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[PMID]:28463086
[Au] Autor:Mann EH; Ho TR; Pfeffer PE; Matthews NC; Chevretton E; Mudway I; Kelly FJ; Hawrylowicz CM
[Ad] Endereço:1 MRC and Asthma-UK Centre for Allergic Mechanisms in Asthma, and.
[Ti] Título:Vitamin D Counteracts an IL-23-Dependent IL-17A IFN-γ Response Driven by Urban Particulate Matter.
[So] Source:Am J Respir Cell Mol Biol;57(3):355-366, 2017 09.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health. This is hypothesized to be due in part to regulation of IL-17A, which UPM is reported to promote. Here, we used a myeloid dendritic cell (DC)-memory CD4 T cell co-culture system to characterize UPM-driven IL-17A cells, investigate the mechanism by which UPM-primed DCs promote this phenotype, and address evidence for cross-regulation by vitamin D. CD1c myeloid DCs were cultured overnight with or without a reference source of UPM and/or active vitamin D (1,25[OH] D ) before they were co-cultured with autologous memory CD4 T cells. Supernatants were harvested for cytokine analysis on Day 5 of co-culture, and intracellular cytokine staining was performed on Day 7. UPM-primed DCs increased the proportion of memory CD4 T cells expressing the T helper 17 cell (Th17)-associated cytokines IL-17A, IL-17F, and IL-22, as well as IFN-γ, granulocyte-macrophage colony-stimulating factor, and granzyme B. Notably, a large proportion of the UPM-driven IL-17A cells co-expressed these cytokines, but not IL-10, indicative of a proinflammatory Th17 profile. UPM-treated DCs expressed elevated levels of il23 mRNA and increased secretion of IL-23p40. Neutralization of IL-23 in culture reduced the frequency of IL-17A IFN-γ cells without affecting cell proliferation. 1,25(OH) D counteracted the UPM-driven DC maturation and inhibited the frequency of IL-17A IFN-γ cells, most prominently when DCs were co-treated with the corticosteroid dexamethasone, while maintaining antiinflammatory IL-10 synthesis. These data indicate that UPM might promote an inflammatory milieu in part by inducing an IL-23-driven proinflammatory Th17 response. Restoring vitamin D sufficiency may counteract these UPM-driven effects without obliterating important homeostatic immune functions.
[Mh] Termos MeSH primário: Cidades
Interferon gama/metabolismo
Interleucina-17/metabolismo
Interleucina-23/metabolismo
Material Particulado/toxicidade
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Calcitriol/farmacologia
Diferenciação Celular/efeitos dos fármacos
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Dexametasona/farmacologia
Seres Humanos
Células Mieloides/efeitos dos fármacos
Células Mieloides/metabolismo
Fenótipo
Células Th17/imunologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Particulate Matter); 1406-16-2 (Vitamin D); 7S5I7G3JQL (Dexamethasone); 82115-62-6 (Interferon-gamma); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0409OC


  2 / 13518 MEDLINE  
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[PMID]:29366785
[Au] Autor:Ryan ZC; Craig TA; Wang X; Delmotte P; Salisbury JL; Lanza IR; Sieck GC; Kumar R
[Ad] Endereço:Department of Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
[Ti] Título:1α,25-dihydroxyvitamin D mitigates cancer cell mediated mitochondrial dysfunction in human skeletal muscle cells.
[So] Source:Biochem Biophys Res Commun;496(2):746-752, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cachexia is associated with muscle weakness and atrophy. We investigated whether 1α,25-dihydroxyvitamin D (1α,25(OH) D ), which has previously been shown to increase skeletal myoblast oxygen consumption rate, could reverse the deleterious effects of tumor cell conditioned medium on myoblast function. Conditioned medium from Lewis lung carcinoma (LLC1) cells inhibits oxygen consumption, increases mitochondrial fragmentation, inhibits pyruvate dehydrogenase activity, and enhances proteasomal activity in human skeletal muscle myoblasts. 1α,25(OH) D reverses the tumor cell-mediated changes in mitochondrial oxygen consumption and proteasomal activity, without changing pyruvate dehydrogenase activity. 1α,25(OH) D might be useful in treatment of weakness seen in association with CC.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Mitocôndrias/efeitos dos fármacos
Debilidade Muscular/tratamento farmacológico
Debilidade Muscular/etiologia
Mioblastos Esqueléticos/efeitos dos fármacos
Neoplasias/complicações
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Lewis/complicações
Carcinoma Pulmonar de Lewis/metabolismo
Carcinoma Pulmonar de Lewis/patologia
Linhagem Celular
Linhagem Celular Tumoral
Seres Humanos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Debilidade Muscular/metabolismo
Debilidade Muscular/patologia
Mioblastos Esqueléticos/metabolismo
Mioblastos Esqueléticos/patologia
Neoplasias/metabolismo
Neoplasias/patologia
Consumo de Oxigênio/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Vitamins); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


  3 / 13518 MEDLINE  
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[PMID]:28458359
[Au] Autor:Takeda H; Tominari T; Hirata M; Watanabe K; Matsumoto C; Grundler FMW; Inada M; Miyaura C
[Ad] Endereço:Cooperative Major of Advanced Health Science, Tokyo University of Agriculture and Technology.
[Ti] Título:Lutein Enhances Bone Mass by Stimulating Bone Formation and Suppressing Bone Resorption in Growing Mice.
[So] Source:Biol Pharm Bull;40(5):716-721, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Lutein is a member of the xanthophyll family of carotenoids, which are known to prevent hypoxia-induced cell damage in the eye by removing free radicals. However, its role in other tissues is controversial, and the effects of lutein on bone tissues are unknown. To identify a possible role of lutein in bone tissues, we examined the effects of lutein on bone formation and bone resorption and on femoral bone mass in mice. Lutein enhanced the formation of mineralized bone nodules in cultures of osteoblasts. On the other hand, lutein clearly suppressed 1α, 25-dihydroxyvitamin D -induced bone resorption as measured by pit formation in organ culture of mouse calvaria. In co-cultures of bone marrow cells and osteoblasts, lutein suppressed 1α, 25-dihydroxyvitamin D -induced osteoclast formation. In cultures of bone marrow macrophages, lutein suppressed soluble RANKL, the receptor activator of nuclear factor-kappaB (NF-κB) ligand, induced osteoclast formation. When five-week-old male mice were orally administered lutein for 4 weeks, the femoral bone mass was clearly enhanced in cortical bone, as measured by bone mineral density in dual X-ray absorptiometry and micro computed tomography (µCT) analyses. The present study indicates that lutein enhances bone mass in growing mice by suppressing bone resorption and stimulating bone formation. Lutein may be a natural agent that promotes bone turnover and may be beneficial for bone health in humans.
[Mh] Termos MeSH primário: Desenvolvimento Ósseo/efeitos dos fármacos
Reabsorção Óssea/prevenção & controle
Osso e Ossos/anatomia & histologia
Luteína/farmacologia
[Mh] Termos MeSH secundário: Absorciometria de Fóton
Animais
Densidade Óssea/efeitos dos fármacos
Osso e Ossos/diagnóstico por imagem
Calcificação Fisiológica/efeitos dos fármacos
Calcitriol/antagonistas & inibidores
Calcitriol/farmacologia
Células Cultivadas
Fêmur/anatomia & histologia
Fêmur/efeitos dos fármacos
Luteína/uso terapêutico
Masculino
Camundongos
NF-kappa B/antagonistas & inibidores
Osteoblastos/efeitos dos fármacos
Ligante RANK/antagonistas & inibidores
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse); FXC9231JVH (Calcitriol); X72A60C9MT (Lutein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00897


  4 / 13518 MEDLINE  
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[PMID]:29374758
[Au] Autor:Friedrich M; Reichert K; Woeste A; Polack S; Fischer D; Hoellen F; Rody A; Köster F; Thill M
[Ad] Endereço:Department of Gynecology and Obstetrics, Helios Hospital Krefeld, Krefeld, Germany michael.friedrich@helios-kliniken.de.
[Ti] Título:Effects of Combined Treatment with Vitamin D and COX2 Inhibitors on Breast Cancer Cell Lines.
[So] Source:Anticancer Res;38(2):1201-1207, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Vitamin D is known for its anticancer potential. Prostaglandin E (PGE ) is a proliferative and inflammation-activating agent. The production of PGE is dependent on the activity of cyclooxygenase-2 (COX2). A link between vitamin D and PGE metabolism was shown recently. MATERIALS AND METHODS: In MDA-MB-231 and MCF-7 breast cancer cell lines, we investigated the influence of calcitriol and the COX2 inhibitor celecoxib on cell growth via the MTT test, as well as on the protein and mRNA expression of COX2 using western blot and quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: The proliferation of MCF-7 and MDA-MB-231 was inhibited by both calcitriol and the COX2 inhibitor celecoxib and even more strongly by their combination. Moreover, calcitriol inhibited COX2 protein expression in MDA-MB-231 cells, as well as COX2 mRNA expression in both cell lines. CONCLUSION: The combination of calcitriol and celecoxib demonstrated a synergistic growth-inhibitory effect in breast cancer cell lines.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Calcitriol/farmacologia
Celecoxib/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Neoplasias da Mama/tratamento farmacológico
Proliferação Celular/efeitos dos fármacos
Quimioterapia Combinada
Feminino
Seres Humanos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclooxygenase 2 Inhibitors); 0 (Vitamins); FXC9231JVH (Calcitriol); JCX84Q7J1L (Celecoxib)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  5 / 13518 MEDLINE  
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[PMID]:29272316
[Au] Autor:Jamali N; Wang S; Darjatmoko SR; Sorenson CM; Sheibani N
[Ad] Endereço:Departments of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States of America.
[Ti] Título:Vitamin D receptor expression is essential during retinal vascular development and attenuation of neovascularization by 1, 25(OH)2D3.
[So] Source:PLoS One;12(12):e0190131, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vitamin D provides a significant benefit to human health, and its deficiency has been linked to a variety of diseases including cancer. Vitamin D exhibits anticancer effects perhaps through inhibition of angiogenesis. We previously showed that the active form of vitamin D (1, 25(OH)2D3; calcitriol) is a potent inhibitor of angiogenesis in mouse model of oxygen-induced ischemic retinopathy (OIR). Many of vitamin D's actions are mediated through vitamin D receptor (VDR). However, the role VDR expression plays in vascular development and inhibition of neovascularization by 1, 25(OH)2D3 remains unknown. Here using wild type (Vdr +/+) and Vdr-deficient (Vdr -/-) mice, we determined the impact of Vdr expression on postnatal development of retinal vasculature and retinal neovascularization during OIR. We observed no significant effect on postnatal retinal vascular development in Vdr -/- mice up to postnatal day 21 (P21) compared with Vdr +/+ mice. However, we observed an increase in density of pericytes (PC) and a decrease in density of endothelial cells (EC) in P42 Vdr -/- mice compared with Vdr +/+ mice, resulting in a significant decrease in the EC/PC ratio. Although we observed no significant impact on vessel obliteration and retinal neovascularization in Vdr -/- mice compared with Vdr +/+ mice during OIR, the VDR expression was essential for inhibition of retinal neovascularization by 1, 25(OH)2D3. In addition, the adverse impact of 1, 25(OH)2D3 treatment on the mouse bodyweight was also dependent on VDR expression. Thus, VDR expression plays a significant role during retinal vascular development, especially during maturation of retinal vasculature by promoting PC quiescence and EC survival, and inhibition of ischemia-mediated retinal neovascularization by 1, 25(OH)2D3.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Receptores de Calcitriol/metabolismo
Neovascularização Retiniana/prevenção & controle
Vasos Retinianos/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Receptors, Calcitriol); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190131


  6 / 13518 MEDLINE  
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[PMID]:29182680
[Au] Autor:Ahrens JM; Jones JD; Nieves NJ; Mitzey AM; DeLuca HF; Clagett-Dame M
[Ad] Endereço:Biochemistry Department, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
[Ti] Título:Differential activity of 2-methylene-19-nor vitamin D analogs on growth factor gene expression in rhino mouse skin and comparison to all-trans retinoic acid.
[So] Source:PLoS One;12(11):e0188887, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While all 2-methylene-19-nor analogs of 1α,25-dihydroxyvitamin D3 (1α,25(OH)2D3) tested produce an increase in epidermal thickness in the rhino mouse, only a subset reduce utricle size (comedolysis). All-trans retinoic acid (atRA) also causes epidermal thickening and a reduction in utricle size in the rhino mouse. We now report that 2-methylene-19-nor-(20S)-1α-hydroxybishomopregnacalciferol (2MbisP), a comedolytic analog, increases epidermal thickening more rapidly than does atRA, while both reduce utricle area at an equal rate. Whereas unlike atRA, 2MbisP does not alter the epidermal growth factor receptor ligand, heparin-binding epidermal growth factor-like growth factor, it does increase the expression of both amphiregulin and epigen mRNA, even after a single dose. In situ hybridization reveals an increase in these transcripts throughout the closing utricle as well as in the interfollicular epidermis. The mRNAs for other EGFR ligands including betacellulin and transforming growth factor-α, as well as the epidermal growth factor receptor are largely unaffected by 2MbisP. Another analog, 2-methylene-19-nor-(20S)-26,27-dimethylene-1α,25-dihydroxyvitamin D3 (CAGE-3), produces epidermal thickening but fails to reduce utricle size or increase AREG mRNA levels. CAGE-3 modestly increases epigen mRNA levels, but only after 5 days of dosing. Thus, 2-MbisP produces unique changes in epidermal growth factor receptor ligand mRNAs that may be responsible for both epidermal proliferation and a reduction in utricle size.
[Mh] Termos MeSH primário: Calcitriol/análogos & derivados
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Pele/efeitos dos fármacos
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Animais
Calcitriol/química
Calcitriol/farmacologia
Feminino
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/metabolismo
Ligantes
Masculino
Camundongos
RNA Mensageiro/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptores de Calcitriol/metabolismo
Pele/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-methylene-1,25-dihydroxy-19-norvitamin D3); 0 (Heparin-binding EGF-like Growth Factor); 0 (Ligands); 0 (RNA, Messenger); 0 (Receptors, Calcitriol); 5688UTC01R (Tretinoin); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188887


  7 / 13518 MEDLINE  
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[PMID]:29187432
[Au] Autor:Kuittinen T; Rovio P; Staff S; Luukkaala T; Kallioniemi A; Grénman S; Laurila M; Mäenpää J
[Ad] Endereço:Department of Obstetrics and Gynaecology, Tampere University Hospital, Tampere, Finland tea.kuittinen@xfimnet.fi.
[Ti] Título:Paclitaxel, Carboplatin and 1,25-D3 Inhibit Proliferation of Endometrial Cancer Cells .
[So] Source:Anticancer Res;37(12):6575-6581, 2017 12.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Endometrial cancer cells are known to be sensitive to carboplatin and paclitaxel. Furthermore, vitamin D (1,25-D3) has been reported to inhibit endometrial cancer cell growth both as a single agent and combined with carboplatin. However, there are no studies comparing the effect of paclitaxel and carboplatin as single agents vs. in combination in endometrial cancer cell lines. Neither has the effect of 1,25-D3 been studied with paclitaxel. The present study investigated the effect of paclitaxel, carboplatin and 1,25-D3 on the growth of endometrial cancer cells in vitro. MATERIALS AND METHODS: Two endometrial adenocarcinoma cell lines (UT-EC-1 and UT-EC-3) were cultured with different doses of paclitaxel, carboplatin and 1,25-D3. The cellular VDR (vitamin D receptor) mRNA levels were measured and the expression of estrogen (ER) and progesterone (PR) receptors by the cells was determined. RESULTS: In the UT-EC-1 cell line the growth inhibition was 72% with paclitaxel, 54% with carboplatin and 73% with the combination of these compounds. The corresponding numbers in UT-EC-3 were 70%, 33% and 65%, respectively. 1,25-D3 suppressed cell growth 88% with paclitaxel, 63% with carboplatin and 87% with their combination in the UT-EC-1 cell line. CONCLUSION: In both cell lines, single-agent paclitaxel was as effective as the combination of the compounds and more effective than single carboplatin. 1,25-D3 may further contribute to the cytotoxic effect of these agents.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Carboplatina/farmacologia
Proliferação Celular/efeitos dos fármacos
Paclitaxel/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Sinergismo Farmacológico
Neoplasias do Endométrio/genética
Neoplasias do Endométrio/metabolismo
Neoplasias do Endométrio/patologia
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Receptores de Calcitriol/genética
Receptores Estrogênicos/genética
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/genética
Receptores de Progesterona/metabolismo
Vitaminas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Receptors, Calcitriol); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 0 (Vitamins); BG3F62OND5 (Carboplatin); FXC9231JVH (Calcitriol); P88XT4IS4D (Paclitaxel)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


  8 / 13518 MEDLINE  
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[PMID]:29042175
[Au] Autor:Trujillo V; Marín-Luevano P; González-Curiel I; Rodríguez-Carlos A; Ramírez-Reyes M; Layseca-Espinosa E; Enciso-Moreno JA; Díaz L; Rivas-Santiago B
[Ad] Endereço:Unidad de Investigación Biomédica-Zacatecas, IMSS, Mexico; Centro de Investigacion en Ciencias de la Salud y Biomedicina, Facultad de Medicina, Universidad Autónoma de San Luis Potosi, Mexico.
[Ti] Título:Calcitriol promotes proangiogenic molecules in keratinocytes in a diabetic foot ulcer model.
[So] Source:J Steroid Biochem Mol Biol;174:303-311, 2017 Nov.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Foot ulceration is one of the most common and complex sequelae of diabetes mellitus, generally posing a therapeutic challenge due to poor healing responses and high rates of complications, including peripheral vascular disease, ischemia and infections. Calcitriol, the most active vitamin D metabolite, induces antimicrobial peptides production in keratinocytes from diabetic foot ulcers (DFU); however, little is known about its effects on angiogenic factors in this pathology. Herein we aimed at studying whether calcitriol induces angiogenic molecules in keratinocytes under normoxic and hypoxic conditions, and if these molecules are able to improve cell migration in vitro. Evaluation of DFU samples by immunohistochemistry showed increased VEGF and decreased angiogenin and HIF-1α expression compared to controls, suggesting an altered pattern of angiogenic factors in DFU. Interestingly, incubation of keratinocytes with calcitriol significantly upregulated VEGFA, HIF-1α and angiogenin gene expression, while the resulting cell culture media stimulated both endothelial cells and keratinocytes migration in an in vitro wound closure assay under a normoxic environment (p<0.05). Moreover, the culture media of calcitriol-treated keratinocytes stimulated cell migration in a similar extent as exogenous VEGF or EGF in endothelial and keratinocytes cells. These results suggest that the altered profile of angiogenic molecules in DFU might be improved by local or systemic treatment with calcitriol under normoxic conditions, which could probably be achieved with hyperbaric oxygen therapy. Given that calcitriol not only augments proangiogenic factors but also induces antimicrobial peptides expression, this hormone should be further investigated in clinical trials of DFU.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Pé Diabético/metabolismo
Queratinócitos/efeitos dos fármacos
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Adulto
Linhagem Celular
Pé Diabético/genética
Feminino
Expressão Gênica
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Queratinócitos/metabolismo
Masculino
Meia-Idade
Neovascularização Fisiológica
Ribonuclease Pancreático/genética
Ribonuclease Pancreático/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
Cicatrização/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (Vitamins); EC 3.1.27.- (angiogenin); EC 3.1.27.5 (Ribonuclease, Pancreatic); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE


  9 / 13518 MEDLINE  
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[PMID]:28953655
[Au] Autor:Lu C; Zuo K; Lu Y; Liang S; Huang X; Zeng C; Zhang J; An Y; Wang J
[Ad] Endereço:Department of National Clinical Research Center of Kidney Disease, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
[Ti] Título:Apolipoprotein A-1-related amyloidosis 2 case reports and review of the literature.
[So] Source:Medicine (Baltimore);96(39):e8148, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Apolipoprotein A-1 (ApoA-1)-related amyloidosis is characterized by the deposition of ApoA-1 in various organs and can be either hereditary or nonhereditary. It is rare and easily misdiagnosed. Renal involvement is common in hereditary ApoA-1 amyloidosis, but rare in the nonhereditary form. PATIENT CONCERNS: We reported two cases with ApoA-1 amyloidosis, a 64-year-old man suffering from nephrotic syndrome and a 40-year-old man with nephrotic syndrome and splenomegaly. Renal biopsies revealed glomerular, interstitial and vascular amyloid deposits and positive phospholipase A2 receptor staining in the glomerular capillary loop in case 1, and mesangial amyloid deposits in case 2. DIAGNOSES: After immunostaining failed to determine the specific amyloid protein, proteomic analysis of amyloid deposits by mass spectrometry was performed and demonstrated the ApoA-1 origin of the amyloid. Genetic testing revealed no mutation of the APOA1 gene in case 1 but a heterozygous mutation, Trp74Arg, in case 2. Case 1 was thus diagnosed as nonhereditary ApoA-1 associated renal amyloidosis with membranous nephropathy, and case 2 as hereditary ApoA-1 amyloidosis with multiorgan injuries (kidney and spleen) and a positive family history. INTERVENTIONS: Case 1 was treated with glucocorticoid combined with cyclosporine. Case 2 was treated with calcitriol and angiotensin converting enzyme inhibitors. OUTCOMES: Two cases were followed up for 5 months and 2 years, respectively; and case 1 was found to have attenuated proteinuria while case 2 had an elevation of cholestasis indices along with renal insufficiency. LESSONS: Proteomic analysis by mass spectrometry of the amyloid deposits combined with genetic analysis can provide accurate diagnosis of ApoA-1 amyloidosis. Besides, these 2 cases expand our knowledge of ApoA-1-related renal amyloidosis.
[Mh] Termos MeSH primário: Amiloidose Familiar
Amiloidose
Apolipoproteína A-I/metabolismo
Rim/patologia
Síndrome Nefrótica
Placa Amiloide
Esplenomegalia
[Mh] Termos MeSH secundário: Adulto
Amiloidose/diagnóstico
Amiloidose/metabolismo
Amiloidose/fisiopatologia
Amiloidose Familiar/diagnóstico
Amiloidose Familiar/metabolismo
Amiloidose Familiar/fisiopatologia
Inibidores da Enzima Conversora de Angiotensina/administração & dosagem
Calcitriol/administração & dosagem
Agonistas dos Canais de Cálcio/administração & dosagem
Ciclosporina/administração & dosagem
Diagnóstico Diferencial
Inibidores Enzimáticos/administração & dosagem
Glucocorticoides/administração & dosagem
Seres Humanos
Imunossupressores/administração & dosagem
Masculino
Espectrometria de Massas/métodos
Conduta do Tratamento Medicamentoso
Meia-Idade
Síndrome Nefrótica/diagnóstico
Síndrome Nefrótica/etiologia
Seleção de Pacientes
Placa Amiloide/metabolismo
Placa Amiloide/patologia
Receptores da Fosfolipase A2/metabolismo
Esplenomegalia/diagnóstico
Esplenomegalia/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Apolipoprotein A-I); 0 (Calcium Channel Agonists); 0 (Enzyme Inhibitors); 0 (Glucocorticoids); 0 (Immunosuppressive Agents); 0 (Receptors, Phospholipase A2); 83HN0GTJ6D (Cyclosporine); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008148


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[PMID]:28926770
[Au] Autor:Zhou Q; Qin S; Zhang J; Zhon L; Pen Z; Xing T
[Ad] Endereço:Department of General Surgery, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200080, China.
[Ti] Título:1,25(OH) D induces regulatory T cell differentiation by influencing the VDR/PLC-γ1/TGF-ß1/pathway.
[So] Source:Mol Immunol;91:156-164, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Vitamin D has been recommended as an immune modulator in recent years, in addition to regulating calcium-phosphorous-bone metabolism. Clinical studies on organ transplantation found that vitamin D sufficiency patients were less likely to develop acute cellular rejection within one year after transplantation compared to those with vitamin D deficiency. Thus, a high percentage of regulatory T cells might play a key role in preventing acute cellular rejection (ACR). In this report, we studied the specific effects of 1,25(OH)2D3 on human T cell diff ;erentiation, and determined the potential molecule mechanism behind. Results showed that 1,25(OH)2D3 induced the differentiation of T-regulatory cells (Treg cells), while inhibiting Th17 cell proliferation. In addition, 1,25(OH)2D3 promoted secretion of the anti-inflammatory cytokine, transforming Growth Factor beta1 (TGF-ß1) but suppressed pro-inflammatory cytokines such as interleukin-17 (IL-17). Phospholipase C gamma 1 (PLC-γ1) is an indispensable signaling protein downstream of the classical TCR signaling pathway and was shown to play a crucial role in T cell activation, while Naive T cells expressed less PLC-γ1. Here we showed that Vitamin D could significantly upregulate PLC-γ1 expression, which then induced expression of TGF-ß1. In summary, 1,25(OH)2D3 indirectly modulates the differentiation of Treg/Th17 cells by aff ;ecting the VDR/PLC-γ1/TGF-ß1pathway. These results indicate that administration 1,25(OH)2D3 supplements may be a beneficial treatment for organ transplantation recipients.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Diferenciação Celular/efeitos dos fármacos
Fosfolipase C gama/imunologia
Receptores de Calcitriol/imunologia
Transdução de Sinais/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Fator de Crescimento Transformador beta1/imunologia
[Mh] Termos MeSH secundário: Diferenciação Celular/genética
Diferenciação Celular/imunologia
Seres Humanos
Células Jurkat
Fosfolipase C gama/genética
Receptores de Calcitriol/genética
Transdução de Sinais/genética
Transdução de Sinais/imunologia
Células Th17/imunologia
Fator de Crescimento Transformador beta1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Calcitriol); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); EC 3.1.4.11 (PLCG1 protein, human); EC 3.1.4.3 (Phospholipase C gamma); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE



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