Premium
Insulin like growth factor‐I, protein kinase‐C, calcium and cyclic AMP: Partners in the regulation of chondrocyte mitogenesis and metabolism
Author(s) -
Taylor A.M.,
Dandona P.,
Morrell D.J.,
Preece M.A.
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)80280-1
Subject(s) - protein kinase c , verapamil , medicine , endocrinology , activator (genetics) , calcium , chondrocyte , stimulation , protein kinase a , phorbol , growth factor , insulin like growth factor , chemistry , biology , kinase , biochemistry , receptor , in vitro
The possible role of protein kinase‐C (PKC), calcium and cyclic AMP (cAMP) in mediating the metabolic and mitogenic effects of insulin‐like growth factor‐I (IGF‐I) on chondrocytes was investigated using a PKC activator (phorbol ester 12,13‐dibutyrate, PDBU), a PKC inhibitor (compound H7), a calcium channel blocker, (verapamil) and a cAMP analogue (dibutyryl cAMP). IGF‐I and PDBU stimulated sulphate and thymidine incorporation by chondrocytes. Both of these effects were inhibited by compound H7. Verapamil inhibited IGF‐I and PDBU‐stimulated sulphate incorporation, but contrastingly stimulated basal and enhanced IGF‐I and PDBU stimulation of thymidine incorporation. Dibutyryl cAMP increased basal and IGF‐I‐stimulated sulphate incorporation but inhibited both basal and IGF‐I stimulation of thymidine incorporation. These results suggest a harmonic overlap between the activities of PKC and cAMP‐dependent PKA enzyme systems, and calcium balance in the mitogenic and metabolic process of the chondrocyte.