Steroid regulation of growth hormone (GH) receptor and GH-binding protein messenger ribonucleic acids in the rat

Gabrielsson, Britt G.

doi:10.1210/en.136.1.209

Cited by 72 publications

(48 citation statements)

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“…Alternatively, the reduction in GH receptor/GHBP mRNA may reflect a reduction in a subpopulation of hepatic GH receptor transcripts containing a specific 5 -UTR sequence, termed GHR1 (Baumbach & Bingham 1995). Hypophysectomy vastly reduced GHR1 mRNA expression (Baumbach & Bingham 1995) while GH administration increased its abundance in GH-deficient dwarf rats (Gabrielsson et al 1995). This subclass of GH receptor/GHBP mRNA is expressed only in the liver (which may account for the absence of change of GH receptor mRNA in EGP) and is far more abundant in females, which may explain the results in female rats (Maiter et al 1992).…”

Section: Discussionmentioning

confidence: 99%

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats

Zung

Phillip²,

Chalew³

et al. 1999

Journal of Molecular Endocrinology

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Several studies have suggested that testosterone may have a direct, GH-independent effect on growth. In order to assess possible mechanism(s) whereby testosterone exerts its growth-promoting effect, we evaluated its effect on growth mediators of the GH-IGF-I axis, in both the liver and the epiphyseal growth plate (EGP). Testosterone was administered to peripubertal rats and the responses of mRNA of GH receptor, IGF-I, IGF-I receptor and IGF-binding proteins-1 and -3 (IGFBP-1 and IGFBP-3) as well as circulating IGF-I were evaluated in two time-related models: over 12 h after a single injection (short-term study) and 10 days after continuous administration (long-term study). Rats in the short-term study were castrated and were killed 1, 4, 6 and 12 h post injection. Rats in the long-term study were divided into two groups: castrated vs castrated and hypophysectomized, in order to assess the effect of testosterone in the presence and absence of GH. mRNA levels were determined by RNase protection assay, and serum IGF-I by RIA.Testosterone enhanced weight gain in the rats treated for 10 days, a change that was similar in the presence or absence of GH. This effect was relatively small, however, by comparison with the total weight gained without testosterone. Testosterone had no effect on hepatic IGF-I mRNA abundance but induced a reduction in circulating IGF-I levels, in both the short-and long-term study. Testosterone had no effect on hepatic GH receptor and IGFBP-3 mRNA levels but resulted in a transient, short-term elevation in IGFBP-1 mRNA levels that was maximal 4 h post injection.In the EGP, neither testosterone administration nor hypophysectomy had any effect on IGF-I and IGF-I receptor mRNA levels. However, testosterone increased GH receptor mRNA abundance after 10 days of continuous administration in hypophysectomized rats only.These data suggest that the effect of testosterone on growth (as assessed by weight gain) is small and is not mediated by changes in hepatic gene expression of IGF-I, IGF-I receptor, IGFBP-1, IGFBP-3 or circulating IGF-I. At the EGP, the testosterone effect on linear growth is not mediated through changes in mRNA abundance of IGF-I and IGF-I receptor. The small but significant elevation of GH receptor mRNA levels in hypophysectomized rats may suggest a testosterone-mediated augmentation of a GH effect at the target organ.

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Section: Discussionmentioning

confidence: 99%

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats

Zung

Phillip²,

Chalew³

et al. 1999

Journal of Molecular Endocrinology

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“…However, pharmacological doses of testosterone decrease serum GHBP concentrations in hypogonadal men, independently of GH status (Ip et al 1995). Estrogens increase hepatic concentrations of GHBP mRNA and circulating concentrations of GHBP in rats (Carmignac et al 1993, Gabrielsson et al 1995, Bennett et al 1996. In humans, circulating GHBP concentrations are generally negatively correlated with endogenous estrogen concentrations and are reduced by physiological doses of estrogen (Massa et al 1993, Kobayashi et al 1994, Tato et al 1995, although another study (Klein et al 1996) did not find that plasma GHBP concentrations differed with stage of the ovulatory cycle in women.…”

Section: Journal Of Endocrinology (2002) 175 55-59mentioning

confidence: 99%

Structure and regulation of expression of the mouse GH receptor

Talamantes¹,

Ortiz²

2002

Journal of Endocrinology

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GH-binding protein (GHBP) in the mouse consists of a ligand-binding domain, which is identical to the extracellular portion of the GH receptor (GHR), and a hydrophilic C-terminal domain, in place of the transmembrane and intracellular domains of the GHR. The two proteins are encoded by separate mRNAs which are derived from a single gene by alternative splicing. Determination of the gestational profiles of GHR and GHBP mRNA expression in mouse liver and placenta shows that in the liver, the 1·4 kb mRNA corresponding to the mouse GHBP increases approximately 20-fold between non-pregnant and late pregnant mice, whereas the relative increase in the expression of the 4·2 kb mouse GHR was 8-fold. The rise in the steady-state levels of both mRNAs began on day 9 of gestation. Mouse GHBP mRNA levels continue to rise until day 15 of pregnancy, while GHR mRNA abundance reaches a plateau by day 13. By elucidating the temporal changes in GHR and GHBP mRNA abundance during pregnancy and lactation in multiple maternal tissues and by assessing the ontogeny of these mRNAs in fetal and early postnatal mouse liver, our studies have demonstrated that the alternative splicing of mouse GHR/GHBP mRNA precursor is regulated in a tissue-, developmental stage-and physiological state-specific manner. In vitro studies using hepatocytes in culture have begun to elucidate the hormonal factor(s) involved in the gestation control of the expression of GHR and GHBP. Treatment of hepatocytes with GH or estradiol (E2) alone did not have any effect on the cellular concentrations of GHBP and GHR. However, the combination of E2 and GH up-regulated the cellular concentrations of GHBP and GHR 2-to 3-fold. GHBP and GHR mRNA concentrations were also up-regulated 2-to 3-fold. ICI 182-780, a competitive inhibitor of E2 for the estrogen receptor (ER), at different concentrations inhibited the E2-and GH-induced stimulation of GHBP and GHR. Furthermore, ER concentrations increased 5-to 7-fold in hepatocytes treated with E2 and GH compared with those in untreated cells or cells treated with either E2 or GH alone. Our studies in the mouse suggest that GHBP is an important cell-surface receptor for GH in the liver. These studies postulate that an arginine-glycine-aspartic acid sequence found on mouse GHBP but absent in other species is responsible for the association of GHBP with the plasma membrane by binding to one or more integrins on the surface of liver cells.

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“…Dexamethasone inhibited the induction of GHR mRNA by GH in rat primary cultured hepatocytes [20]. In vivo, dexamethasone down-regulated hepatic GHR mRNA and protein in the rats [4]. It is well known that there is a circadian pattern of circulating cortisol in the human; higher in the morning than in the evening [7,29].…”

Section: Discussionmentioning

confidence: 99%

“…However, some possible factors are considered to be the candidates; these include insulin [3,19], glucocorticoids [4,20] and GH [5,[21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

“…The number and function of GHR affect the ability of a tissue to respond to GH [2]. GHR messenger ribonucleic acid (mRNA) expression has been reported to be regulated by various factors, including insulin [3], glucocorticoids [4], GH [5] and nutritional status [6], and the regulation is tissue specific. It is known that there is a circadian pattern of circulating cortisol in rodents and humans [7,8] and GH secretion is pulsatile in these species [9,10].…”

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confidence: 99%

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Diurnal Variation in Growth Hormone Receptor Messenger Ribonucleic Acid in Liver and Skeletal Muscle of lit/+ and lit/lit Mice

et al. 2004

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Steroid regulation of growth hormone (GH) receptor and GH-binding protein messenger ribonucleic acids in the rat

Cited by 72 publications

References 0 publications

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats

Testosterone effect on growth and growth mediators of the GH-IGF-I axis in the liver and epiphyseal growth plate of juvenile rats

Structure and regulation of expression of the mouse GH receptor

Diurnal Variation in Growth Hormone Receptor Messenger Ribonucleic Acid in Liver and Skeletal Muscle of lit/+ and lit/lit Mice

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