Insulin like growth factor‐I, protein kinase‐C, calcium and cyclic AMP: Partners in the regulation of chondrocyte mitogenesis and metabolism

FEBS Letters

Taylor, A.M.¹  Dandona, P.²  Morrell, D.J.¹  Preece, M.A.¹ 

[1] Department of Growth and Development, Institute of Child Health, Royal Free Hospital and School of Medicine, University of London, London, England;Department of Chemical Pathology and Human Metabolism, The Royal Free Hospital and School of Medicine, University of London, London, England

关键词: Insulin-like growth factor-I;    Protein kinase C;    Ca2+;    cyclic AMP;    Chondrocyte;   

DOI  :  10.1016/0014-5793(88)80280-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown