Modulation of IGF‐I receptors by exogenous hGH treatment in constitutionally short children

Eshet, R; Klinger, B.; Silbergeld, A.; Laron, Zvi

doi:10.1111/j.1365-2265.1993.tb02428.x

Cited by 8 publications

(2 citation statements)

References 27 publications

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“…As previously demonstrated by us (Eshet et al 1991(Eshet et al , 1992 and others (Hochberg et al 1992), serum IGF-I levels are inversely correlated with IGF-I binding. The increase in the number of IGF-I binding sites which we have found in the present study may reflect the decreased plasma IGF-I levels seen in the patients with IGHD or LTD.…”

Section: Igf-i Receptors Have Been Demonstrated In Bothsupporting

confidence: 70%

Up-regulation of insulin-like growth factor-I (IGF-I) receptor gene expression in patients with reduced serum IGF-I levels

Eshet¹,

Werner²,

Klinger³

et al. 1993

Journal of Molecular Endocrinology

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We have analysed the expression of the IGF-I receptor gene in lymphocytes of patients with low levels of circulating IGF-I (four patients with isolated GH deficiency (IGHD) and one Laron-type dwarf (LTD)) in comparison with a control group exhibiting normal serum IGF-I levels and endocrine profiles. 125I-Labelled IGF-I binding assays were performed on erythrocytes to determine the number of IGF-I binding sites per cell and their dissociation constants. Erythrocytes from patients with IGHD or LTD contained significantly (P = 0.002) more receptors per cell (10.9 +/- 3.1 binding sites/cell), with a reduced affinity (Kd = 0.49 +/- 0.05 nM), than erythrocytes from controls (2.0 +/- 0.4 sites/cell; Kd = 0.14 nM). The levels of IGF-I receptor mRNA in circulating lymphocytes were determined by an RNA template-specific reverse transcription/polymerase chain reaction method. There was a statistically significant increase in IGF-I receptor mRNA levels in lymphocytes from patients with LTD or IGHD when compared with controls (3108.1 +/- 775.9 vs 576.0 +/- 465.7 arbitrary units, P = 0.006). The increased level of IGF-I binding due to increased IGF-I receptor gene expression may represent a compensatory up-regulation process activated in response to the low levels of IGF-I in the circulation of patients with LTD or IGHD.

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Section: Igf-i Receptors Have Been Demonstrated In Bothsupporting

confidence: 70%

Up-regulation of insulin-like growth factor-I (IGF-I) receptor gene expression in patients with reduced serum IGF-I levels

Eshet¹,

Werner²,

Klinger³

et al. 1993

Journal of Molecular Endocrinology

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“…In addition, during hGH therapy of constitutionally short children, the number of IGF-I receptors on erythrocytes decreased when IGF-I serum levels increased (67).…”

mentioning

confidence: 98%

Effects of growth hormone and insulin-like growth factor I on the immune system

Auernhammer

Strasburger²

1995

European Journal of Endocrinology

139

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Growth hormone-releasing hormone (GHRH), growth hormone (GH), prolactin (PRL) and insulin-like growth factor I (IGF-I) are synthesized and secreted by various immunocompetent cells. In addition, GHRH, GH, PRL and IGF-I receptors are expressed on immune cells. Growth hormone, PRL and IGF-I stimulate the proliferation of immunocompetent cells and modulate humoral and cellular immune functions, i.e. immunoglobuline secretion of B cells, thymulin secretion of thymic epithelial cells, natural killer cell activity, phagocytosis, oxidative burst and killing capacity of neutrophils and macrophages. No clinically significant cellular or humoral immunodeficiency has been found in GH-deficient patients. However, several immunological parameters and functions are altered in GH-deficient patients when compared to normal controls. The data available to date indicate that endocrine and pleiotropic para- and autocrine mechanisms of action are involved in a neuropeptide immune network, including GH, PRL and IGF-I as modulators of immune function.

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