Insulin-like growth factor binding protein-1 inhibits the DNA amplification induced by insulin-like growth factor I in human granulosa—luteal cells

Angervo, Maarit; Koistinen, Riitta; Suikkari, Anne‐Maria; Seppälä, Markku

doi:10.1093/oxfordjournals.humrep.a137426

Cited by 66 publications

(27 citation statements)

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“…They influence IGF bioavailability and can either inhibit or potentiate IGF action. Inhibition is achieved by sequestration of IGFs from their receptors (Angervo et al, 1991;Cohen. et al, 1993) and the mechanism of potentiation involves a cellular association by IGFBPs bound to IGFBP receptors or otherwise (Conover, 1992).…”

Section: Resultsmentioning

confidence: 99%

Recombinant insulin-like growth factor-I (IGF-I) production in Super-CHO results in the expression of IGF-I receptor and IGF binding protein 3

Sunstrom¹,

Baig²,

Cheng³

et al. 1998

Current Applications of Cell Culture Engineering

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Previously, we described the genetic construction Super-CHO, a cell line capable of autocrine growth under fully defined protein-free conditions. Super-CHO cells constitutively express insulin growth factor-I (IGF-I) and transferrin in sufficient amounts to support long-term, stable growth without the addition of exogenous growth factors, thus making it an ideal host for the production of recombinant biopharmaceuticals. although IGF-I has been successfully expressed in Chinese Hamster Ovary (CHO) cells, the long term effects of recombinant IGF-I expression have not been explored. In particular, the expression of the endogenous IGF-I receptor in response to IGF-I production has not been reported. We report here the transcriptional induction of the type I IGF receptor gene in Super-CHO. In addition, we examined the conditioned medium for the presence of IGF-I binding proteins. Ligand blot analysis reveals the presence of IGF binding proteins present in the medium conditioned by Super-CHO cells as well as CHO cells incubated in the presence of IGF-I. Furthermore, immunoaffinity reveals that Super-CHO expresses IGF binding protein-3 in response to IGF-I production. These results suggest the autocrine growth of Super-CHO involves a complex interaction of cell type specific factors which regulate its utility of IGF-I.

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Section: Resultsmentioning

confidence: 99%

Recombinant insulin-like growth factor-I (IGF-I) production in Super-CHO results in the expression of IGF-I receptor and IGF binding protein 3

Sunstrom¹,

Baig²,

Cheng³

et al. 1998

Current Applications of Cell Culture Engineering

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“…In the circulation of normal, non-pregnant individuals, IGFBP-1 is present as a highly phosphorylated form. Other studies have used either recombinant IGFBP-1 which is non-phosphorylated (Cox et al 1994, Lee et al 1996 or IGFBP-1 purified from amniotic fluid which is deficient in the highly phosphorylated form (Frauman et al 1989, Burch et al 1990, Angervo et al 1991, Liu et al 1991, Lewitt et al 1993. We therefore purified phosphorylated IGFBP-1 from HepG2-conditioned medium and found it was more potent than npIGFBP-1 since it completely reversed the effects of IGF-I at a 1:1 molar ratio, while at this molar ratio npIGFBP-1 did not significantly inhibit IGF mitogenic actions.…”

Section: Discussionmentioning

confidence: 99%

IGF-binding protein-1 inhibits IGF effects on adipocyte function: implications for insulin-like actions at the adipocyte

Siddals¹,

Westwood²,

Gibson³

et al. 2002

Journal of Endocrinology

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IGF action in vivo is acutely regulated by IGF-binding protein-1 (IGFBP-1) and its phosphorylation state is implicated in modulating these effects. Since IGFs have an important regulatory role in adipocyte function, we investigated the effects of phosphorylated IGFBP-1 (pIGFBP-1) and non-phosphorylated IGFBP-1 (npIGF BP-1) on 3T3-L1 preadipocyte proliferation and adipocyte metabolism.IGFs stimulated clonal expansion of 3T3-L1 cells (IGF-I more potently than IGF-II (EC 50 : 30 nM and 50 nM)). npIGFBP-1 inhibited IGF-I (50 nM) clonal expansion at a 5:1 molar ratio (P<0·01), whereas pIGFBP-1 (purified from HepG2 cell medium) abolished clonal expansion at a 1:1 molar ratio (P<0·005). In contrast, IGF-II-induced clonal expansion was inhibited 100% at a 1:1 molar ratio of npIGFBP-1.In mature adipocytes, IGF-I was equipotent with insulin in stimulating glucose uptake (EC 50 : 10 nM) and inhibiting isoproterenol-induced lipolysis (EC 50 : 15 nM). npIGFBP-1 completely reversed IGF-I effects at a 1:1 molar ratio (P<0·01).In summary, IGFs rather than insulin are potent regulators of clonal expansion in 3T3-L1 preadipocytes. Importantly, IGFs are equipotent with insulin in regulating adipocyte metabolism. IGFBP-1 inhibits IGF effects on preadipocyte proliferation and adipocyte metabolism, with pIGFBP-1 being more potent than npIGFBP-1 at inhibiting mitogenic actions. Since IGFBP-1 is acutely regulated by insulin, this could have important consequences in hyperinsulinaemic and insulin-resistant states.

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“…However, the production and secretion of IGFBP-1 in human luteinized granulosa cells has been reported (Angervo et al, 1991;Holst et al,1997). In addition, IGFBP-3 mRNA is expressed in the endothelial cells of the human corpus luteum (Fraser et al, 2000).…”

Section: Effect Of Nitric Oxide On the Expression Of Insulin-like Gromentioning

confidence: 99%

Effect of nitric oxide on the expression of insulin-like growth factors and the insulin-like growth factor binding proteins throughout the lifespan of the human corpus luteum

Iniguez¹

2001

Reproduction

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ResearchThe presence of insulin-like growth factors (IGF), IGF binding proteins (IGFBP) and IGF receptor type 1 (IGF-IR) in the human corpus luteum was investigated by examining the expression and production of related proteins throughout the lifespan of the corpus luteum and the action of nitric oxide upon their production. The expression of proteins in corpora lutea from the early, midand late luteal phases was assessed by immunohistochemistry, evaluated by a semi-quantitative analysis and the functional study was performed in corpus luteum explants incubated with nitric oxide donors. IGF-I and -II and IGFBP-1 and -3 were measured in the culture media by specific immunoassays. The results showed that IGF-I and -II, IGFBP-1 to -6 and IGF-IR were detected in the human corpus luteum throughout the luteal phase. Moreover, the expression and production of IGF-I and IGFBP-1 increased progressively from corpora lutea from the early to late luteal phases (P < 0.05), whereas the expression and production of IGFBP-2, -4 and -5 were significantly higher in corpora lutea from the mid-luteal phase (P < 0.05). No differences were observed in the expression of IGF-II, IGFBP-3 and -6 and IGF-IR throughout the lifespan of the corpus luteum. However, functional studies showed that nitric oxide donors elicited a stimulatory action on production of IGF-I in corpora lutea from the early luteal phase (80%) and on production of IGFBP-1 in corpora lutea from the late luteal phase (50%) (P < 0.05), whereas production of IGF-II and IGFBP-3 was not affected by nitric oxide. In conclusion, the components of the IGF-IGFBP system are expressed in the human corpus luteum throughout its lifespan. Nitric oxide regulates IGF-I and IGFBP-1 production, indicating that the growth factors may serve, at least in part, as mediators of the action of nitric oxide in the human corpus luteum.

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Insulin-like growth factor binding protein-1 inhibits the DNA amplification induced by insulin-like growth factor I in human granulosa—luteal cells

Cited by 66 publications

References 0 publications

Recombinant insulin-like growth factor-I (IGF-I) production in Super-CHO results in the expression of IGF-I receptor and IGF binding protein 3

Recombinant insulin-like growth factor-I (IGF-I) production in Super-CHO results in the expression of IGF-I receptor and IGF binding protein 3

IGF-binding protein-1 inhibits IGF effects on adipocyte function: implications for insulin-like actions at the adipocyte

Effect of nitric oxide on the expression of insulin-like growth factors and the insulin-like growth factor binding proteins throughout the lifespan of the human corpus luteum

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