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Journal of Clinical Endocrinology & Metabolism Vol. 71, No. 2 464-469
doi:10.1210/jcem-71-2-464
Copyright © 1990 by the Endocrine Society.
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Growth Hormone Mediates the Growth of TLymphoblast Cell Lines via Locally Generated Insulin-Like Growth Factor-I*

MITCHELL E. GEFFNER, NOELLE BERSCH, BARBARA M. LIPPE, RON G. ROSENFELD, RAYMOND L. HINTZ and DAVID W. GOLDE

Departments of Pediatrics (M.E.G., B.M.L.) and Medicine (N.B., D.W.G.), University of California- Los Angeles Medical Center Los Angeles, California 90024
The Department of Pediatrics, Stanford University Medical Center (R.G.R., R.L.H.) Stanford, California 94305

Address requests for reprints to: Mitchell E. Geffner, M.D., Department of Pediatrics, University of California-Los Angeles Medical Center, Los Angeles, California 90024.

It has become evident that locally produced insulin-like growth factors-I and -II (IGF-I and IGF-II) play an important role in the mediation of GH action upon tissues. To explore this concept with respect to immunocompetent cells, we analyzed IGF production and clonogenic responsiveness of immortalized human T-cell lines established from seven normal controls and four Laron dwarfs. While the normal T-cell lines showed significant augmentation of basal colony formation in response to both IGF-I and GH, little increase in clonogenesis in response to GH was seen with the Laron T-cell lines. Assay of basal and GH-stimulated conditioned media demonstrated low, but measurable, levels of IGF-I and IGF-II from both normaland Laron T-cells. Under serum-free incubation conditions, GH stimulation of normal T-cell lines failed to generate significant increases in mean IGF-I or IGF-II concentrations. Only a marginal increase in the mean IGF-I concentration and no increase in the mean IGF-II concentration in conditioned medium were observed after GH stimulation of Laron T-cell lines. Nevertheless, the increased cloning efficiency of the normal T-cell lines in response to either GH or IGF-I was nearly completely abrogated by preincubation of cells with antibodies to either IGF-I or the type I IGF receptor. These studies, thus, support a role for locally generated IGF-I in the mediation of GH action on Tlymphocytes and indicate that this effect is mediated via the type I IGF receptor.

* This work was supported in part by Grants DK-28229 (to R.G.R.), DK-36054 (to R.G.R.), DK-01275 (to R.G.R.), CA-42106 (to R.G.R.), DK-24085 (to R.L.H.), CA-32737 (to D.W.G.), and CA-30388 (D.W.G.) from the NIH.

Received January 22, 1990.




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