Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interrelationship between estrogen and insulin-like growth factor-I (IGF-I) in the regulation of uterine growth was studied in the rat. The levels of the estrogen receptor (ER), ER mRNA, and IGF-I mRNA in rat uterus and liver were monitored. Uterine ER in normal cycling rats was highest in proestrus and diestrus, as was IGF-I mRNA. ER mRNA and plasma estradiol peaked in proestrus. Hepatic ER mRNA and IGF-I mRNA were highest in diestrus, whereas ER was not significantly changed during the estrous cycle. The temporal effects of multiple injections or continuous infusion of 17 beta-estradiol in ovariectomized rats were examined. In the uterus of animals subjected to multiple injections, a 10-fold increase in IGF-I mRNA was seen 24 h after the start of the treatment, whereas rats given continuous infusion of estradiol showed a more than 16-fold increase. In both groups, the increase of IGF-I mRNA was transient although estrogen treatment was continued. To study local hormonal effects, ovariectomized rats were given estradiol in vaginal implants. The uterine IGF-I mRNA level increased two-fold in 3 days. The ER mRNA level increased 1.5-fold and the uterine weights were doubled. The plasma estradiol concentration did not change during the treatment. A separate experiment was carried out to establish whether IGF-I itself exercises estrogen-like effects. Ovariectomized rats were given hrIGF-I in osmotic minipumps for 3 days. The uteri of the treated animals weighted significantly more than did the controls. Quantitation of the level of uterine estrogen receptors revealed a significant decrease.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1994 Jul
PMID:Estrogen regulation of the estrogen receptor and insulinlike growth factor-I in the rat uterus: a potential coupling between effects of estrogen and IGF-I. 797 26

Short-term lower leg growth, the insulin-like growth factor axis, and collagen turnover were assessed in 16 adolescents with asthma during treatment with inhaled budesonide, 800 micrograms/d, from a pressurized metered dose inhaler with a volume spacer. The design was a randomized double blind, placebo-controlled two-period crossover trial with treatment periods of 4 weeks and a 1-week wash-out. Lower leg growth was assessed by knemometry. Serum levels of insulin-like growth factor-I, insulin-like growth factor-binding protein-3, and the following markers of collagen turnover were evaluated: Serum markers of type I collagen formation and degradation; the carboxy-terminal propeptide of type I procollagen and the carboxy terminal pyridinoline cross-linked telopeptide of type I procollagen (ICTP), the serum marker of type III collagen formation; the amino-terminal propeptide of type III procollagen (PIIINP) and the urinary concentrations of the type I collagen degradation products pyridinoline (PYD) and deoxypyridinoline (DPD) cross-links. Mean lower leg growth velocity was suppressed from 0.51 mm/week during placebo to 0.18 mm/week during budesonide treatment (p < 0.001). No statistically significant effects on insulin-like growth factor-1, insulin-like growth faster-binding protein-3, or carboxy-terminal propeptide of type I procollagen were observed. ICTP and PIIINP were reduced with 2.3 and 2.5 micrograms/liter (p < 0.001 and p < 0.001, respectively) during budesonide treatment, urinary concentrations of PYD and DPD with 32.9 nmol/mmol creatinine (p < 0.005) and 6.8 nmol/mmol creatinine (p < 0.005), respectively. Significant correlations between lower leg growth velocity and ICTP, PIIINP, PYD, and DPD during placebo (p < 0.01, p < 0.05, p < 0.01, and p < 0.01) and budesonide (p < 0.05, p < 0.05, p < 0.05, and p < 0.05) periods were found. Short term lower leg growth suppression in adolescents treated with inhaled budesonide, 800 micrograms/d, reflects suppression of type I and III collagen turnover.
Steroids 1997 Oct
PMID:Short-term growth and collagen turnover in asthmatic adolescents treated with the inhaled glucocorticoid budesonide. 938 13

In prostatic tissue, androgen action may be mediated by growth factors such as insulin-like growth factor-I (IGF-I) and II (IGF-II), which are mitogenic for prostatic cells and modulate the stroma-epithelium interaction. IGF-binding proteins (IGFBPs) have an autocrine and/or paracrine role in regulating the local actions of the IGFs. In this study, testosterone, dihydrotestosterone (DHT), 3 alpha androstanediol (3 alpha diol), IGF-I, IGF-II, IGFBP2, and IGFBP3 concentrations were evaluated in human benign prostatic hyperplasia (BPH) tissue. Samples of prostate tissue were removed by suprapubic prostatectomy from twelve BPH patients. Androgen tissue levels were determined by radioimmunoassay after purification on celite microcolumns. IGF-I, IGFBP2, and IGFBP3 were measured by radioimmunoassay, and IGF-II by immunoradio metric assay, after acidification and chromatography on Sep-pak C18 Cartridges for IGF-I and IGF-II. Androgen concentrations, expressed in ng/g tissue (mean +/- SE), were 0.51 +/- 0.05 for testosterone, 5.3 +/- 0.16 for DHT, and 1.1 +/- 0.07 for 3 alpha diol. IGF-I, IGF-II, IGFBP2, and IGFBP3 levels were 24 +/- 3.7, 121 +/- 14 ng/g tissue and 0.44 +/- 0.05 and 1.2 +/- 0.17 micrograms/g tissue, respectively. No correlation between IGF-I, androgens, and IGFBPs was found. IGF-II was positively correlated with DHT (r = 0.78; p = 0.003) and 3 alpha diol (r = 0.66; p = 0.021) but not with IGFBPs. These data suggest that in BPH, DHT modulates the IGF system by increasing IGF-II without modifying IGFBPs. Therefore, the stroma-epithelium interaction, which plays an important role in prostatic growth, may be regulated by DHT through IGF-II.
Steroids
PMID:Insulin-like growth factor-I and -II in human benign prostatic hyperplasia: relationship with binding proteins 2 and 3 and androgens. 961 3

Estradiol signaling through estrogen receptors in the nervous system involves a variety of rapid membrane/cytoplasm-initiated events that are integrated with different mechanisms of transcriptional regulation. Here we review the role of glycogen synthase kinase 3 (GSK3) and beta-catenin in the coordination of membrane/cytoplasm-initiated and nuclear-initiated estrogen receptor signaling. Estradiol activates in vitro and in vivo the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway in neural cells. By activating this pathway through estrogen receptors, estradiol increases the levels of inactive GSK3beta (phosphorylated in serine 9). In turn, the inhibition of GSK3beta increases the stability of beta-catenin and its nuclear translocation. Then, beta-catenin exerts two different transcriptional effects: (i) regulates beta-catenin/T cell factor (TCF) mediated transcription in a similar but not identical way as Wnt ligands and (ii) regulates estrogen receptor mediated transcription after its association with estrogen receptor alpha. In addition, by the regulation of PI3K/Akt/GSK3/beta-catenin pathway, other factors such as insulin-like growth factor-I (IGF-I) regulate estrogen receptor mediated transcription. Therefore, GSK3 and beta-catenin allow the interaction of membrane/cytoplasm-initiated estrogen receptor signaling, IGF-I signaling, Wnt signaling and nuclear-initiated estrogen receptor signaling in the nervous system.
Steroids
PMID:Interaction of estrogen receptors with insulin-like growth factor-I and Wnt signaling in the nervous system. 1977 47

Breast cancer risk is strongly related to several reproductive and hormonal factors, but the nature of the effects of endogenous oestrogens has been difficult to establish. Data are now available from several large prospective studies with biobanks of stored serum, enabling better characterization of the associations of endogenous oestrogens, and other endogenous hormones, with breast cancer risk. In postmenopausal women, relatively high serum concentrations of oestradiol are associated with a more than twofold increase in the risk for breast cancer, and this probably explains the increase in risk in obese postmenopausal women. In premenopausal women the data available on oestrogens are more limited and difficult to interpret due to the large variations in endogenous oestrogens during the menstrual cycle, but are compatible with a positive association between oestradiol and breast cancer risk. There is also evidence that breast cancer risk is positively associated with androgens, prolactin and insulin-like growth factor-I. Further data are required, with better assays and repeat measures, to provide more accurate estimates of risk and to clarify the role of oestrogens in premenopausal women and the roles of other endogenous hormones.
Steroids 2011 Jul
PMID:Endogenous oestrogens and breast cancer risk in premenopausal and postmenopausal women. 2147 10

Prenatal exposure to excessive glucocorticoids (GCs) leads to intrauterine growth retardation and fetal programming of adult health and disease through deregulation of placental functions. Placental secretion of insulin-like growth factor-I (IGF-I) plays a critical role in the regulation of placental development and function. However, it remains elusive whether GCs affect placental functions through glucocorticoid receptor (GR)-mediated transcriptional regulation of IGF-I gene. In this study, human placental choriocarcinoma (BeWo) cells before and after syncytialization were used as cytotrophoblast and syncytiotrophoblast models, respectively, to explore the effects of dexamethasone (Dex) on transcriptional regulation of IGF-I gene at both stages. Dex significantly inhibited (P<0.05) cell proliferation in cytotrophoblasts and down-regulated amino acid transporter SLC7A5 in syncytiotrophoblasts. Concurrently, the abundance of IGF-I mRNA and its transcript variants, together with IGF-I level in culture media, were significantly reduced, in association with significantly enhanced (P<0.05) GR phosphorylation. GR antagonist RU486 was able to abolish all these effects. Two glucocorticoid response elements (GREs) were predicted in the promoter regions of IGF-I gene. GR binding to GRE1 was significantly enriched (P<0.05) in both cytotrophoblasts and syncytiotrophoblasts, but that to GRE2 was significantly diminished (P<0.05) in cytotrophoblasts but not in syncytiotrophoblasts, in response to Dex treatment. IGF-I supplementation completely rescued Dex-induced cell cycle arrest but not SLC7A5 down-regulation, indicating different regulatory mechanisms. Taken together, our results suggest that GR-mediated transcriptional regulation of IGF-I is involved in Dex-induced inhibition of placental cell proliferation and function.
Steroids 2016 11
PMID:Glucocorticoid receptor-mediated insulin-like growth factor-I transcriptional regulation in BeWo trophoblast cells before and after syncytialisation. 2750 Jun 92