Base de dados : MEDLINE
Pesquisa : D08.244.453.496 [Categoria DeCS]
Referências encontradas : 4 [refinar]
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  1 / 4 MEDLINE  
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[PMID]:27327272
[Au] Autor:Bartonkova I; Grycova A; Dvorak Z
[Ad] Endereço:Department of Cell Biology and Genetics, Faculty of Science, Palacky University , Slechtitelu 27, 783 71 Olomouc, Czech Republic.
[Ti] Título:Profiling of Vitamin D Metabolic Intermediates toward VDR Using Novel Stable Gene Reporter Cell Lines IZ-VDRE and IZ-CYP24.
[So] Source:Chem Res Toxicol;29(7):1211-22, 2016 Jul 18.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Variety of xenobiotics, including therapeutically used vitamin D analogues or environmental and alimentary endocrine disruptors, may interfere with vitamin D receptor (VDR) signaling, with serious physiological or pathophysiological consequences. Therefore, it is of topical interest to have reliable and efficient in vitro screening tools for the identification of agonists and activators of human VDR. We present here two novel stably transfected human reporter cell lines allowing rapid, high-throughput, and selective identification of VDR agonists and activators. Human colon adenocarcinoma cells LS180 were stably transfected with reporter plasmids CYP24_minP-pNL2.1[Nluc/Hygro] (IZ-CYP24 cells contain the -326/-46 sequence from the human CYP24A1 promoter) or VDREI3_SV40-pNL2.1[Nluc/Hygro] (IZ-VDRE cells contain three copies of vitamin D response elements VDRE-I from the human CYP24A1 promoter). Both cell lines remained fully functional for over two months in the culture and also after cryopreservation. Luciferase inductions ranged from 10-fold to 25-fold (RLU 10(6)-10(7)) and from 30-fold to 80-fold (RLU 10(3)-10(4)) in IZ-VDRE and IZ-CYP24 cells, respectively. Time-course analyses revealed that detection of VDR activators is possible as soon as after 8 h of incubation. Cell lines were highly selective toward VDR agonists, displaying no cross-activation by retinoids, thyroids, and steroids. As a proof of concept, we used IZ-VDRE and IZ-CYP24 cells for profiling analogues of vitamin D, and intermediates in vitamin D2 and vitamin D3 metabolic pathways against VDR transcriptional activity. The data obtained revealed significant activation of VDR not only by obligatory ligands calcitriol and ergocalcitriol but also by their precursors and degradation products.
[Mh] Termos MeSH primário: Família 24 do Citocromo P450/genética
Genes Reporter
Receptores de Calcitriol/metabolismo
Vitamina D/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Calcitriol); 1406-16-2 (Vitamin D); EC 1.14.15.16 (Cytochrome P450 Family 24)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160622
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.6b00170


  2 / 4 MEDLINE  
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[PMID]:27173620
[Au] Autor:Vuica A; Vukojevic K; Ferhatovic Hamzic L; Jeric M; Puljak L; Grkovic I; Filipovic N
[Ad] Endereço:Laboratory for Neurocardiology, Department of Anatomy, Histology and Embryology, University of Split School of Medicine, Croatia.
[Ti] Título:Expression pattern of CYP24 in liver during ageing in long-term diabetes.
[So] Source:Acta Histochem;118(5):486-95, 2016 Jun.
[Is] ISSN:1618-0372
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Association of liver calcitriol (active vitamin D metabolite) catabolism with osteomalacia during prolonged use of certain drugs was reported in several recent studies. To examine whether the increased calcitriol catabolism could be a potential link between ageing/diabetes mellitus (DM) and bone loss, we studied the dynamic of expression of CYP24, the main calcitriol catabolising enzyme in the liver of rats during ageing and a long-term experimental DM1. DM1 model was induced with intraperitoneally injected streptozotocin (STZ) (55mg/kg). Sprague-Dawley rats were sacrificed 6 and 12 months after the DM1 induction. The immunohistochemical analyses of CYP24 and transforming growth factor ß 1 (TGF-ß1) expression in the liver were performed. We found that ageing and long-term DM1 resulted in a significantly increased expression of CYP24 in hepatocytes, as well as in non-hepatocyte liver cells (Kupffer cells, hepatic stellate cells and sinusoidal endothelial cells). Ageing and long-term DM1 resulted in an increased expression of TGF-ß1 as well. Expression of CYP24 coexisted with the expression of TGF-ß1 in all types of hepatic cells. We concluded that liver has the capacity for an active vitamin D catabolism in different populations of liver cells, especially in sinusoidal endothelial cells, through an expression of CYP24. That capacity is substantially increased during ageing and long-term diabetes mellitus. Increased liver calcitriol catabolism could be one of the mechanisms of the bone metabolism impairment related to ageing and diabetes.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Família 24 do Citocromo P450/metabolismo
Diabetes Mellitus Experimental/enzimologia
Fígado/enzimologia
[Mh] Termos MeSH secundário: Animais
Fígado/patologia
Masculino
Ratos Sprague-Dawley
Fator de Crescimento Transformador beta1/fisiologia
Vitamina D/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tgfb1 protein, rat); 0 (Transforming Growth Factor beta1); 1406-16-2 (Vitamin D); EC 1.14.15.16 (Cytochrome P450 Family 24)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170116
[Lr] Data última revisão:
170116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160514
[St] Status:MEDLINE


  3 / 4 MEDLINE  
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[PMID]:26567049
[Au] Autor:Wang L; Gao Z; Wang L; Gao Y
[Ad] Endereço:Division of Blood Purification, The Second Hospital of Hebei Medical University, No. 215 Peace Road, Shijiazhuang, 053000, Hebei, China.
[Ti] Título:Upregulation of nuclear factor-κB activity mediates CYP24 expression and reactive oxygen species production in indoxyl sulfate-induced chronic kidney disease.
[So] Source:Nephrology (Carlton);21(9):774-81, 2016 Sep.
[Is] ISSN:1440-1797
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:AIM: Chronic kidney disease (CKD) is associated with an inflammation-mediated process, and the vitamin D (3) catabolizing enzyme, CYP24, is frequently overexpressed in CKD, where it may play a crucial role in kidney disease. METHODS: Herein, in this study, we investigated CYP24, reactive oxygen species (ROS), and inflammatory responses in an indoxyl sulfate (IS)-induced CKD model to elucidate the role of CYP24 in CKD. RESULTS: Our results showed that IS upregulates proinflammatory cytokine, CYP24 and nuclear factor-κB (NF-κB) expression in human renal proximal tubule epithelial cells. In addition, IS treatment increased ROS production and simultaneously upregulated CYP24 expression and NF-κB translocation. Moreover, the IS-induced upregulation of CYP24 expression was alleviated by an inhibitor of NF-κB, as well as a siRNA specific to NF-κB p65. Furthermore, the renal cortex of DN (Dahl salt-resistant normotensive) + IS, DH (Dahl salt-sensitive hypertensive), and DH + IS rats showed increased expression of NF-κB p65, CYP24, 8-hydroxydeoxyguanosine (8-OHdG), a marker of ROS and macrophage infiltration compared with DN rats. CONCLUSIONS: These results provide evidence that administration of IS in human renal tubular epithelial cells upregulates NF-κB, which leads to increase CYP24 expression and ROS production. They also suggest that suppressing NF-κB signalling is promising for the development into a strategy for CKD treatment.
[Mh] Termos MeSH primário: Família 24 do Citocromo P450/metabolismo
Indicã/toxicidade
Rim/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Insuficiência Renal Crônica/induzido quimicamente
Fator de Transcrição RelA/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Família 24 do Citocromo P450/genética
Citocinas/metabolismo
Desoxiguanosina/análogos & derivados
Desoxiguanosina/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Seres Humanos
Hipertensão/complicações
Mediadores da Inflamação/metabolismo
Rim/enzimologia
Interferência de RNA
Ratos Endogâmicos Dahl
Insuficiência Renal Crônica/enzimologia
Insuficiência Renal Crônica/genética
Fator de Transcrição RelA/genética
Transfecção
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (RELA protein, human); 0 (Reactive Oxygen Species); 0 (Rela protein, rat); 0 (Transcription Factor RelA); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); EC 1.14.15.16 (Cytochrome P450 Family 24); G9481N71RO (Deoxyguanosine); N187WK1Y1J (Indican)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170227
[Lr] Data última revisão:
170227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151115
[St] Status:MEDLINE
[do] DOI:10.1111/nep.12673


  4 / 4 MEDLINE  
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[PMID]:26361014
[Au] Autor:van der Meijden K; Buskermolen J; van Essen HW; Schuurman T; Steegenga WT; Brouwer-Brolsma EM; Langenbach GEJ; van Ruijven LJ; den Heijer M; Lips P; Bravenboer N
[Ad] Endereço:Department of Endocrinology/Internal Medicine, VU University Medical Center, MOVE Research Institute, Amsterdam, The Netherlands.
[Ti] Título:Long-term vitamin D deficiency in older adult C57BL/6 mice does not affect bone structure, remodeling and mineralization.
[So] Source:J Steroid Biochem Mol Biol;164:344-352, 2016 Nov.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Animal models show that vitamin D deficiency may have severe consequences for skeletal health. However, most studies have been performed in young rodents for a relatively short period, while in older adult rodents the effects of long-term vitamin D deficiency on skeletal health have not been extensively studied. Therefore, the first aim of this study was to determine the effects of long-term vitamin D deficiency on bone structure, remodeling and mineralization in bones from older adult mice. The second aim was to determine the effects of long-term vitamin D deficiency on mRNA levels of genes involved in vitamin D metabolism in bones from older adult mice. Ten months old male C57BL/6 mice were fed a diet containing 0.5% calcium, 0.2% phosphate and 0 (n=8) or 1 (n=9) IU vitamin D /gram for 14 months. At an age of 24 months, mice were sacrificed for histomorphometric and micro-computed tomography (micro-CT) analysis of humeri as well as analysis of CYP27B1, CYP24 and VDR mRNA levels in tibiae and kidneys using RT-qPCR. Plasma samples, obtained at 17 and 24 months of age, were used for measurements of 25-hydroxyvitamin D (25(OH)D) (all samples), phosphate and parathyroid hormone (PTH) (terminal samples) concentrations. At the age of 17 and 24 months, mean plasma 25(OH)D concentrations were below the detection limit (<4nmol/L) in mice receiving vitamin D deficient diets. Plasma phosphate and PTH concentrations did not differ between both groups. Micro-CT and histomorphometric analysis of bone mineral density, structure and remodeling did not reveal differences between control and vitamin D deficient mice. Long-term vitamin D deficiency did also not affect CYP27B1 mRNA levels in tibiae, while CYP24 mRNA levels in tibiae were below the detection threshold in both groups. VDR mRNA levels in tibiae from vitamin D deficient mice were 0.7 fold lower than those in control mice. In conclusion, long-term vitamin D deficiency in older adult C57BL/6 mice, accompanied by normal plasma PTH and phosphate concentrations, does not affect bone structure, remodeling and mineralization. In bone, expression levels of CYP27B1 are also not affected by long-term vitamin D deficiency in older adult C57BL/6 mice. Our results suggest that mice at old age have a low or absent response to vitamin D deficiency probably due to factors such as a decreased bone formation rate or a reduced response of bone cells to 25(OH)D and 1,25(OH) D. Older adult mice may therefore be less useful for the study of the effects of vitamin D deficiency on bone health in older people.
[Mh] Termos MeSH primário: Calcificação Fisiológica/genética
Calcitriol/deficiência
Úmero/metabolismo
Osteogênese/genética
Tíbia/metabolismo
Deficiência de Vitamina D/metabolismo
[Mh] Termos MeSH secundário: 25-Hidroxivitamina D3 1-alfa-Hidroxilase/genética
25-Hidroxivitamina D3 1-alfa-Hidroxilase/metabolismo
Animais
Densidade Óssea
Calcitriol/sangue
Família 24 do Citocromo P450/genética
Família 24 do Citocromo P450/metabolismo
Regulação da Expressão Gênica
Úmero/anatomia & histologia
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Hormônio Paratireóideo/sangue
Fosfatos/sangue
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Calcitriol/genética
Receptores de Calcitriol/metabolismo
Tíbia/anatomia & histologia
Vitamina D/análogos & derivados
Vitamina D/sangue
Deficiência de Vitamina D/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Parathyroid Hormone); 0 (Phosphates); 0 (RNA, Messenger); 0 (Receptors, Calcitriol); 1406-16-2 (Vitamin D); 64719-49-9 (25-hydroxyvitamin D); EC 1.14.13.13 (25-Hydroxyvitamin D3 1-alpha-Hydroxylase); EC 1.14.15.16 (Cytochrome P450 Family 24); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150912
[St] Status:MEDLINE



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