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PTH induces modification of transductive events in otosclerotic bone cell cultures
Author(s) -
Fanó G.,
VentiDonti G.,
Belia S.,
Paludetti G.,
Antonica A.,
Donti E.,
Maurizi M.
Publication year - 1993
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.290110406
Subject(s) - cyclase , adenylate kinase , calcitonin , receptor , parathyroid hormone , endocrinology , intracellular , medicine , osteoblast , stimulation , chemistry , calcitonin receptor , hormone , microbiology and biotechnology , biology , calcium , biochemistry , neuropeptide , in vitro , calcitonin gene related peptide
We studied the effect of PTH (10–100 nM) on transductive mechanisms (adenylate cyclase activity, Ca 2+ metabolism, IP 3 levels) in cell cultures derived from normal and otosclerotic human bone fragments. The cultured cells were osteoblast‐like but with calcitonin‐receptors still present and with PTH receptors coupled with the adenylate cyclase system. The results showed that PTH activated adenylate cyclase and increased the intracellular Ca 2+ levels with qualitative and quantitative differences between the two cellular populations. In particular, otosclerotic cells responded less to hormone stimulation, which is in accord with the current hypothesis of a desensitization of the receptor/enzyme complex associated with the pathological status.