Добірка наукової літератури з теми "Vitamine D 24-hydroxylase"
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Статті в журналах з теми "Vitamine D 24-hydroxylase"
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Shanmugasundaram, R., та R. K. Selvaraj. "Vitamin D-1α-hydroxylase and vitamin D-24-hydroxylase mRNA studies in chickens". Poultry Science 91, № 8 (серпень 2012): 1819–24. http://dx.doi.org/10.3382/ps.2011-02129.
Повний текст джерела
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Rahmaniyan, Mehrdad, Kennerly Patrick, and Norman H. Bell. "Characterization of recombinant CYP2C11: a vitamin D 25-hydroxylase and 24-hydroxylase." American Journal of Physiology-Endocrinology and Metabolism 288, no. 4 (April 2005): E753—E760. http://dx.doi.org/10.1152/ajpendo.00201.2004.
Повний текст джерелаАнотація:
Studies were performed to further characterize the male-specific hepatic recombinant microsomal vitamin D 25-hydroxlase CYP2C11, expressed in baculovirus-infected insect cells, and determine whether it is also a vitamin D 24-hydroxylase. 25- and 24-hydroxylase activities were compared with those of 10 other recombinant hepatic microsomal cytochrome P-450 enzymes expressed in baculovirus-infected insect cells. Each of them 25-hydroxylated vitamin D2, vitamin D3, 1α-hydroxyvitamin D2(1αOHD2), and 1α-hydroxyvitamin D3(1αOHD3). CYP2C11 had the greatest activity with these substrates, except vitamin D3, which had the same activity as four of the other enzymes. The descending order of 25-hydroxylation by CYP2C11 was 1αOHD3> 1αOHD2> vitamin D2> vitamin D3. Each of the recombinant cytochrome P-450 enzymes 24-hydroxylated 1αOHD2. CYP2C11 had the greatest activity. 24-Hydroxylation of 1αOHD3was very low, and there was none with vitamin D3. Only CYP2C11 24-hydroxylated vitamin D2. Structures of vitamin D metabolites, including 24-hydroxyvitamin D2, 1,24( S)-dihydroxyvitamin D2, and 1,24-dihydroxyvitamin D3, were confirmed by HPLC and gas chromatography retention times and characteristic mass spectrometric fragmentation patterns. In male rats, hypophysectomy significantly reduced body weight, liver weight, hepatic CYP2C11 mRNA expression, and 24- and 25-hydroxylation of 1αOHD2. Expression of CYP2J3 and CYP2R1 mRNA did not change. In male rat hepatocytes, CYP2C11 mRNA expression and 24- and 25-hydroxylation were significantly reduced after culture for 24 h compared with uncultured cells. Expression of CYP2J3 and CYP2R1 either increased or did not change. It is concluded that CYP2C11 is a male-specific hepatic microsomal vitamin D 25-hydroxylase that hydroxylates vitamin D2, vitamin D3, 1αOHD2, and 1αOHD3. CYP2C11 is also a vitamin D 24-hydroxylase.
3
Ren, Songyang, Lisa Nguyen, Shaoxing Wu, Carlos Encinas, John S. Adams, and Martin Hewison. "Alternative Splicing of Vitamin D-24-Hydroxylase." Journal of Biological Chemistry 280, no. 21 (March 23, 2005): 20604–11. http://dx.doi.org/10.1074/jbc.m414522200.
Повний текст джерела
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Warner, M., and A. Tenenhouse. "Regulation of renal vitamin D hydroxylase activity in vitamin D deficient rats." Canadian Journal of Physiology and Pharmacology 63, no. 8 (August 1, 1985): 978–82. http://dx.doi.org/10.1139/y85-161.
Повний текст джерелаАнотація:
The regulation of renal mitochondrial 1-hydroxylase activity in chronic vitamin D deficiency was studied in male rats. These rats were born of mothers who had been raised from weaning (21 days) on a vitamin D deficient diet and who had no detectable serum 1,25-dihydroxycholecalciferol (1,25-(OH)2D) at the time their offspring were weaned (28 days). In the pups, renal mitochondrial 1-hydroxylase activity was undetectable before the 3rd week of life even though the animals were severely hypocalcemic from birth. The 1-hydroxylase activity first became detectable at 26 days of age, rapidly reached a maximum at day 34, then decreased to become undetectable again by 65 days. Throughout this time serum calcium concentration was <5.0 mg/dL and serum parathyroid hormone (PTH) concentration, measured by a midmolecule radioimmunoassay, was two-to five-fold greater than that found in vitamin D replete rats. 1-Hydroxylase activity could be restored in the +65-day-old animals by administration of a single dose of 2.5 μg vitamin D3. Enzyme activity was detected within 24 h, was maximal at 72 h, and returned to undetectable levels by 96 h after administration of the vitamin. Serum 1,25-(OH)2D which was undetectable before administration of the vitamin D3, was 108 and 458 pg/mL at 16 and 40 h, respectively, after the injection. The serum concentration of this metabolite then decreased progressively to 80 pg/mL by 6 days. 24-Hydroxylase activity first became detectable 48 h after vitamin D administration, increased to a maximum at 96 h, and thereafter decreased to become undetectable by 7 days. The urinary excretion of phosphate and cyclic AMP was 10% of control values between 65 and 90 days of age. These values became normal 4 days after a single dose of 2.5 μg vitamin D3. From these data it is concluded that there are two distinct levels of regulation of 1-hydroxylase activity: a vitamin D independent induction of the activity at the time of weaning that is transient and is not associated with any detectable 24-hydroxylase activity; and the second is a vitamin D dependent induction of enzyme activity seen in animals which prior to administration of the vitamin manifest the characteristics of PTH resistance and have no detectable renal hydroxylase activity. The mechanisms of these effects remain to be determined.
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Akeno, N., A. Matsunuma, T. Maeda, T. Kawane, and N. Horiuchi. "Regulation of vitamin D-1alpha-hydroxylase and -24-hydroxylase expression by dexamethasone in mouse kidney." Journal of Endocrinology 164, no. 3 (March 1, 2000): 339–48. http://dx.doi.org/10.1677/joe.0.1640339.
Повний текст джерелаАнотація:
We investigated the effects of dexamethasone on vitamin D-1alpha-hydroxylase and -24-hydroxylase expression and on vitamin D receptor (VDR) content in the kidneys of mice fed either a normal (NCD) diet or a calcium- and vitamin D-deficient (LCD) diet for 2 weeks. For the last 5 days mice received either vehicle or dexamethasone (2 mg/kg per day s.c.). Dexamethasone significantly increased plasma calcium concentrations without changing plasma concentrations of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) in both NCD and LCD groups. Northern blot and enzyme activity analyses in NCD mice revealed that dexamethasone increased renal VDR mRNA expression modestly and greatly increased 24-hydroxylase mRNA abundance and enzyme activity, but did not affect 1alpha-hydroxylase mRNA abundance and enzyme activity. In mice fed an LCD diet, dexamethasone increased renal VDR mRNA expression 1.5-fold, decreased 1alpha-hydroxylase mRNA abundance (52%) and activity (34%), and markedly increased 24-hydroxylase mRNA abundance (16-fold) and enzyme activity (9-fold). Dexamethasone treatment did not alter functional VDR number (B(max) 125-141 fmol/mg protein) or ligand affinity (K(d) 0.13-0.10 nM) in LCD mice. Subcutaneous injections of 1,25(OH)(2)D(3) (0.24 nmol/kg per day for 5 days) into NCD mice strongly increased renal 24-hydroxylase mRNA abundance and enzyme activity, while there was no effect of dexamethasone on renal 24-hydroxylase expression in these mice. This may be due to overwhelming induction of 24-hydroxylase by 1,25(OH)(2)D(3). These findings suggest that glucocorticoid-induced osteoporosis is caused by direct action of the steroids on bone, and the regulatory effect of glucocorticoids on renal 25-hydroxyvitamin D(3) metabolism may be less implicated in the initiation and progression of the disease.
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Agu, Chinyere, Ei Cho, Christine Resta, and Rakhlin Luba. "LBSAT130 Hypercalcemia In Pregnancy Due To CYP24A1 Mutation." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A149. http://dx.doi.org/10.1210/jendso/bvac150.303.
Повний текст джерелаАнотація:
Abstract Background The active form of vitamin D (1,25 OH2 vitamin D) is catabolized by a key enzyme 1,25 OH vitamin D-24 hydroxylase, which is encoded by the CYP24A1 gene. Loss of function mutation in the CYP24A1 leads to elevated levels of active vitamin D, causing PTH independent hypercalcemia with nephrolithiasis and nephrocalcinosis. Two phenotypic variants have been identified: idiopathic infantile hypercalcemia, which is a more severe form presenting in infancy, and a milder form with onset in adulthood as is this case. Pregnancy is known to initiate or worsen the hypercalcemia. Clinical Case A 27-year-old woman presented at 11 weeks gestation with hyperemesis, noted to have hypercalcemia calcium 15.7mg/dl (8.2 to 10.1 pg/ml), low PTH 2pg/ml (24 -85 pg/ml) with high serum 1,25 OHD 309pg/ml (nl 19.9-79.3 pg/ml). She had low PTHrp, normal ACE level, and negative TB testing. Pre-pregnancy calcium was normal (9.8mg/dl). She had a history of hypercalcemia in previous pregnancy (Calcium 13mg/dl) that ended in IUFD. Family history revealed nephrolithiasis in her sister, mother, and paternal aunt as well as a consanguineous marriage in our patient and her parents. Vitamin D metabolites evaluated via liquid chromatography showed low serum 24,25(OH)2D (0.29ng/ml nl N/A) and elevated 25OHD 138 ng/mL (20-80 ng/ml). Ratio of 25 (OH) Vit D to 24,25(OH)2D was 475.86 (values >80 indicate probable bi-allelic CYP24A1 deletion or mutation. Genetic test pending. Conclusion This case highlights the fact that patients with 24 hydroxylase deficiency may be normocalcemic with hypercalcemia unveiled during pregnancy due to increased 1alpha hydroxylase production by the placenta and kidneys as well as intake of prenatal vitamins containing calciferol. An index of suspicion for CYP24A1 mutation is needed in patients with high active vitamin D metabolites, high or normal calcium, low PTH, family history of kidney stones or worsening hypercalcemia in pregnancy. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Lee, Sang R., Mi-Young Park, Hyun Yang, Geun-Shik Lee, Beum-Soo An, Bae-kuen Park, Eui-Bae Jeung та Eui-Ju Hong. "5α-dihydrotestosterone reduces renal Cyp24a1 expression via suppression of progesterone receptor". Journal of Molecular Endocrinology 60, № 2 (лютий 2018): 159–70. http://dx.doi.org/10.1530/jme-17-0187.
Повний текст джерелаАнотація:
Androgens act in concert with vitamin D to influence reabsorption of calcium. However, it is unclear whether androgens directly regulate vitamin D homeostasis or control other cellular events that are related to vitamin D metabolism. To examine whether the expression of vitamin D-related genes in mouse kidney is driven by androgens or androgen-dependent effects, the androgen receptor and other sex steroid receptors were monitored in orchidectomized mice treated with 5α-dihydrotestosterone (DHT). Our results revealed that exposing orchidectomized mice to DHT inhibited the expression of progesterone receptor (Pgr) with or without estrogen receptor α expression, the latter was confirmed by ER-positive (MCF7 and T47D) or -negative (PCT) cells analysis. The loss of Pgr in turn decreased the expression of renal 24-hydroxylase via transcriptional regulation because Cyp24a1 gene has a progesterone receptor-binding site on promoter. When male kidneys preferentially hydroxylate 25-hydroxyvitamin D3 using 24-hydroxylase rather than 25-hydroxyvitamin D3-1-alpha hydroxylase, DHT suppressed the Pgr-mediated 24-hydroxylase expression, and it is important to note that DHT increased the blood 25-hydroxyvitamin D3 levels. These findings uncover an important link between androgens and vitamin D homeostasis and suggest that therapeutic modulation of Pgr may be used to treat vitamin D deficiency and related disorders.
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Mata-Greenwood, Eugenia, Hans C. A. Westenburg, Stacy Zamudio, Nicholas P. Illsley, and Lubo Zhang. "Decreased Vitamin D Levels and Altered Placental Vitamin D Gene Expression at High Altitude: Role of Genetic Ancestry." International Journal of Molecular Sciences 24, no. 4 (February 8, 2023): 3389. http://dx.doi.org/10.3390/ijms24043389.
Повний текст джерелаАнотація:
High-altitude hypoxia challenges reproduction; particularly in non-native populations. Although high-altitude residence is associated with vitamin D deficiency, the homeostasis and metabolism of vitamin D in natives and migrants remain unknown. We report that high altitude (3600 m residence) negatively impacted vitamin D levels, with the high-altitude Andeans having the lowest 25-OH-D levels and the high-altitude Europeans having the lowest 1α,25-(OH)2-D levels. There was a significant interaction of genetic ancestry with altitude in the ratio of 1α,25-(OH)2-D to 25-OH-D; with the ratio being significantly lower in Europeans compared to Andeans living at high altitude. Placental gene expression accounted for as much as 50% of circulating vitamin D levels, with CYP2R1 (25-hydroxylase), CYP27B1 (1α-hydroxylase), CYP24A1 (24-hydroxylase), and LRP2 (megalin) as the major determinants of vitamin D levels. High-altitude residents had a greater correlation between circulating vitamin D levels and placental gene expression than low-altitude residents. Placental 7-dehydrocholesterol reductase and vitamin D receptor were upregulated at high altitude in both genetic-ancestry groups, while megalin and 24-hydroxylase were upregulated only in Europeans. Given that vitamin D deficiency and decreased 1α,25-(OH)2-D to 25-OH-D ratios are associated with pregnancy complications, our data support a role for high-altitude-induced vitamin D dysregulation impacting reproductive outcomes, particularly in migrants.
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Buffenstein, R., I. N. Sergeev, and J. M. Pettifor. "Vitamin D hydroxylases and their regulation in a naturally vitamin D-deficient subterranean mammal, the naked mole rat (Heterocephalus glaber)." Journal of Endocrinology 138, no. 1 (July 1993): 59–64. http://dx.doi.org/10.1677/joe.0.1380059.
Повний текст джерелаАнотація:
ABSTRACT The vitamin D hormone 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is generated by a series of hydroxylation steps in the liver and kidneys. We investigated whether naturally vitamin D-deficient subterranean mammals (naked mole rats, Heterocephalus glaber) employ the same enzymatic pathways, and whether these are regulated in a similar manner to that established for other mammals. Vitamin D3-25-hydroxylase in the liver and both 25-hydroxyvitamin D3-l-hydroxylase and 25-hydroxyvitamin D3-24 hydroxylase (1-OHase and 24-OHase) in the kidney were detectable in mole rats. As expected for vitamin D-deficient mammals, the 1-OHase activity predominated over the 24-OHase. After mole rats received a supraphysiological supplement of vitamin D3, 1-OHase activity was suppressed and 24-OHase activity was enhanced. Irrespective of vitamin D status, forskolin (a protein kinase A activator) and dibutyryl cyclic AMP did not alter the activity of either 1-OHase or 24-OHase. These findings suggest that the response of renal hydroxylases to parathyroid hormone was blunted. Phorbol esters, 12-O-tetradecanoylphorbol 13-acetate (TPA) and 1-oleoyl-2-acetylglycerol (OAG) (protein kinase C activators), suppressed 1-OHase activity. 24-OHase activity was induced by TPA but not by OAG. These effects were similar to those illicited by vitamin D3 supplementation but were additive in that they increased the responses shown in vitamin D-replete mole rats. These data confirm that naturally vitamin D-deficient mole rats can convert vitamin D3 to the hormone, 1,25(OH)2D3. Furthermore, the enzymes 1-OHase and 24-OHase present in the kidneys of these mammals are regulated independently by 1,25(OH)2D3 and protein kinase C-mediated pathways of intracellular signalling, but are not regulated by the cyclic AMP–protein kinase A signal transduction pathway. Journal of Endocrinology (1993) 138, 59–64
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Agic, Admir, Hong Xu, Christopher Altgassen, Frank Noack, Monika M. Wolfler, Klaus Diedrich, Michael Friedrich, Robert N. Taylor та Daniela Hornung. "Relative Expression of 1,25-Dihydroxyvitamin D3 Receptor, Vitamin D 1α-Hydroxylase, Vitamin D 24-Hydroxylase, and Vitamin D 25-Hydroxylase in Endometriosis and Gynecologic Cancers". Reproductive Sciences 14, № 5 (липень 2007): 486–97. http://dx.doi.org/10.1177/1933719107304565.
Повний текст джерелаДисертації з теми "Vitamine D 24-hydroxylase"
1
Boutinet, Stéphane. "Rôle du calcium intracellulaire dans la compliance de l'artère carotide de rat : effets d'un inhibiteur de l'enzyme de conversion de l'angiotensine 1." Nancy 1, 1995. http://docnum.univ-lorraine.fr/public/SCD_T_1995_0449_BOUTINET.pdf.
Повний текст джерелаАнотація:
L'objectif de ce travail s'est focalisé sur le rôle du calcium intracellulaire dans la compliance carotidienne chez le rat au cours d'études in vitro sur les effets (1) du vieillissement vasculaire, (2) d'un traitement par la vitamine D3 et la nicotine, et (3) d'un traitement chronique par un inhibiteur de l'enzyme de conversion de l'angiotensine l, le périndopril, sur la surcharge calcique vasculaire. Pour cela nous avons développé une nouvelle technique d'évaluation de la capacité de l'artère carotide à amortir un signal de pression pulsée nous permettant de mesurer simultanément le Ca2+ cytosolique par l'utilisation d'une sonde fluorescente, le fura-2. La capacité d'amortissement artériel est maximale à basse pression (25 mmHg) et minimale à partir de 100 mmHg. A basse pression, la stimulation par la noradrénaline induit une augmentation du niveau de Ca2+ intracellulaire et une baisse conjointe de la capacité d'amortissement artériel, indiquant le rôle modulateur du Ca2+ intracellulaire. Les effets du vieillissement vasculaire tels qu'une rigidification de l'artère carotide et une calcification pariétale sont nettement accentués lors d'un traitement vitamine D3-nicotine avec en plus une hypertrophie ventriculaire gauche. Cette calcification pariétale, qui se caractérise par un dépôt de calcium sur les fibres élastiques, aboutit à une perte de la capacité d'amortissement artériel, peu marquée au cours du vieillissement vasculaire mais très prononcée après le traitement vitamine D3-nicotine. La concentration de Ca2+ cytosolique de base ne semble pas être significativement modifiée dans les deux cas. La stimulation par la noradrénaline entraîne une augmentation de Ca2+ cytosolique et une baisse de la capacité d'amortissement artériel. La réactivité vasculaire augmente avec la maturation mais n'est pas altérée par le vieillissement. Au contraire, cette réactivité est anmlIée après le traitement vitamine D3-nicotine. Le traitement chronique par le périndopril n'a aucun effet sur la calcification, la capacité d'amortissement artériel et la réactivité vasculaire de l'artère carotide. Seule la pression artérielle systolique et la masse cardiaque sont diminuées par ce traitement. En conclusion, le Ca2+ cytosolique peut jouer un rôle important dans la modulation de la capacité d'amortissement artériel. Cependant, ce rôle devient mineur lors d'altérations fonctionnelles de la matrice extracellulaire notamment des fibres élastiques.
2
Boutinet, Stéphane. "Rôle du calcium intracellulaire dans la compliance de l'artère carotide de rat : effets d'un inhibiteur de l'enzyme de conversion de l'angiotensine 1." Nancy 1, 1995. http://docnum.univ-lorraine.fr/public/SCD_T_1995_0449_BOUTINET.pdf.
Повний текст джерелаАнотація:
L'objectif de ce travail s'est focalisé sur le rôle du calcium intracellulaire dans la compliance carotidienne chez le rat au cours d'études in vitro sur les effets (1) du vieillissement vasculaire, (2) d'un traitement par la vitamine D3 et la nicotine, et (3) d'un traitement chronique par un inhibiteur de l'enzyme de conversion de l'angiotensine l, le périndopril, sur la surcharge calcique vasculaire. Pour cela nous avons développé une nouvelle technique d'évaluation de la capacité de l'artère carotide à amortir un signal de pression pulsée nous permettant de mesurer simultanément le Ca2+ cytosolique par l'utilisation d'une sonde fluorescente, le fura-2. La capacité d'amortissement artériel est maximale à basse pression (25 mmHg) et minimale à partir de 100 mmHg. A basse pression, la stimulation par la noradrénaline induit une augmentation du niveau de Ca2+ intracellulaire et une baisse conjointe de la capacité d'amortissement artériel, indiquant le rôle modulateur du Ca2+ intracellulaire. Les effets du vieillissement vasculaire tels qu'une rigidification de l'artère carotide et une calcification pariétale sont nettement accentués lors d'un traitement vitamine D3-nicotine avec en plus une hypertrophie ventriculaire gauche. Cette calcification pariétale, qui se caractérise par un dépôt de calcium sur les fibres élastiques, aboutit à une perte de la capacité d'amortissement artériel, peu marquée au cours du vieillissement vasculaire mais très prononcée après le traitement vitamine D3-nicotine. La concentration de Ca2+ cytosolique de base ne semble pas être significativement modifiée dans les deux cas. La stimulation par la noradrénaline entraîne une augmentation de Ca2+ cytosolique et une baisse de la capacité d'amortissement artériel. La réactivité vasculaire augmente avec la maturation mais n'est pas altérée par le vieillissement. Au contraire, cette réactivité est anmlIée après le traitement vitamine D3-nicotine. Le traitement chronique par le périndopril n'a aucun effet sur la calcification, la capacité d'amortissement artériel et la réactivité vasculaire de l'artère carotide. Seule la pression artérielle systolique et la masse cardiaque sont diminuées par ce traitement. En conclusion, le Ca2+ cytosolique peut jouer un rôle important dans la modulation de la capacité d'amortissement artériel. Cependant, ce rôle devient mineur lors d'altérations fonctionnelles de la matrice extracellulaire notamment des fibres élastiques.
3
Roy, Stéphane. "Regulation of 1,25 dihydroxyvitamin D3-24-hydroxylase gene expression." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=34441.
Повний текст джерелаАнотація:
The first three studies in this thesis address the mechanism for the aberrant fall in serum 1,25-dihydroxyvitamin D$ sb3$ (1,25-(OH)$ sb2$D$ sb3 rbrack$ and increase in renal 1,25-(OH)$ sb2$D$ sb3$-24-hydroxylase(24-hydroxylase) activity in X-linked hypophosphatemic mice (Hyp). The 24-hydroxylase is the first enzyme in the C-24 oxidation pathway that degrades the vitamin D hormone to its final inactivation product, calcitroic acid. We demonstrated that: (i) the aberrant increase in 24-hydroxylase activity in Pi-deprived Hyp mice is specific to the kidney and is the result of an increase in enzyme Vmax, immunoreactive protein and mRNA abundance; (ii) the increase in 24-hydroxylase mRNA in both Pi-deprived Hyp mice and 1,25-(0H)$ sb2$D$ sb3$-treated normal littermates can be ascribed to an increase in the transcriptional activity of the 24-hydroxylase gene; (iii) 24-hydroxylase transcripts in normal mice, Pi-deprived Hyp and normal mice and 1,25-(OH)$ sb2$D$ sb3$-treated normal mice are localized to the proximal tubule by in situ hybridization; and (iv) recombinant human growth hormone administration normalizes the aberrant increase in 24-hydroxylase but that this response is not sufficient to correct serum 1,25-(OH)$ sb2$D$ sb3$ levels in Pi-deprived Hyp mice.The fourth study addresses the mechanism whereby EB 1089, an analogue of 1,25-(OH)$ sb2$D$ sb3,$ is less calcemic than the vitamin D hormone, while being more potent in its antiproliferative action. We demonstrate that: (i) EB 1089 has a 50-fold lower affinity than 1,25-(OH)$ sb2$D$ sb3$ for the vitamin D catabolic enzyme, 24-hydroxylase; and (ii) EB 1089 and 1,25-(OH)$ sb2$D$ sb3$ exhibit tissue-specific differences in vitamin D receptor-mediated responses in vivo that may be ascribed, at least in part, to differences in binding affinities for the vitamin D receptor.
4
Agić, Admir [Verfasser]. "Relative expression of 1,25-dihydroxyvitamin D3-receptor, vitamin D 1alpha-hydroxylase, vitamin D 24-hydroxylase and vitamin D 25-hydroxylase in endometriosis and gynecologic cancers / eingereicht von Admir Agic." 2008. http://d-nb.info/988454319/34.
Повний текст джерела
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Pöppelmeier, Olaf. "Funktionelle Analyse des Polymorphismus im Promotor des 24-Hydroxylase-Gens." Doctoral thesis, 2006. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-23977.
Повний текст джерелаАнотація:
Funktionelle Analyse des Polymorphismus im Promotor des 24-Hydroxylase-Gens Ziel dieser Arbeit war es, in der Arbeitsgruppe eindeutig nachgewiesene Polymorphismen im Promotor des 24Hydroxylasegens, auf eine funktionelle Relevanz zu untersuchen. Die Substrate des Enzyms CYP24 sind 1,25(OH)2D3 und 25(OH)D3. Die entsprechenden Produkte der Katalyse sind 1,24,25(OH)3D3 und 24,25(OH)2D3. Über das erste Produkt wird das hochpotente 1,25(OH)2D3 im Sinne einer negativen Rückkopplung abgebaut. Dem zweiten Produkt 24,25(OH)2D3, konnte die Funktion als Botenstoff in der Knochenheilung und -entstehung nachgewiesen werden. Detailliertere Ergebnisse gibt es insbesondere für Chondrozyten in der Ruhezone der Epiphysefuge. Der Promotor des CYP24-Gens ist mit zwei Vitamin D-responsiven Elementen (VDREs) ausgestattet, welche die Transkriptionsrate des Gens in Anwesenheit von 1,25(OH)2D3 schnell und deutlich steigern. In einer poly-A-Strecke, die 488bp upstream des Transkriptionsstarts auffiel, konnte ein Polymorphismus nachgewiesen werden, die häufigsten Allele wurden als +A, +2A, und +C5AC bezeichnet. Mittels PCR wurden aus humaner, genomischer DNA, 672-680bp lange Promotorfragmente mit TATA-box, den beiden bekannten VDREs und dem polymorphen Bereich hergestellt. Diese Promotorfragmente wurden in den pGL3 Basic Vektor (ein für Luziferase kodierendes Plasmid ohne Promotor) kloniert und die Sequenz dieser Vektor-Promotorkonstrukte durch Fragmentanalyse und Sequenzierung kontrolliert. Die Vektor-Promotorkonstrukte wurden dann mittels Elektroporation in hFOB und T/C28 Zellen transfiziert. Es wurden Versuchsreihen unter basalen Bedingungen und unter Stimulation mit1,25(OH)2D3 durchgeführt. Anhand von Kontrollkonstrukten konnte die Spezifität der Promotoraktivität gezeigt werden. Für die Promotoren, die das Allel +A enthielten, konnte eine Verdoppelung und für die mit dem Allel +2A eine Verdreifachung der Luziferaseaktivität gezeigt werden. Das Allel +C5AC wies ähnliche Promotoraktivitäten wie der Wildtyp auf. Unter Stimulation mit 1,25(OH)2D3 war in allen Konstrukten mit einem Promotor in korrekter Orientierung eine mindestens dreifache Steigerung der Luziferaseaktivität zu messen. Sowohl Abwesenheit als auch in Anwesenheit von 1,25(OH)2D3 wird die Aktivität des Promotors des CYP24-Gens durch die Allele +A und +2A signifikant (p<0,001) gesteigert. Demzufolge könnte der Polymorphismus auch unter physiologischen Bedingungen Einfluss auf die Transkriptionsrate des CYP24-Gens haben. Da die CYP24-Aktivität vor allem über die Transkription reguliert wird, müsste durch den beschriebenen Polymorphismus die Aktivität des Enzyms in vivo gesteigert werden. In Folge könnte es lokal oder systemisch zu niedrigeren 1,25(OH)2D3- oder erhöhten 24,25(OH)2D3-Spiegeln kommen. Potentielle Bedeutung hat dieser Befund in der Pathogenese von Osteoporose, dem Prostatakarzinom oder anderen Erkrankungen die mit veränderten 1,25(OH)2D3 Aktivitäten einhergehen. Gegenwärtig wird bereits nach SNPs gefahndet die mit dem beschriebenen Polymorphismus assoziiert sind, um Untersuchungen von größeren Kollektiven auf diesen Polymorphismus hin zu erleichtern. Bell et al. konnten Veränderungen von CYP24-aktivitäten in Fibroblastenkulturen in Abhängigkeit von ethnischer Herkunft zeigen. Möglicherweise könnte das CYP24-Gen eines von zahlreichen Kandidatengenen sein, die bei der Entstehung von Osteoporose von Relevanz sind, und in ein System zur Risikoanalyse mit einfließen. Es könnten zum Beispiel über den Einsatz von zu entwickelnden „Single Nucleotid Polymorphims Gen-Chips“ solche Risikoprofile relativ einfach erstellt werden. In Folge könnten sowohl in der Prophylaxe als auch in der Therapie von Osteoporose neue Möglichkeiten geschaffen und neue Perspektiven eröffnen werdenFunctional analysis of the polymorphism in the promotor of the 24-Hydroxylase gene Aim: A functional characterisation of the Polymorphism in the promotor of the 24-hydroxylase (CYP24) gene. The enzyme CYP24 initiates the degradation of the active vitamin D metabolite 1,25(OH)D3 as well as catalysing the production of 24,25(OH)D3, an active metabolite bone metabolism. If the polymorphism influenced the activity of CYP24, local or systemic levels of vitamin D could be altered or bone metabolism disturbed by varying 24,25(OH)D3 levels. The polymorphism could a factor in the pathogenesis of osteoporosis or other diseases of the skeletal system. Methods: Four different alleles of the polymorphism in the promotor of the CYP24 gene (WT, +A, +2A and +C5AC) as well as controls were amplified using PCR and cloned into a luciferase assay vector (pgl3-basic). Using electroporation the vector was transfected into two different cell systems, h-fob cells (human Osteoblasts) and T/C28a2 cells (human Chondrocytes). The cells were cultivated with and without the influence of vitamin D. The promotor activity was quantified using the luciferase assay. Results: By comparison with the controls a specific promotor activity could be demonstrated. For the allele +A a two fold increase and for the allele +2A a three fold increase in promotor activity compared to the wild type promotor was measured (p<0,001). The allele +C5AC showed no significant influence on the promotor activity. Under influence of vitamin D promotor activity was increase at least three times as high as in the basic setting. Discussion: Since the activity of the enzyme CYP24 is controlled mainly by the rate of transcription, the polymorphism in the promotor of the gene could influence CYP24 activity in vivo. The result could be a local or systemic decrease of 1,25(OH)D3 levels or increase of 24,25(OH)D3 levels. The polymorphism might therefore be relevant in the pathogenesis of osteoporosis, prostate cancer or other diseases associated with decreased levels of vitamin D
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Zierold, Claudia. "The 24-hydroxylase promoter identification and characterization of its vitamin D response elements /." 1995. http://catalog.hathitrust.org/api/volumes/oclc/34654762.html.
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Ismail, Rohaizah. "Chicken vitamin D₃ 24-hydroxylase cDNA cloning and mRNA regulation by 1,25-dihydroxyvitamin Dr₃ and parathyroidectomy /." 1994. http://catalog.hathitrust.org/api/volumes/oclc/32033525.html.
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Tan, Cheng Ta Joseph. "Regulation of the 24 - hydroxylase gene promoter by 1,25 - dihydroxyvitamin D3 and chemotherapeutics drugs." Thesis, 2005. http://hdl.handle.net/2440/37863.
Повний текст джерелаАнотація:
Chemotherapy in childhood cancer patients is associated with reduced bone density that can result in osteoporotic fracture in survivors. A significant proportion of paediatric patients experience a reduction in plasma 25 - hydroxyvitamin D3 [ 25 ( OH ) D3 ] and 1,25 - dihydroxyvitamin D3 [ 1,25 ( OH ) 2D3 ] levels during treatment, the basis of which is unknown. A balance between the bioactivation and degradation of 1,25 ( OH ) 2D3 is responsible for maintaining homoeostatic levels of 1,25 ( OH ) 2D3 at the correct set - point. Whereas the cytochrome P450 enzyme, CYP27B1 ( 25 - hydroxyvitamin D3 1 α - hydroxylase ), catalyses the hydroxylation of the precursor 25 ( OH ) D3 to generate 1,25 ( OH ) 2D3, catabolic inactivation and cleavage of 1,25 ( OH ) 2D3 is achieved by the mitochondrial cytochrome P450 enzyme, 25 - hydroxyvitamin D3 24 - hydroxylase ( CYP24 ), which is highly expressed in bone and kidney cells. Since many of the signalling pathways which regulate the expression of CYP24 are also activated by chemotherapeutic drugs, we hypothesised that the drugs could cause the degradation of plasma 25 ( OH ) D3 and 1,25 ( OH ) 2D3 by increasing CYP24 expression, the principal means of facilitating the bio - inactivation and degradation of plasma 25 ( OH ) D3 and 1,25 ( OH ) 2D3. Using the kidney cell - lines, COS - 1 and HEK293T cells, we now report that chemotherapeutic drugs, represented by daunorubicin hydrochloride ( an anthracycline antibiotics ), etoposide and vincristine sulphate ( vinca alkaloids and related compounds ) and cisplatin ( an alkylating agent ), were able to enhance CYP24 promoter activity in kidney cell lines transfected with a CYP24 promoter - luciferase construct, either by themselves or in the presencedaunorubicin hydrochloride and etoposide, two of the strongest inducers of CYP24 promoter activation under our experimental conditions, demonstrate that these drugs acted in a concentration - dependent manner. In addition to stimulating promoter activity on their own, the drugs also amplified the induction of the CYP24 promoter by 1,25 ( OH ) 2D3. Synergistic increases were generally observed when the cells were treated simultaneously with 1,25 ( OH ) 2D3 and a drug. The two kidney cell lines generally responded in a similar manner when challenged with the drugs, either in the presence or absence of 1,25 ( OH ) 2D3. Interestingly, the hydroxylated derivative of daunorubicin hydrochloride, doxorubicin hydrochloride which is also a commonly used chemotherapeutic drug, had no effect of promoter activity. Further studies with daunorubicin hydrochloride demonstrated that the effects of the drug per se were not mediated by oxidative stress and the vitamin D receptor was not required for daunorubicin hydrochloride per se to stimulate CYP24 promoter activity. However, daunorubicin hydrochloride caused a modest increase in the expression of the vitamin D receptor and this could contribute to its synergistic activity with 1,25 ( OH ) 2D3. In the presence of etoposide, there was also a tendency for the kidney cells to express higher levels of the vitamin D receptor. A key role for the extracellular signal - regulated protein kinase ( ERK ) 1, ERK2 and ERK5 mitogen - activated protein ( MAP ) kinases was demonstrated for the inductive action of daunorubicin hydrochloride and etoposide, with CYP24 promoter - specific transcription factors located in the first - 298bp being likely targets of the ERK activity. Studies with a dominant negative mutant of MKK4, one of the two immediate upstream activators of the c - jun N - terminal kinase isoforms, demonstrated that this MAP kinase also played a crucial role in inductive actions of the of 1,25 ( OH ) 2D3. Dose - response studies with drugs. Consistent with their use in anti - cancer therapy, all of the above drugs killed the human promyelocytic HL60 leukaemic cells at very low concentrations but had no effect on the viability of kidney or liver cells, either at concentrations used in our experiments or at higher levels. Our data provide novel biochemical evidence that some of the commonly used chemotherapeutic drugs could cause an increase in the transcriptional activation of the promoter, most likely via the MAP kinases activating the transcription factors which bind to the CYP24 promoter. Such an effect could contribute to the reduction in plasma 25 ( OH ) D3 and 1,25 ( OH ) 2D3 in some of the patients undergoing chemotherapy.Thesis (Ph.D.)--University of Adelaide, School of Paediatrics and Reproductive Health, 2005.
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Tan, Cheng Ta Joseph. "Regulation of the 24 - hydroxylase gene promoter by 1,25 - dihydroxyvitamin D3 and chemotherapeutics drugs." 2005. http://hdl.handle.net/2440/37863.
Повний текст джерелаАнотація:
Chemotherapy in childhood cancer patients is associated with reduced bone density that can result in osteoporotic fracture in survivors. A significant proportion of paediatric patients experience a reduction in plasma 25 - hydroxyvitamin D3 [ 25 ( OH ) D3 ] and 1,25 - dihydroxyvitamin D3 [ 1,25 ( OH ) 2D3 ] levels during treatment, the basis of which is unknown. A balance between the bioactivation and degradation of 1,25 ( OH ) 2D3 is responsible for maintaining homoeostatic levels of 1,25 ( OH ) 2D3 at the correct set - point. Whereas the cytochrome P450 enzyme, CYP27B1 ( 25 - hydroxyvitamin D3 1 α - hydroxylase ), catalyses the hydroxylation of the precursor 25 ( OH ) D3 to generate 1,25 ( OH ) 2D3, catabolic inactivation and cleavage of 1,25 ( OH ) 2D3 is achieved by the mitochondrial cytochrome P450 enzyme, 25 - hydroxyvitamin D3 24 - hydroxylase ( CYP24 ), which is highly expressed in bone and kidney cells. Since many of the signalling pathways which regulate the expression of CYP24 are also activated by chemotherapeutic drugs, we hypothesised that the drugs could cause the degradation of plasma 25 ( OH ) D3 and 1,25 ( OH ) 2D3 by increasing CYP24 expression, the principal means of facilitating the bio - inactivation and degradation of plasma 25 ( OH ) D3 and 1,25 ( OH ) 2D3. Using the kidney cell - lines, COS - 1 and HEK293T cells, we now report that chemotherapeutic drugs, represented by daunorubicin hydrochloride ( an anthracycline antibiotics ), etoposide and vincristine sulphate ( vinca alkaloids and related compounds ) and cisplatin ( an alkylating agent ), were able to enhance CYP24 promoter activity in kidney cell lines transfected with a CYP24 promoter - luciferase construct, either by themselves or in the presencedaunorubicin hydrochloride and etoposide, two of the strongest inducers of CYP24 promoter activation under our experimental conditions, demonstrate that these drugs acted in a concentration - dependent manner. In addition to stimulating promoter activity on their own, the drugs also amplified the induction of the CYP24 promoter by 1,25 ( OH ) 2D3. Synergistic increases were generally observed when the cells were treated simultaneously with 1,25 ( OH ) 2D3 and a drug. The two kidney cell lines generally responded in a similar manner when challenged with the drugs, either in the presence or absence of 1,25 ( OH ) 2D3. Interestingly, the hydroxylated derivative of daunorubicin hydrochloride, doxorubicin hydrochloride which is also a commonly used chemotherapeutic drug, had no effect of promoter activity. Further studies with daunorubicin hydrochloride demonstrated that the effects of the drug per se were not mediated by oxidative stress and the vitamin D receptor was not required for daunorubicin hydrochloride per se to stimulate CYP24 promoter activity. However, daunorubicin hydrochloride caused a modest increase in the expression of the vitamin D receptor and this could contribute to its synergistic activity with 1,25 ( OH ) 2D3. In the presence of etoposide, there was also a tendency for the kidney cells to express higher levels of the vitamin D receptor. A key role for the extracellular signal - regulated protein kinase ( ERK ) 1, ERK2 and ERK5 mitogen - activated protein ( MAP ) kinases was demonstrated for the inductive action of daunorubicin hydrochloride and etoposide, with CYP24 promoter - specific transcription factors located in the first - 298bp being likely targets of the ERK activity. Studies with a dominant negative mutant of MKK4, one of the two immediate upstream activators of the c - jun N - terminal kinase isoforms, demonstrated that this MAP kinase also played a crucial role in inductive actions of the of 1,25 ( OH ) 2D3. Dose - response studies with drugs. Consistent with their use in anti - cancer therapy, all of the above drugs killed the human promyelocytic HL60 leukaemic cells at very low concentrations but had no effect on the viability of kidney or liver cells, either at concentrations used in our experiments or at higher levels. Our data provide novel biochemical evidence that some of the commonly used chemotherapeutic drugs could cause an increase in the transcriptional activation of the promoter, most likely via the MAP kinases activating the transcription factors which bind to the CYP24 promoter. Such an effect could contribute to the reduction in plasma 25 ( OH ) D3 and 1,25 ( OH ) 2D3 in some of the patients undergoing chemotherapy.Thesis (Ph.D.)--School of Paediatrics and Reproductive Health, 2005.
Частини книг з теми "Vitamine D 24-hydroxylase"
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Kharb, Simmi. "Role of Vitamin D in Preeclampsia." In Preeclampsia. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100139.
Повний текст джерелаАнотація:
Pathogenesis of preeclampsia involves immune dysfunction, placental implantation, abnormal angiogenesis, excessive inflammation, hypertension that may be affected by vitamin D. Human placenta expresses all the components for vitamin D signaling: Vitamin D receptor (VDR), retinoid X receptor (RXR), 1-alpha- hydroxylase (CYP27B1) and 24- hydroxylase (CYP24A1). Vitamin D binding protein plays a role in binding and transportation of 25 hydroxyvitamin D [25(OH)D] and 1,25(OH)2D3. Vitamin D is activated by 25-hydroxylase (CYP2R1) and 1-alpha -hydroxylase (CYP27B1) and is degraded by 24-hydroxylase (CYP24A1). Vitamin D supplementation is not recommended by WHO for pregnant women and allows recommended nutrient intake (RNI) of 200 IU (5 μg) per day. Further research requires serum 25(OH)D analysis and assessment of maternal and infant outcomes; pre-conceptional vitamin D status.
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OMDAHL, JOHN, and BRIAN MAY. "The 25-Hydroxyvitamin D 24-Hydroxylase." In Vitamin D, 85–104. Elsevier, 2005. http://dx.doi.org/10.1016/b978-012252687-9/50009-7.
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Veldurthy, Vaishali, Ran Wei, Megan Campbell, Kamil Lupicki, Puneet Dhawan, and Sylvia Christakos. "25-Hydroxyvitamin D3 24-Hydroxylase." In Vitamin D Hormone, 137–50. Elsevier, 2016. http://dx.doi.org/10.1016/bs.vh.2015.10.005.
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"PURIFICATION OF 25-HYDROXYVITAMIN D3 24-HYDROXYLASE FROM RAT KIDNEY MITOCHONDRIA." In Vitamin D, 257–58. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-071.
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"In Vivo Regulation of Rat Intestinal 24-Hydroxylase (I-24-OHase): Potential New Role of Calcitonin." In Vitamin D, 170–71. De Gruyter, 1994. http://dx.doi.org/10.1515/9783110882513-059.
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"Differences of the Regulation of 24-Hydroxylase Gene Expression in the Kidney and Intestine." In Vitamin D, 113–21. De Gruyter, 1994. http://dx.doi.org/10.1515/9783110882513-042.
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"Regulation of 24-Hydroxylase mRNA Expression by 1a,25(OH)2D3 and its Fluorinated Analogues." In Vitamin D, 155–56. De Gruyter, 1994. http://dx.doi.org/10.1515/9783110882513-056.
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"EVIDENCE THAT RAT KIDNEY 25-HYDROXYVIΤΑΜIN D-24-HYDROXYLASE CAN EXIST IN AN INACTIVE STATE." In Vitamin D, 196–97. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.196.
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"Influence of Extracellular Calcium in the Kinetic Behaviour of 1-Hydroxylase (1-OHase) and 24-Hydroxylase (24-OHase) in Walker Carcinosarcoma 256 Cells (WS) and in the Renal Proximal Tube Phenotype Cells (LLC-PK1)." In Vitamin D, 149–50. De Gruyter, 1994. http://dx.doi.org/10.1515/9783110882513-053.
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"Protein Kinase C Up-Regulates 1 a,25-Dihydroxyvitamin D3-Induced Expression of 24-Hydroxylase Gene." In Vitamin D, 133–34. De Gruyter, 1994. http://dx.doi.org/10.1515/9783110882513-045.
Повний текст джерелаТези доповідей конференцій з теми "Vitamine D 24-hydroxylase"
1
Luo, Wei, Adam R. Karpf, Kristin K. Deeb, Josephia R. Muindi, Carl D. Morrison, Donald L. Trump, and Candace S. Johnson. "Abstract 4944: Regulation of vitamin D 24-hydroxylase gene expression in human prostate cancer by epigenetic mechanisms." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4944.
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