Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Rosato, Roberto R.; Lindenbergh-Kortleve, Dicky J.; Neck, J. van; Drop, Stenvert L. S.; Jahn, Graciela A.

doi:10.1530/eje.0.1460729

Cited by 19 publications

(13 citation statements)

References 46 publications

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“…Our observation that IGFBP‐5 is detectable in medium conditioned by primary cultures of mouse mammary epithelial cells (derived from P14–P18 mice) agrees with a previous study demonstrating the presence of this binding protein in medium conditioned by primary cultures of epithelial cells derived from P9 or P15 mice (Marshman et al, 2003). It also agrees with in vivo data which confirm the presence of IGFBP‐5 mRNA in whole mammary gland at different stages of pregnancy (Rosato et al, 2002; Boutinaud et al, 2004) and with in situ data showing expression of IGFBP‐5 in mid‐pregnant ductal and alveolar epithelial cells (Wood et al, 2000; Allar and Wood, 2004). Similarly, the lactogen‐induced upregulation of IGFBP‐5 in primary mouse mammary epithelial cell cultures agrees with our previous observations of lactogen‐induced upregulation of this gene at both the protein and mRNA level in HC11 cells (Phillips et al, 2003; Boutinaud et al, 2004) and may represent the upregulated binding protein reported in the earlier study by Fielder et al (1992).…”

Section: Discussionsupporting

confidence: 89%

Insulin‐like growth factor binding protein (IGFBP)‐5 is upregulated during both differentiation and apoptosis in primary cultures of mouse mammary epithelial cells

Lochrie

Phillips

Tonner

et al. 2006

Journal Cellular Physiology

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We have previously demonstrated that insulin-like growth factor binding protein-5 (IGFBP-5) is upregulated following treatment of the mouse mammary epithelial cell line HC11 with lactogenic hormones (dexamethasone, insulin, and prolactin-DIP). In addition, we have also shown that IGFBP-5 is upregulated in mammary epithelial cells in vivo during involution of the rodent mammary gland. We have, therefore, postulated that there may be a dual regulation of IGFBP-5 expression during the temporally separated processes of differentiation and apoptosis of mammary epithelial cells. To test this hypothesis further, we have used a phenotypically differentiated model, which comprises primary cultures of mouse mammary epithelial cells grown on a layer of EHS (Engelbreth-Holm-Swarm) extracellular matrix. We show that lactogenic hormone treatment (hydrocortisone, insulin, and prolactin-HIP) of these cultures induces the upregulation of IGFBP-5 thus replicating the results obtained with the HC11 cell line. In addition, following the induction of apoptosis in primary cultures of mammary epithelial cells by treatment with TGFbeta-3, IGFBP-5 expression is also upregulated. In parallel with this upregulation of IGFBP-5, there is also an increase in the levels of cleaved caspase-3, a well-characterized marker of cellular apoptosis. These findings confirm previous in vivo work demonstrating an increase in IGFBP-5 expression during involution of the mouse mammary gland. When HC11 cells are cultured under serum-free conditions (a well-characterized apoptotic insult in cell culture), there is also an increase in cleaved caspase-3 levels. Unexpectedly, in the presence of TGFbeta-3, caspase-3 levels are attenuated. In the presence of DIP, caspase-3 levels are also decreased in HC11 cells. As described previously, TGFbeta-3 inhibits beta-casein synthesis in HC11 cells. In the HC11 cell line (in contrast to primary cultures of mammary epithelial cells), there is no evidence for TGFbeta-3 induction of IGFBP-5 under either serum-free or DIP-supplemented conditions. We believe our data with primary cultures of mammary epithelial cells support the hypothesis of dual regulation of IGFBP-5 expression during both differentiation and apoptosis in the mammary gland and emphasizes the importance of using appropriate cell culture models to investigate such phenomena in this tissue. We discuss the possible implications of our observations in relation to the physiological processes of pregnancy, lactation, and involution in the mammary gland and the associated changes in mammary epithelial cell function.

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Section: Discussionsupporting

confidence: 89%

Insulin‐like growth factor binding protein (IGFBP)‐5 is upregulated during both differentiation and apoptosis in primary cultures of mouse mammary epithelial cells

Lochrie

Phillips

Tonner

et al. 2006

Journal Cellular Physiology

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“…Three of the four c-erbA gene products—erbA-α1, erbA-β1, and erbA-β2—encode biologically active thyroid hormone receptors (Teboul and Torresani 1993). Hyperthyroidism in rats produces organ hypertrophy and an increase in circulating levels of IGF and its binding proteins (IGFBP) (Rosato et al 2002). IGF-1 is the major mediator of growth hormone effects (Iglesias et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Acute Ozone-Induced Differential Gene Expression Profiles in Rat Lung

Nadadur¹,

Costa²,

Slade³

et al. 2005

Environ Health Perspect

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Ozone (O3) is an oxidant gas that can directly induce lung injury. Knowledge of the initial molecular events of the acute O3 response would be useful in developing biomarkers of exposure or response. Toward this goal, we exposed rats to toxic concentrations of O3 (2 and 5 ppm) for 2 hr and the molecular changes were assessed in lung tissue 2 hr postexposure using a rat cDNA expression array containing 588 characterized genes. Gene array analysis indicated differential expression in almost equal numbers of genes for the two exposure groups: 62 at 2 ppm and 57 at 5 ppm. Most of these genes were common to both exposure groups, suggesting common roles in the initial toxicity response. However, we also identified the induction of nine genes specific to 2-ppm (thyroid hormone-β receptor c-erb-A-β and glutathione reductase) or 5-ppm exposure groups (c-jun, induced nitric oxide synthase, macrophage inflammatory protein-2, and heat shock protein 27). Injury markers in bronchoalveolar lavage fluid (BALF) were used to assess immediate toxicity and inflammation in rats similarly exposed. At 2 ppm, injury was marked by significant increases in BALF total protein, N-acetylglucosaminidase, and lavageable ciliated cells. Because infiltration of neutrophils was observed only at the higher 5 ppm concentration, the distinctive genes suggested a potential amplification role for inflammation in the gene profile. Although the specific gene interactions remain unclear, this is the first report indicating a dose-dependent direct and immediate induction of gene expression that may be separate from those genes involved in inflammation after acute O3 exposure.

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“…In contrast to IGFBP-3, IGFBP-5 expression appeared to be highly regulated. In situ analyses have also localised IGFBP-5 transcripts to epithelial cells in mouse and rat mammary glands (Tonner et al 1997, Wood et al 2000, Rosato et al 2002. In the mammary gland, the induction of IGFBP-5 mRNA between L10 and I2 is extremely pronounced (54-fold) and reaches levels of expression at least an order of magnitude greater than any of the other IGFBPs (Fig.…”

Section: Knight 2002)mentioning

confidence: 91%

A quantitative RT-PCR study of the mRNA expression profile of the IGF axis during mammary gland development

Boutinaud¹,

Shand²,

Park³

et al. 2004

Journal of Molecular Endocrinology

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We have used quantitative RT-PCR to analyse the mRNA expression profile of the major components of the IGF axis in different stages of murine mammary gland development, including late pregnancy, lactation and involution. We have shown that all the genes studied, IGF-I, IGF-II, IGF receptor (IGFR) and IGF-binding protein (IGFBP)-1 to -6, were expressed in every stage, albeit at greatly differing levels and displaying unique expression profiles between developmental stages. IGF-I was always expressed at significantly higher levels than either IGF-II or IGFR. This suggests that IGF-I may be the more important IGF during mammary morphogenesis. Overall, IGFBP-3 demonstrated the highest level of expression of any of the IGFBP genes throughout all the developmental stages studied. However, within developmental stages, by far the highest level of expression of any of the IGFBPs was that of IGFBP-5 at day 2 of involution; this was almost an order of magnitude higher than any of the other IGFBP levels recorded. This corroborated our previous findings that the levels of IGFBP-5 protein are highly elevated in the involuting mammary gland, and demonstrated that this up-regulation of IGFBP-5 operates at the level of transcriptional control or message stability. Comparison of the expression profile for these different genes would strongly suggest that they are likely to have differential functions throughout mammary gland development, and also highlights potential interactions and co-regulation between different members of this axis. In addition, our results have identified some similarities and differences in the expression of IGFBPs between the mouse mammary epithelial cell line, HC11, and the normal mammary gland which are worthy of study, most notably the differential regulation of IGFBP-2 and the site of expression of IGFBP-4 and -6. Overall, this study has demonstrated the importance and complexity of the IGF axis during mammary gland development and provides a valuable resource for future research in this area.

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Effect of chronic thyroxine treatment on IGF-I, IGF-II and IGF-binding protein expression in mammary gland and liver during pregnancy and early lactation in rats

Cited by 19 publications

References 46 publications

Insulin‐like growth factor binding protein (IGFBP)‐5 is upregulated during both differentiation and apoptosis in primary cultures of mouse mammary epithelial cells

Insulin‐like growth factor binding protein (IGFBP)‐5 is upregulated during both differentiation and apoptosis in primary cultures of mouse mammary epithelial cells

Acute Ozone-Induced Differential Gene Expression Profiles in Rat Lung

A quantitative RT-PCR study of the mRNA expression profile of the IGF axis during mammary gland development

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