Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abstract Triiodothyronine (T(3)) stimulates the synthesis of growth hormone and enhances the growth of neoplastic rat pituitary somatomam-motrophs (GH cells) in culture. Moreover, T(3) has been shown to stimulate the production and secretion of an autocrine growth factor by these cells. We have previously demonstrated the presence of specific receptors for insulin-like growth factors (IGF) on GH cells. Since GH(3) cells contain mRNA encoding IGF-I, it has been suggested that IGF-I might act in an autocrine fashion in these cells. Therefore, it was of interest to learn how T(3) affects IGF-I binding to GH(3) cells. T(3) increased [(125)I]IGF-I binding in a time - and dose-dependent manner. After 48 h of exposure to T(3), an increase in IGF-I binding was seen with 10(-11)M T(3), maximizing with 10(-8)M T(3). When cells were exposed to 10(-8) T(3), [(125)I]IGF-I binding reached a maximum of 218 +/- 20.8% of control (+/-SEM, P < 0.002) after 72 h of incubation. Scatchard analysis indicated that T(3) did not alter the K(d) of IGF-I for its receptor, but that the total receptor number was increased. Dexamethasone (10(-7)M) inhibited the T(3)-induced increase in IGF-I binding, but glucocorticoid alone did not substantially alter receptor number. No significant change in insulin or IGF-II binding was seen after hormone treatment. 10(-8) M T(3) or IGF-I increased the growth of the GH(3) cells by >/=30%. Our data indicate that T(3) upregulates IGF-I binding in GH(3) cells without altering insulin binding and thereby provides a means for enhancing potential autocrine regulation in this cell line.
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PMID:Triiodothyronine regulates insulin-like growth factor-I binding to cultured rat pituitary cells. 1921 Apr 52

One hundred and ninety-three Sprague-Dawley (SD) rats (average body weight 100-120g) were randomly divided into five groups (I-V). Groups I and II rats served as the negative and positive controls respectively and both received 0.1mg/kg Se from sodium selenite supplemented diets for the 18-week experimental period. Groups III-V rats were fed Se from SEM supplemented diets (0.3, 1 and 3mg/kg respectively). To induce hepatocarcinoma, groups II-V rats received diethylnitrosamine solution (100mg/L) at the dosage of 10mg/kg body weight in drinking water daily for 16 weeks, followed by sterilized water for a further 2 weeks. Group I rats received sterilized water throughout. At weeks 4, 8, 12 and 16 five rats in each group were sacrificed by cervical decapitation. At the termination of the study, at week 18, the surplus rats were sacrificed by cervical decapitation. Feed was withheld from the rats for 12 h before sampling. The following items including TNF-alpha, IGF-II, NO and T-NOS levels in plasma were tested using kit techniques. At the same time the expression of vascular endothelial growth factor (VEGF) in tumor tissue was analyzed by immunohistochemistry using the envision two-step methods with a kit. The results indicated that SEM could increase the levels of TNF-alpha in the early stages of hepatocarcinoma formation, however there was a decrease in the later stage of hepatocarcinogenesis. SEM could also significantly decrease the levels of IGF-II and NO, and inhibit the expression of VEGF in tumor tissue. SEM delayed the development of hepatocarcinoma in rats and that could be partially attributed to inhibition of angiogenesis.
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PMID:Effect of selenium-enriched malt on VEGF and several relevant angiogenic cytokines in diethylnitrosamine-induced hepatocarcinoma rats. 2012 81


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