TY - JOUR
T1 - Growth hormone dependent stimulation of osteoblast-like cells in serum-free cultures via local synthesis of insulin-like growth factor I
AU - Ernst, M.
AU - Froesch, E. R.
PY - 1988/2/29
Y1 - 1988/2/29
N2 - Gene-recombinant human growth hormone (rhGH) elicited a dose-dependent stimulation of the proliferation of osteoblast-like cells (OB), when grown in strictly serum-free longterm cultures. A half-maximal effect was observed at concentrations of 15-20ng/ml and the maximal stimulation was 160% of hormone-free controls. The rhGH-induced effect on proliferation could be inhibited dose-dependently by the addition of an insulin-like growth factor (IGF) I-antiserum to the medium. Moreover, IGF I and rhGH had additive effects only when the exogeneous IGF I concentration exceeded that of endogenously produced IGF I by a large margin. Thus, direct stimulation of OB proliferation by rhGH is, at least in part, mediated by IGF I-like immunoreactivity.
AB - Gene-recombinant human growth hormone (rhGH) elicited a dose-dependent stimulation of the proliferation of osteoblast-like cells (OB), when grown in strictly serum-free longterm cultures. A half-maximal effect was observed at concentrations of 15-20ng/ml and the maximal stimulation was 160% of hormone-free controls. The rhGH-induced effect on proliferation could be inhibited dose-dependently by the addition of an insulin-like growth factor (IGF) I-antiserum to the medium. Moreover, IGF I and rhGH had additive effects only when the exogeneous IGF I concentration exceeded that of endogenously produced IGF I by a large margin. Thus, direct stimulation of OB proliferation by rhGH is, at least in part, mediated by IGF I-like immunoreactivity.
UR - http://www.scopus.com/inward/record.url?scp=0023857232&partnerID=8YFLogxK
U2 - 10.1016/0006-291X(88)90570-0
DO - 10.1016/0006-291X(88)90570-0
M3 - Article
C2 - 3348770
AN - SCOPUS:0023857232
SN - 0006-291X
VL - 151
SP - 142
EP - 147
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -