Isolation of an inhibitory insulin-like growth factor (IGF) binding protein from bone cell-conditioned medium: a potential local regulator of IGF action.

Mohan, Subburaman; Bautista, Catalino M.; Wergedal, Jon E.; Baylink, David J.

doi:10.1073/pnas.86.21.8338

Cited by 331 publications

(142 citation statements)

References 31 publications

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“…Although its physiological role is still unclear, IGFBP-4 appears to inhibit IGF mitogenic actions under most experimental conditions, suggesting that it is an important negative regulator of cellular proliferation (17,53). A major factor regulating IGFBP action is its distribution between the soluble phase (interstitial fluid) and the extracellular matrix (ECM) or cell surface; inhibitory effects of IGFBP on IGF action are associated typically with high-affinity soluble forms.…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in prepubertal pig sertoli cells

Bottazzi

Demori

et al. 1999

European Journal of Endocrinology

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A large body of evidence suggests the existence of an intratesticular IGF system complete with ligands, receptors and binding proteins (IGFBPs); the aim of the present study was to evaluate tri-iodothyronine (T 3 ) and retinoic acid (RA) effects on IGFBP production by Sertoli cells. A significant dose-dependent increase in IGFBP-4 mRNA levels was observed in Sertoli cells cultured in the presence of physiological concentrations of T 3 or RA. This response was inhibited by cycloheximide, indicating that de novo protein synthesis is required, as well as by actinomycin D, suggesting that the increase in mRNA levels requires transcriptional activation. As shown by ligand blot assays the stimulatory effects of both agents on IGFBP-4 mRNA expression appears to be consistent with an enhanced synthesis and secretion of IGFBP-4, thus suggesting that the transcriptional response is transduced to the protein level. Our data establish an important direct role for T 3 and RA in regulating IGFBP-4 expression and consequently IGF activity at the testis level.

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Section: Discussionmentioning

confidence: 99%

Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in prepubertal pig sertoli cells

Bottazzi

Demori

et al. 1999

European Journal of Endocrinology

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“…The growth-promoting activity of IGF-I is determined not only by the concentration of IGF-I but also by the amounts of various IGFBPs (21,22). Of these, IGFBP-3 is the major binding protein (23).…”

Section: Discussionmentioning

confidence: 99%

GH response to provocation and circulating IGF-I and IGF-binding protein-3 concentrations, the IGF-I generation test and clinical response to GH therapy in children with beta-thalassaemia

Soliman

Banna

Ansari

1998

European Journal of Endocrinology

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The causes of growth retardation of children with thalassaemia major are multifactorial. We studied the GH response to provocation by clonidine and glucagon, measured the circulating concentrations of insulin, IGF-I, IGF-binding protein-3 (IGFBP-3) and ferritin, and evaluated IGF-I generation after a single dose of GH (0.1 mg/kg per dose) in 15 prepubertal patients with thalassaemia, 15 age-matched children with constitutional short stature (CSS) (height standard deviation score less than ¹2, with normal GH response to provocation) and 11 children with isolated GH deficiency (GHD). Children with thalassaemia had significantly lower peak GH response to provocation by clonidine and glucagon (6:2 Ϯ 2:3 and 6:8 Ϯ 2:1 mg/l respectively) than the CSS group (18:6 Ϯ 2:7 and 16:7 Ϯ 3:7 mg/l respectively). They had significantly decreased circulating concentrations of IGF-I and IGFBP-3 (47:5 Ϯ 19 ng/ml and 1:2 Ϯ 0:27 mg/l respectively) compared with those with CSS (153 Ϯ 42 ng/ ml and 2:06 Ϯ 0:37 mg/l respectively), but the IGF-I and IGFBP-3 concentrations were not different from those with GHD (56 Ϯ 25 ng/ml and 1:1 Ϯ 0:32 mg/l respectively). These data demonstrate that the GH-IGF-I-IGFBP-3 axis in thalassaemic children is defective. Serum ferritin concentration correlated significantly with GH peak response to provocation (r ¼ ¹0:36, P < 0:05) and circulating IGF-I (r ¼ ¹0:47, P < 0:01) and IGFBP-3 (r ¼ ¹0:42, P < 0:01) concentrations. In the IGF-I generation test, after GH injection, the thalassaemic children had significantly lower IGF-I and IGFBP-3 levels 86:7 Ϯ 11:2 ng/ml and 2:05 Ϯ 0:51 mg/l respectively) than those in the CSS group (226 Ϯ 45:4 ng/ ml and 2:8 Ϯ 0:43 mg/l respectively). The IGF-I response was significantly higher in children with GHD (158 Ϯ 50 ng/ml) than in thalassaemic children. Six short (height standard deviation score less than ¹2) thalassaemic children who had defective GH response to provocation (<10 mg/l), all the children with GHD and eight short normal children (CSS) were treated for 1 year with human GH (18 units/m 2 per week divided into daily s.c. doses). After 1 year of GH therapy there was a marked acceleration of growth velocity in both thalassaemic children (from 3:8 Ϯ 0:6 cm/year to 7:2 Ϯ 0:8 cm/year) and controls. However, the linear acceleration of growth velocity on GH therapy was significantly slower in thalassaemic children (3:3 Ϯ 0:3 cm/year increment) compared with those with CSS (5:3 Ϯ 0:4 cm/year increment) and GHD (6:9 Ϯ 1:2 cm/year increment) (P < 0:05). Their circulating IGF-I concentration (105 Ϯ 36 ng/ml) was significantly lower than those for CSS (246 Ϯ 58 ng/ml) and GHD (189 Ϯ 52 ng/ml) after 1 year of GH therapy. These data prove that some children with b-thalassaemia major have a defective GH-IGF-I-IGFBP-3 axis and suggest the presence of partial resistance to GH.

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“…In contrast to IGFBP-4, which exerts exclusively inhibitory actions on bone cells both in vitro (Mohan et al 1989(Mohan et al , 1995b and in vivo (Miyakoshi et al 1999), IGFBP-5 was identified as a stimulator of osteoblast mitogenesis (Andress & Birnbaum 1991, 1992, Bautista et al 1991, Andress et al 1993, Mohan et al 1995b). The stimulatory Schmid et al (1996) i=inhibition; s=stimulation; TSH=thyroid-stimulating hormone.…”

Section: Bone Physiology and Pathologymentioning

confidence: 99%

IGF-binding protein-5: flexible player in the IGF system and effector on its own

Schneider¹,

Wolf²,

Hoeflich³

et al. 2002

Journal of Endocrinology

162

137

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The multiple activities of IGF-I and -II are modulated by a family of IGF-binding proteins (IGFBP-1 to -6). Although structurally related, each IGFBP has unique properties and exerts specific functions. IGFBP-5 is the most conserved IGFBP across species and was identified as an essential regulator of physiological processes in bone, kidney and mammary gland. In addition, IGFBP-5 appears to play a decisive role in the control of proliferation of specific tumour cell types. In many situations IGFBP-5 exerts biological activities in the absence of IGFs, indicating the existence of IGF-independent actions. This concept was supported by the unexpected localisation of IGFBP-5 in the nucleus and the description of IGFBP-5-specific membrane-bound IGFBP-5 receptor(s). The scope of this review is to summarise the available information about the structure of IGFBP-5 and the regulation of its expression. Furthermore, the potential significance of IGFBP-5 in the regulation of physiological processes will be critically analysed in the light of recent experimental data.

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Isolation of an inhibitory insulin-like growth factor (IGF) binding protein from bone cell-conditioned medium: a potential local regulator of IGF action.

Cited by 331 publications

References 31 publications

Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in prepubertal pig sertoli cells

Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in prepubertal pig sertoli cells

GH response to provocation and circulating IGF-I and IGF-binding protein-3 concentrations, the IGF-I generation test and clinical response to GH therapy in children with beta-thalassaemia

IGF-binding protein-5: flexible player in the IGF system and effector on its own

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