM) or the adenylate cyclase activator forskolin (10-100 microM). Cultures were processed for indirect immunofluorescence microscopy using an anti-human p75 mAb. The treatment of cultured muscle cells with cAMP analogues or forskolin for two days induced a decrease of immunoreactivity for p75 and a reduction of both myotube formation and morphological cell differentiation. Removal of cAMP derivatives from the medium resulted in a return of immunoreactive cells to the levels of untreated controls. These data indicate that adenylate cyclase is involved in the regulation of human muscle p75.
Baron
P
P
Institute of Neurology, Dino Ferrari Center, University of Milan, IRCCS Ospedale Maggiore Policlinico, Italy.
Scarpini
E
E
Pizzul
S
S
Zotti
F
F
Conti
G
G
Pleasure
D
D
Scarlato
G
G
D000262:Adenylyl Cyclases / Q000187:drug effects; D000328:Adult; D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism*; D015536:Down-Regulation; D004789:Enzyme Activation; D006801:Humans; D007150:Immunohistochemistry; D009132:Muscles / Q000737:chemistry* / Q000166:cytology; D017475:Receptors, Nerve Growth Factor / Q000032:analysis*
D017475:Receptors, Nerve Growth Factor; D005576:Colforsin; D000242:Cyclic AMP; D000262:Adenylyl Cyclases