Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anterior pituitary gland RNA isolated from Meishan (MS) and White Composite (WC) sexually mature boars was compared by a newly developed method of differential expression cloning called differential display. A number of cDNAs were identified that differed distinctly in expression between these breeds. The gene for beta-subunit of thyroid-stimulating hormone (TSH-beta) was initially identified as more highly expressed in MS than in WC boars. Subsequently, RNase protection assays and TSH RIA were used to quantify the magnitude of differences in transcription and translation in both males and females. Mature MS pigs had threefold greater expression of TSH-beta (P < .05) and greater plasma TSH concentrations than mature WC pigs (P < .01). The cDNA cloning and sequence analyses indicate identity in TSH-beta mRNA between MS and WC males. Elevated plasma TSH concentration may contribute MS pigs reaching sexual maturity earlier than WC or other European breeds. The method used in this study provides a useful molecular tool 1) to detect differentially expressed genes, 2) to study genetic variation that occurs at the transcription level between individuals, populations, or breeds; and additionally, 3) to identify candidate genes that control economically important quantitative traits in livestock.
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PMID:Overexpression of beta-subunit of thyroid-stimulating hormone in Meishan swine identified by differential display. 888 Apr 12

The beta subunit of thyroid-stimulating hormone (TSHbeta) has been isolated and sequenced in many species, including several mammals and the frog, but not in any avian species. Therefore, the objective of this study was to isolate and sequence a cDNA for chicken TSHbeta. Degenerate oligonucleotide primers were designed, based on conserved regions of TSHbeta from four other species, and used for reverse transcription and polymerase chain reaction amplification of a cDNA fragment from total cellular RNA of pituitary glands from 7-day-old chicks. The remaining sequence was completed by rapid amplification of cDNA ends. The predicted amino acid sequence was 70. 4% identical between bovine and chicken, 69.6% identical between chicken and rat, and 57.4% identical between chicken and frog. To test for tissue specificity of the cDNA, total cellular RNA samples from testicle, liver, pituitary, lung, and heart were analyzed by Northern blot. The 32P-labeled antisense riboprobe hybridized to an RNA species of approximately 600-700 bases in pituitary RNA alone, corresponding with the length of TSHbeta mRNA in other species. Gene expression in Day 1 posthatch chickens was then analyzed by ribonuclease protection assay. Anterior pituitary cells of Day 1 chickens were treated for 20 to 24 hr in serum-free medium alone or with medium containing either thyrotropin-releasing hormone (TRH) (10(-8) M) or triiodothyronine (T3) (10(-9) M). The RNA was then harvested from these cells and hybridized with a 32P-labeled antisense riboprobe. Treatment with TRH had no effect on TSHbeta mRNA levels, while T3 significantly decreased (P < 0.05; n = 6 trials) TSHbeta mRNA levels by 45%. Taken together these results indicate that the cDNA sequence derived represents chicken TSHbeta mRNA, and that TSHbeta gene expression is downregulated by thyroid hormones as it is in mammals.
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PMID:Cloning and sequence analysis of a cDNA for the beta subunit of chicken thyroid-stimulating hormone. 924 26

Growth hormone (GH) secretion is altered in poorly controlled diabetic animals. However, modifications in the hypothalamic neuropeptides that control GH secretion, somatostatin and GH-releasing hormone (GHRH), as well as changes in the sensitivity of the hypothalamus and pituitary to the feedback effects of GH, are less clear. We have used RNase protection assays and in-situ hybridization to address whether the mRNA expression of GH, somatostatin and GHRH, as well as of the GH receptor (GHR) in the hypothalamus and anterior pituitary, are altered in streptozotocin-induced diabetic rats. After induction of diabetes, rats were treated with insulin twice daily for 3 weeks to obtain either poorly controlled (mean plasma glucose >300 mg/dl) or well-controlled diabetic rats. Although no significant change in pituitary GH mRNA expression was found, the hypothalamic expression of GHRH and somatostatin mRNA was reduced in poorly-controlled diabetic rats and returned to control values with normalisation of plasma glucose concentrations (P<0.0001 and P<0.002, respectively). Somatostatin mRNA expression was reduced only in the central portion of the periventricular nucleus, with no change being seen in the other areas of the periventricular nucleus or in the arcuate, suprachiasmatic or paraventricular nuclei. A significant decline in GHRH mRNA expression was observed in both the arcuate nucleus and ventromedial hypothalamus. Anterior pituitary GHR mRNA expression was significantly reduced in both well and poorly-controlled diabetic rats, while there was no change in the hypothalamus. To examine whether the evolution time of the diabetes influences these parameters, in a subsequent experiment, diabetic rats received no insulin for 2 months. A significant decline in GHRH and somatostatin mRNA expression was also observed in these rats. In addition, pituitary GH mRNA expression declined significantly in long-term diabetic rats. These results demonstrate that: (1) the expression of both GHRH and somatostatin declines specifically in anatomical areas involved in anterior pituitary hormone control; (2) GHR mRNA expression is decreased in the pituitary of diabetic rats, but not in the hypothalamus, and does not return to control values with normalisation of mean blood glucose concentrations; and (3) the evolution time of the diabetes is important for detecting some changes, including the decrease in pituitary GH mRNA expression.
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PMID:Anatomically specific changes in the expression of somatostatin, growth hormone-releasing hormone and growth hormone receptor mRNA in diabetic rats. 1069 41

Prior research indicates that growth hormone (GH) cell differentiation can be induced prematurely by treatment with glucocorticoids in vitro and in vivo. However, the nature of these responses has not been fully characterized. In this study, the time course of corticosterone induction of GH-secreting cells in cultures of chicken embryonic pituitary cells, responsiveness of differentiated somatotrophs to GH secretagogues, localization of somatotroph precursor cells within the pituitary gland, and the effect of corticosterone on GH gene expression were determined to better define the involvement of glucocorticoids in somatotroph recruitment during development. Anterior pituitary cells from embryonic day 12 chicken embryos were cultured in 10(-9) M corticosterone for 4 to 48 h and were then subjected to reverse haemolytic plaque assays (RHPAs) for GH. Corticosterone treatment for as short as 16 h increased the percentage of GH cells compared with the control. When corticosterone was removed after 48 h and cells were cultured for an additional 3 days in medium alone, the percentage of GH secretors decreased but remained greater than the proportion of somatotrophs among cells that were never treated with corticosterone. To determine if prematurely differentiated somatotrophs were responsive to GH secretagogues, cells were exposed to corticosterone for 48 h and then subjected to GH RHPAs in the presence or absence of GH-releasing hormone (GHRH) or thyrotropin-releasing hormone (TRH). Approximately half of the somatotrophs induced to differentiate with corticosterone subsequently released more GH in response to GHRH and TRH than in their absence. The somatotroph precursor cells were localized within the anterior pituitary by culturing cells from the caudal lobe and cephalic lobe of the anterior pituitary separately. Corticosterone induction of GH cells was substantially greater in cultures derived from the caudal lobe of the anterior pituitary, where somatotroph differentiation normally occurs. GH gene expression was evaluated by ribonuclease protection assay and by in situ hybridization. Corticosterone increased GH mRNA in cultured cells by greater than fourfold. Moreover, corticosterone-induced somatotroph differentiation involved GH gene expression in cells not expressing GH mRNA previously, and the extent of somatotroph differentiation was augmented by treatment with GHRH in combination with corticosterone. We conclude that corticosterone increases the number of GH-secreting cells within 16 h, increases GH gene expression in cells formerly not expressing this gene, confers somatotroph sensitivity to GHRH and TRH, and induces GH production in a precursor population found primarily in the caudal lobe of the anterior pituitary, a site consistent with GH localization in adults. These findings support the hypothesis that glucocorticoids function to induce the final stages in the differentiation of fully functional somatotrophs from cells previously committed to this lineage.
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PMID:Somatotroph recruitment by glucocorticoids involves induction of growth hormone gene expression and secretagogue responsiveness. 1137 20

Responsiveness of the hypothalamo-pituitary-adrenal axis is decreased during pregnancy. Therefore, the objective of the present study was to determine if responsiveness at the level of individual corticotrophs to corticotropin-releasing hormone (CRH) or arginine vasopressin (AVP) is decreased during pregnancy in sheep. Anterior pituitaries (APs) were collected from pregnant and nonpregnant ewes. Half of the APs were dispersed, and cells were placed on immobilon and treated with vehicle, CRH (10 nM), or AVP (100 nM) for 2 h. Cells were then fixed and incubated with ACTH or pro-opiomelanocortin (POMC) antibodies. The percentage of cells staining positive for immunoreactive (ir) ACTH or POMC, the percentage of cells secreting irACTH or POMC, and the area of irACTH or POMC secretion were measured. RNA was extracted from the other half of the APs to quantify CRH type 1 (CRH-R1) and vasopressin type 1b (V1b) receptor mRNA by ribonuclease protection assay. CRH treatment increased the percentage of corticotrophs with relatively large areas of irACTH and POMC secretion in nonpregnant, but not in pregnant, ewes. AVP treatment significantly increased the percentage of irACTH- and POMC-secreting cells in nonpregnant, but not in pregnant, ewes. V1b receptor mRNA, but not CRH-R1 receptor mRNA, was significantly decreased during pregnancy. These results suggest that corticotroph responsiveness to CRH and AVP is decreased during pregnancy in sheep. Therefore, reduced corticotroph responsiveness may contribute to stress hyporesponsivity during pregnancy.
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PMID:Attenuation of corticotropin-releasing hormone and arginine vasopressin responsiveness during late-gestation pregnancy in sheep. 1202 Oct 66

The influence of estrogen (E) on corticosterone (CORT) receptor function in neural tissue was investigated in female Sprague-Dawley rats. This was accomplished by using a sensitive solution-hybridization RNase protection assay to examine the effect of E on the regulation of CORT receptor mRNAs. Animals were bilaterally ovariectomized (OVX), and a Silastic capsule (0.5 cm) containing 17beta-estradiol was sc implanted. Control animals received a blank capsule. Animals were killed 1, 7, or 21 days later. Anterior pituitary glucocorticoid receptor (GR) mRNA levels were significantly lower (P < 0.01) in E-treated rats at all time points examined. Hippocampal GR mRNA levels were significantly decreased below OVX values (P < 0.01) after 1 and 21 days of E treatment. Hypothalamic-preoptic area (HPOA) GR mRNA levels were significantly lower (P < 0.01) than OVX values only after 21 days of E treatment. Mineralocorticoid receptor mRNA levels were significantly lower after E treatment (P < 0.01) at all time points and in all three tissues examined. In a second study, we administered the GR-specific agonist RU 28362 (40 mug/100 g BW for 4 days) or the nonspecific agonist dexamethasone (DEX; 40 mug/100 g BW for 4 days) to OVX - and OVX + E-treated animals. The administration of RU 28362 significantly down-regulated hippocampal GR mRNA (P < 0.05) in OVX rats only. In contrast, DEX administration significantly down-regulated hippocampal GR mRNA (P < 0.05) in both control and E-treated animals. The administration of DEX or RU 28362 significantly reduced GR mRNA levels (P < 0.05) in the HPOA of OVX control animals, but not E-treated animals. Thus, E treatment results in a loss of the glucocorticoid receptor's ability to down-regulate its mRNA. These studies, combined with our earlier findings that E treatment impairs the ability of GR to down-regulate its protein (8), provide evidence that E interferes with glucocorticoid receptor function.
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PMID:Estrogen-induced alterations in the regulation of mineralocorticoid and glucocorticoid receptor messenger RNA expression in the female rat anterior pituitary gland and brain. 1991 22