Characterization of the receptor for insulin-like growth factor II in bone cells

S. Mohan, T. Linkhart, Ronald (Ron) Rosenfeld, D. Baylink

Research output: Contribution to journalArticle

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Abstract

We have previously shown that insulin-like growth factor II (IGF-II) is produced by bone cells and that IGF-II stimulates cell proliferation and collagen synthesis in bone cells. We now extend these in vitro findings by demonstrating specific IGF-II binding to bone cells derived from newborn mouse calvaria and embryonic chick calvaria. The kinetics of [125I] IGF-II binding in embryonic chick calvaria cells showed time and temperature dependence. Scatchard analysis of [125I]IGF-II binding to chick calvaria cells showed an apparent K(d) of 1.4 x 10-10 M, with a calculated receptor site concentration of 40,000/cell. The specificity characteristics showed that IGF-II was significantly more potent than IGF-I or insulin in displacing IGF-II tracer. Competition for binding of [125I]IGF-II by unlabeled IGF-II showed a dose-dependent displacement between 0.5 and 25 ng/ml. Fifty percent displacement of [125I]IGF-II binding to chick and mouse calvarial cells was achieved at 1-2 ng/ml; 90% of specific binding of [125I]IGF-II was displaceable in the presence of 125 ng/ml of unlabeled IGF-II. IGF-I showed less than 5% cross reactivity for displacement of [125I]IGF-II binding to chick and mouse bone cells. Type II receptor inhibitory antibodies, R-II-PAB1 inhibited the binding of [125I]IGF-II to mouse bone cells and H-35 rat hepatoma cells (which contain type II but not type I receptors) in a dose-dependent manner. R-II-PAB1 also inhibited basal cell proliferation as well as IGF-II-, IGF-I-, and fibroblast growth factor (FGF)-induced cell proliferation in mouse bone cells. In chick calvaria bone cells, and TE89 human osteosarcoma cells, R-II-PAB1 inhibited neither binding of [125I]IGF-II nor IGF-II-induced cell proliferation. These results together with our findings that IGF-II increased chick bone cell proliferation in the presence of maximal doses of IGF-I suggest that at least part of the mitogenic action of IGF-II is mediated through type II rather than type I receptors in bone cells.

Original languageEnglish (US)
Pages (from-to)169-176
Number of pages8
JournalJournal of Cellular Physiology
Volume140
Issue number1
StatePublished - 1989
Externally publishedYes

Fingerprint

IGF Type 2 Receptor
Insulin-Like Growth Factor II
Bone
Bone and Bones
Cell proliferation
Skull
Insulin-Like Growth Factor I
Cell Proliferation

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

Cite this

Mohan, S., Linkhart, T., Rosenfeld, R. R., & Baylink, D. (1989). Characterization of the receptor for insulin-like growth factor II in bone cells. Journal of Cellular Physiology, 140(1), 169-176.

Characterization of the receptor for insulin-like growth factor II in bone cells. / Mohan, S.; Linkhart, T.; Rosenfeld, Ronald (Ron); Baylink, D.

In: Journal of Cellular Physiology, Vol. 140, No. 1, 1989, p. 169-176.

Research output: Contribution to journalArticle

Mohan, S, Linkhart, T, Rosenfeld, RR & Baylink, D 1989, 'Characterization of the receptor for insulin-like growth factor II in bone cells', Journal of Cellular Physiology, vol. 140, no. 1, pp. 169-176.
Mohan, S. ; Linkhart, T. ; Rosenfeld, Ronald (Ron) ; Baylink, D. / Characterization of the receptor for insulin-like growth factor II in bone cells. In: Journal of Cellular Physiology. 1989 ; Vol. 140, No. 1. pp. 169-176.
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