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[PMID]:28177365
[Au] Autor:Muscher-Banse AS; Marholt L; Eigendorf N; Wilkens MR; Schröder B; Breves G; Cehak A
[Ti] Título:Segmental diversity of phosphate transport along the intestinal axis in horses.
[So] Source:J Anim Sci;95(1):165-172, 2017 Jan.
[Is] ISSN:1525-3163
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:For horses, distinct differences in intestinal phosphate transport have been postulated to account for the unique features of hind gut fermentation compared to other monogastric animals and ruminants. So far published data on mechanisms and underlying transport proteins involved in intestinal phosphate transport in the horse are still missing. Therefore we investigated intestinal phosphate transport in horses at both functional and molecular levels. Segmental diversity of intestinal phosphate transport along the intestinal axis was documented using the Ussing chamber technique. A transcellular phosphate secretion in the jejunum was confirmed. Furthermore, 2 sodium-dependent phosphate cotransporters, NaPiIIb and PiT1, were first detected in the equine intestine at mRNA level with PiT1 being expressed in both the small and large intestine, and NaPiIIb being solely expressed in the large intestine. In the colon, unidirectional net flux rates of phosphate were significantly greater compared to flux rates in other segments ( < 0.005) suggesting the colon as a major site for phosphate absorption in horses. Phosphate transport in the colon was mainly transcellular and mediated by a sodium-gradient as documented by Ussing chamber experiments and uptake of phosphate into colonic brush border membrane vesicles. In summary, the present study demonstrated mechanisms and transporters of intestinal phosphate transport in equine intestinal tissues with distinct differences between intestinal segments providing a new basis for a better understanding of intestinal phosphate transport in horses.
[Mh] Termos MeSH primário: Cavalos/fisiologia
Absorção Intestinal/fisiologia
Transporte de Íons/fisiologia
Fosfatos/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica/fisiologia
Intestinos/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphates); 0 (RNA, Messenger); 0 (Sodium-Phosphate Cotransporter Proteins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.2527/jas.2016.0939


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[PMID]:28049945
[Au] Autor:Shima K; Tsuchiya M; Oizumi T; Takano-Yamamoto T; Sugawara S; Endo Y
[Ad] Endereço:Division of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Tohoku University.
[Ti] Título:Inflammatory Effects of Nitrogen-Containing Bisphosphonates (N-BPs): Modulation by Non-N-BPs.
[So] Source:Biol Pharm Bull;40(1):25-33, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Bisphosphonates (BPs) are used against diseases with enhanced bone resorption. Those classed as nitrogen-containing BPs (N-BPs) exhibit much stronger anti-bone-resorptive effects than non-nitrogen-containing BPs (non-N-BPs). However, N-BPs carry the risk of inflammatory/necrotic side effects. Depending on their side-chains, BPs are divided structurally into cyclic and non-cyclic types. We previously found in mice that etidronate and clodronate (both non-cyclic non-N-BPs) could reduce the inflammatory effects of all three N-BPs tested (cyclic and non-cyclic types), possibly by inhibiting their entry into soft-tissue cells via SLC20 and/or SLC34 phosphate transporters. Tiludronate is the only available cyclic non-N-BP, but its effects on N-BPs' side effects have not been examined. Here, we compared the effects of etidronate, clodronate, and tiludronate on the inflammatory effects of six N-BPs used in Japan [three cyclic (risedronate, zoledronate, minodronate) and three non-cyclic (pamidronate, alendronate, ibandronate)]. Inflammatory effects were evaluated in mice by measuring the hind-paw-pad swelling induced by subcutaneous injection of an N-BP (either alone or mixed with a non-N-BP) into the hind-paw-pad. All of six N-BPs tested induced inflammation. Etidronate, clodronate, and the SLC20/34 inhibitor phosphonoformate inhibited this inflammation. Tiludronate inhibited the inflammatory effects of all N-BPs except ibandronate and minodronate, which have higher molecular weights than the other N-BPs. The mRNAs of SLC20a1, SLC20a2, and SLC34a2 (but not of SLC34a1 and SLC34a3) were detected in the soft-tissues of hind-paw-pads. These results suggest that etidronate, clodronate, and phosphonoformate may act non-selectively on phosphate transporter members, while tiludronate may not act on those transporting N-BPs of higher molecular weights.
[Mh] Termos MeSH primário: Difosfonatos/efeitos adversos
Difosfonatos/uso terapêutico
Edema/induzido quimicamente
Edema/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Reabsorção Óssea/tratamento farmacológico
Difosfonatos/farmacologia
Edema/metabolismo
Masculino
Camundongos
Nitrogênio
RNA Mensageiro/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diphosphonates); 0 (RNA, Messenger); 0 (Sodium-Phosphate Cotransporter Proteins); N762921K75 (Nitrogen)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170203
[Lr] Data última revisão:
170203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170105
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00521


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[PMID]:27956087
[Au] Autor:Vieira-Bernardo R; Gomes-Vieira AL; Carvalho-Kelly LF; Russo-Abrahão T; Meyer-Fernandes JR
[Ad] Endereço:Laboratório de Bioquímica Celular, Instituto de Bioquímica Médica Leopoldo de Meis, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
[Ti] Título:The biochemical characterization of two phosphate transport systems in Phytomonas serpens.
[So] Source:Exp Parasitol;173:1-8, 2017 Feb.
[Is] ISSN:1090-2449
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inorganic phosphate (P ) is an essential nutrient for all organisms because it is required for a variety of biochemical processes, such as signal transduction and the synthesis of phosphate-containing biomolecules. Assays of P uptake performed in the absence or in the presence of Na indicated the existence of a Na -dependent and a Na -independent P transporter in Phytomonas serpens. Phylogenetic analysis of two hypothetical protein sequences of Phytomonas (EM1) showed similarities to the high-affinity P transporters of Saccharomyces cerevisiae: Pho84, a Na -independent P transporter, and Pho89, a Na -dependent P transporter. Plasma membrane depolarization by FCCP, an H ionophore, strongly decreased P uptake via both Na -independent and Na -dependent carriers, indicating that a membrane potential is essential for P influx. In addition, the furosemide-sensitive Na -pump activity in the cells grown in low P conditions was found to be higher than the activity detected in the plasma membrane of cells cultivated at high P concentration, suggesting that the up-regulation of the Na -ATPase pump could be related to the increase of P uptake by the Pho89p Na :P symporter. Here we characterize for the first time two inorganic phosphate transporters powered by Na and H gradients and activated by low P availability in the phytopathogen P. serpens.
[Mh] Termos MeSH primário: Fosfatos/metabolismo
Simportadores de Próton-Fosfato/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/metabolismo
Trypanosomatina/metabolismo
[Mh] Termos MeSH secundário: Adenosina Trifosfatases/genética
Adenosina Trifosfatases/metabolismo
Proteínas de Transporte de Cátions/genética
Proteínas de Transporte de Cátions/metabolismo
Hidrogênio/metabolismo
Concentração de Íons de Hidrogênio
Transporte de Íons
Cinética
Potenciais da Membrana
Simportadores de Próton-Fosfato/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA de Protozoário/genética
RNA de Protozoário/metabolismo
Sódio/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/genética
Trypanosomatina/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cation Transport Proteins); 0 (Phosphates); 0 (Proton-Phosphate Symporters); 0 (RNA, Messenger); 0 (RNA, Protozoan); 0 (Sodium-Phosphate Cotransporter Proteins); 7YNJ3PO35Z (Hydrogen); 9NEZ333N27 (Sodium); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (sodium-translocating ATPase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161214
[St] Status:MEDLINE


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[PMID]:27150146
[Au] Autor:Shima K; Nemoto W; Tsuchiya M; Tan-No K; Takano-Yamamoto T; Sugawara S; Endo Y
[Ad] Endereço:Division of Oral Molecular Regulation, Graduate School of Dentistry, Tohoku University.
[Ti] Título:The Bisphosphonates Clodronate and Etidronate Exert Analgesic Effects by Acting on Glutamate- and/or ATP-Related Pain Transmission Pathways.
[So] Source:Biol Pharm Bull;39(5):770-7, 2016.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Bisphosphonates (BPs) are typical anti-bone-resorptive drugs, with nitrogen-containing BPs (N-BPs) being stronger than non-nitrogen-containing BPs (non-N-BPs). However, N-BPs have inflammatory/necrotic effects, while the non-N-BPs clodronate and etidronate lack such side effects. Pharmacological studies have suggested that clodronate and etidronate can (i) prevent the side effects of N-BPs in mice via inhibition of the phosphate transporter families SLC20 and/or SLC34, through which N-BPs enter soft-tissue cells, and (ii) also inhibit the phosphate transporter family SLC17. Vesicular transporters for the pain transmitters glutamate and ATP belong to the SLC17 family. Here, we examined the hypothesis that clodronate and etidronate may enter neurons through SLC20/34, then inhibit SLC17-mediated transport of glutamate and/or ATP, resulting in their decrease, and thereby produce analgesic effects. We analyzed in mice the effects of various agents [namely, intrathecally injected clodronate, etidronate, phosphonoformic acid (PFA; an inhibitor of SLC20/34), and agonists of glutamate and ATP receptors] on the nociceptive responses to intraplantar injection of capsaicin. Clodronate and etidronate produced analgesic effects, and these effects were abolished by PFA. The analgesic effects were reduced by N-methyl-D-aspartate (agonist of the NMDA receptor, a glutamate receptor) and α,ß-methylene ATP (agonist of the P2X-receptor, an ATP receptor). SLC20A1, SLC20A2, and SLC34A1 were detected within the mouse lumbar spinal cord. Although we need direct evidence, these results support the above hypothesis. Clodronate and etidronate may be representatives of a new type of analgesic drug. Such drugs, with both anti-bone-resorptive and unique analgesic effects without the adverse effects associated with N-BPs, might be useful for osteoporosis.
[Mh] Termos MeSH primário: Analgésicos
Ácido Clodrônico
Ácido Etidrônico
Dor/tratamento farmacológico
[Mh] Termos MeSH secundário: Ácido Acético
Trifosfato de Adenosina/análogos & derivados
Trifosfato de Adenosina/metabolismo
Trifosfato de Adenosina/farmacologia
Analgésicos/farmacologia
Analgésicos/uso terapêutico
Animais
Conservadores da Densidade Óssea/farmacologia
Conservadores da Densidade Óssea/uso terapêutico
Capsaicina
Ácido Clodrônico/farmacologia
Ácido Clodrônico/uso terapêutico
Ácido Etidrônico/farmacologia
Ácido Etidrônico/uso terapêutico
Agonistas de Aminoácidos Excitatórios/farmacologia
Foscarnet/farmacologia
Ácido Glutâmico/metabolismo
Vértebras Lombares
Camundongos
Camundongos Endogâmicos BALB C
N-Metilaspartato/farmacologia
Dor/induzido quimicamente
Dor/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/genética
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
Substância P/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Bone Density Conservation Agents); 0 (Excitatory Amino Acid Agonists); 0 (Sodium-Phosphate Cotransporter Proteins); 0813BZ6866 (Clodronic Acid); 33507-63-0 (Substance P); 364P9RVW4X (Foscarnet); 3KX376GY7L (Glutamic Acid); 6384-92-5 (N-Methylaspartate); 8L70Q75FXE (Adenosine Triphosphate); M2F465ROXU (Etidronic Acid); NYX13NT29D (alpha,beta-methyleneadenosine 5'-triphosphate); Q40Q9N063P (Acetic Acid); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160507
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b15-00882


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[PMID]:26047794
[Au] Autor:Schlingmann KP; Ruminska J; Kaufmann M; Dursun I; Patti M; Kranz B; Pronicka E; Ciara E; Akcay T; Bulus D; Cornelissen EA; Gawlik A; Sikora P; Patzer L; Galiano M; Boyadzhiev V; Dumic M; Vivante A; Kleta R; Dekel B; Levtchenko E; Bindels RJ; Rust S; Forster IC; Hernando N; Jones G; Wagner CA; Konrad M
[Ad] Endereço:Department of General Pediatrics, University Children's Hospital, Münster, Germany;
[Ti] Título:Autosomal-Recessive Mutations in SLC34A1 Encoding Sodium-Phosphate Cotransporter 2A Cause Idiopathic Infantile Hypercalcemia.
[So] Source:J Am Soc Nephrol;27(2):604-14, 2016 Feb.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Idiopathic infantile hypercalcemia (IIH) is characterized by severe hypercalcemia with failure to thrive, vomiting, dehydration, and nephrocalcinosis. Recently, mutations in the vitamin D catabolizing enzyme 25-hydroxyvitamin D3-24-hydroxylase (CYP24A1) were described that lead to increased sensitivity to vitamin D due to accumulation of the active metabolite 1,25-(OH)2D3. In a subgroup of patients who presented in early infancy with renal phosphate wasting and symptomatic hypercalcemia, mutations in CYP24A1 were excluded. Four patients from families with parental consanguinity were subjected to homozygosity mapping that identified a second IIH gene locus on chromosome 5q35 with a maximum logarithm of odds (LOD) score of 6.79. The sequence analysis of the most promising candidate gene, SLC34A1 encoding renal sodium-phosphate cotransporter 2A (NaPi-IIa), revealed autosomal-recessive mutations in the four index cases and in 12 patients with sporadic IIH. Functional studies of mutant NaPi-IIa in Xenopus oocytes and opossum kidney (OK) cells demonstrated disturbed trafficking to the plasma membrane and loss of phosphate transport activity. Analysis of calcium and phosphate metabolism in Slc34a1-knockout mice highlighted the effect of phosphate depletion and fibroblast growth factor-23 suppression on the development of the IIH phenotype. The human and mice data together demonstrate that primary renal phosphate wasting caused by defective NaPi-IIa function induces inappropriate production of 1,25-(OH)2D3 with subsequent symptomatic hypercalcemia. Clinical and laboratory findings persist despite cessation of vitamin D prophylaxis but rapidly respond to phosphate supplementation. Therefore, early differentiation between SLC34A1 (NaPi-IIa) and CYP24A1 (24-hydroxylase) defects appears critical for targeted therapy in patients with IIH.
[Mh] Termos MeSH primário: Hipercalcemia/genética
Doenças do Recém-Nascido/genética
Erros Inatos do Metabolismo/genética
Mutação
Proteínas Cotransportadoras de Sódio-Fosfato Tipo IIa/genética
Proteínas Cotransportadoras de Sódio-Fosfato/genética
[Mh] Termos MeSH secundário: Animais
Genes Recessivos
Seres Humanos
Lactente
Recém-Nascido
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SLC34A1 protein, human); 0 (Slc34a1 protein, mouse); 0 (Sodium-Phosphate Cotransporter Proteins); 0 (Sodium-Phosphate Cotransporter Proteins, Type IIa)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150607
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2014101025


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[PMID]:26598821
[Au] Autor:Segawa H; Shiozaki Y; Kaneko I; Miyamoto K
[Ad] Endereço:Department of Molecular Nutrition, Institute of Medical Nutrition, The University of Tokushima School of Medicine.
[Ti] Título:The Role of Sodium-Dependent Phosphate Transporter in Phosphate Homeostasis.
[So] Source:J Nutr Sci Vitaminol (Tokyo);61 Suppl:S119-21, 2015.
[Is] ISSN:1881-7742
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Inorganic phosphate (Pi) is an essential compound for several biologic functions. Pi levels outside the normal range, however, contribute to several pathological processes. Hypophosphatemia leads to bone abnormalities, such as rickets/osteomalacia. Hyperphosphatemia contributes to vascular calcification in patients with chronic kidney disease and hemodialysis patients and is independently associated with cardiac mortality.Pi homeostasis is regulated by the coordinated function of renal and intestinal sodium-dependent phosphate (NaPi) transporters with dietary Pi, parathyroid hormone, 1,25-dihydroxyvitamin D3, and fibroblast growth factor 23. The type II NaPi transporter/SLC34 family, with three members identified to date, is mainly responsible for Pi homeostasis in the body. SLC34A1 and SCL34A3 are predominantly expressed in the kidney, whereas SLC34A2 is expressed in the small intestine. The role of each SLC34 in the body was recently established by studies of gene-targeted mice. Mutation of SLC34A1 causes Fanconi syndrome and mutation of SLC34A3 causes autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. SLC34A2 is thought to be a major intestinal NaPi transporter and mutation of SLC34A2 causes pulmonary alveolar microlithiasis. A detailed understanding of Pi regulation in the body is important toward maintaining health.
[Mh] Termos MeSH primário: Homeostase
Fosfatos/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato/metabolismo
[Mh] Termos MeSH secundário: Animais
Doenças Ósseas/etiologia
Seres Humanos
Nefropatias/etiologia
Pneumopatias/etiologia
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Phosphates); 0 (Sodium-Phosphate Cotransporter Proteins); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151125
[Lr] Data última revisão:
151125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151125
[St] Status:MEDLINE
[do] DOI:10.3177/jnsv.61.S119


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[PMID]:26551467
[Au] Autor:Katsumata Y; Kajiya H; Okabe K; Fukushima T; Ikebe T
[Ad] Endereço:Research Center for Regenerative Medicine, Fukuoka Dental College, Fukuoka 8140193, Japan; Department of Oral and Maxillofacial Surgery, Fukuoka Dental College, Fukuoka 8140193, Japan.
[Ti] Título:A salmon DNA scaffold promotes osteogenesis through activation of sodium-dependent phosphate cotransporters.
[So] Source:Biochem Biophys Res Commun;468(4):622-8, 2015 Dec 25.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported the promotion of bone regeneration in calvarial defects of both normal and ovariectomy-induced osteoporotic rats, with the use of biodegradable DNA/protamine scaffold. However, the method by which this DNA-containing scaffold promotes bone formation is still not understood. We hypothesize that the salmon DNA, from which this scaffold is derived, has an osteoinductive effect on pre-osteoblasts and osteoblasts. We examined the effects of salmon DNA on osteoblastic differentiation and calcification in MC3T3-E1 cells, mouse osteoblasts, in vitro and bone regeneration in a calvarial defect model of aged mouse in vivo. The salmon DNA fragments (300 bps) upregulated the expression of the osteogenic markers, such as alkaline phosphatase, Runx2, and osterix (Osx) in MC3T3E1 cells compared with incubation with osteogenic induction medium alone. Measurement of phosphate ion concentrations in cultures showed that the DNA scaffold degraded phosphate ions were released to the cell cultures. Interestingly, we found that the inclusion of DNA in osteoblastic cell cultures upregulated the expression of sodium-dependent phosphate (NaPi) cotransporters, SLC20A1 and SLC34A2, in MC3T3-E1 cells in a time dependent manner. Furthermore, the inclusion of DNA in cell cultures increased the transcellular permeability of phosphate. Conversely, the incubation of phosphonoformic acid, an inhibitor of NaPi cotransporters, attenuated the DNA-induced expression and activation of SLC20A1 and SLC34A2 in MC3T3-E1 cells, resulting in suppression of the osteogenic markers. The implantation of a salmon DNA scaffold disk promoted bone regeneration using calvarial defect models in 30-week-old mice. Our results indicate that the phosphate released from salmon DNA upregulated the expression and activation of NaPi cotransporters, resulting in the promotion of bone regeneration.
[Mh] Termos MeSH primário: DNA/genética
Osteoblastos/citologia
Osteogênese/genética
Fraturas Cranianas/terapia
Proteínas Cotransportadoras de Sódio-Fosfato/genética
Tecidos Suporte
[Mh] Termos MeSH secundário: Células 3T3
Animais
Diferenciação Celular/genética
DNA/administração & dosagem
Implantes de Medicamento/administração & dosagem
Desenho de Equipamento
Análise de Falha de Equipamento
Camundongos
Osteoblastos/fisiologia
Radiografia
Salmão/genética
Fraturas Cranianas/diagnóstico por imagem
Fraturas Cranianas/fisiopatologia
Engenharia Tecidual/instrumentação
Engenharia Tecidual/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drug Implants); 0 (Sodium-Phosphate Cotransporter Proteins); 9007-49-2 (DNA)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151110
[St] Status:MEDLINE


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[PMID]:25825784
[Au] Autor:Bobeck EA; Hellestad EM; Sand JM; Piccione ML; Bishop JW; Helvig C; Petkovich M; Cook ME
[Ad] Endereço:Animal Sciences Department, University of Wisconsin-Madison, Madison, WI 53706.
[Ti] Título:Oral peptide specific egg antibody to intestinal sodium-dependent phosphate co-transporter-2b is effective at altering phosphate transport in vitro and in vivo.
[So] Source:Poult Sci;94(6):1128-37, 2015 Jun.
[Is] ISSN:0032-5791
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hyperimmunized hens are an effective means of generating large quantities of antigen specific egg antibodies that have use as oral supplements. In this study, we attempted to create a peptide specific antibody that produced outcomes similar to those of the human pharmaceutical, sevelamer HCl, used in the treatment of hyperphosphatemia (a sequela of chronic renal disease). Egg antibodies were generated against 8 different human intestinal sodium-dependent phosphate cotransporter 2b (NaPi2b) peptides, and hNaPi2b peptide egg antibodies were screened for their ability to inhibit phosphate transport in human intestinal Caco-2 cell line. Antibody produced against human peptide sequence TSPSLCWT (anti-h16) was specific for its peptide sequence, and significantly reduced phosphate transport in human Caco-2 cells to 25.3±11.5% of control nonspecific antibody, when compared to nicotinamide, a known inhibitor of phosphate transport (P≤0.05). Antibody was then produced against the mouse-specific peptide h16 counterpart (mouse sequence TSPSYCWT, anti-m16) for further analysis in a murine model. When anti-m16 was fed to mice (1% of diet as dried egg yolk powder), egg yolk immunoglobulin (IgY) was detected using immunohistochemical staining in mouse ileum, and egg anti-m16 IgY colocalized with a commercial goat anti-NaPi2b antibody. The effectiveness of anti-m16 egg antibody in reducing serum phosphate, when compared to sevelamer HCl, was determined in a mouse feeding study. Serum phosphate was reduced 18% (P<0.02) in mice fed anti-m16 (1% as dried egg yolk powder) and 30% (P<0.0001) in mice fed sevelamer HCl (1% of diet) when compared to mice fed nonspecific egg immunoglobulin. The methods described and the findings reported show that oral egg antibodies are useful and easy to prepare reagents for the study and possible treatment of select diseases.
[Mh] Termos MeSH primário: Imunoglobulinas/imunologia
Fosfatos/sangue
Proteínas Cotransportadoras de Sódio-Fosfato/genética
[Mh] Termos MeSH secundário: Animais
Anticorpos/metabolismo
Células CACO-2
Embrião de Galinha
Galinhas
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Imunoglobulinas/sangue
Imunoglobulinas/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Óvulo/metabolismo
Análise de Sequência de Proteína
Proteínas Cotransportadoras de Sódio-Fosfato/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies); 0 (IgY); 0 (Immunoglobulins); 0 (Phosphates); 0 (Sodium-Phosphate Cotransporter Proteins)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:150528
[Lr] Data última revisão:
150528
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150401
[St] Status:MEDLINE
[do] DOI:10.3382/ps/pev085


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[PMID]:25602517
[Au] Autor:Rizzo F; Staub O
[Ad] Endereço:Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
[Ti] Título:NEDD4-2 and salt-sensitive hypertension.
[So] Source:Curr Opin Nephrol Hypertens;24(2):111-6, 2015 Mar.
[Is] ISSN:1473-6543
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: NEDD4-2 is an ubiquitin-protein ligase that was originally identified as an interactor of the epithelial Na+ channel (ENaC); this interaction is defective in Liddle's syndrome, causing elevated ENaC activity and salt-sensitive hypertension. In this review we aim to highlight progress achieved in recent years demonstrating that NEDD4-2 is involved in the control of Na+ transporters that are different from ENaC, but which also play a role in salt-sensitive hypertension. RECENT FINDINGS: It has been shown that NEDD4-2 interacts with ubiquitylates and negatively regulates the thiazide-sensitive NCC (Na+,Cl- -cotransporter), both in vitro and in vivo in inducible, nephron-specific Nedd4-2 knockout mice. Moreover, evidence has been provided that NEDD4-2 is also involved in the regulation of human NHE3 (Na+,H+-exchanger 3) and NKCC2 (Na+,K+,2Cl- -cotransporter 2). SUMMARY: The emerging role of NEDD4-2 in the regulation of different Na+ transporters along the nephron and the identification of human polymorphisms in the NEDD4-2 gene (Nedd4L) related to salt-sensitive hypertension makes this ubiquitin-protein ligase an interesting target for the development of antihypertensive drugs.
[Mh] Termos MeSH primário: Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Canais Epiteliais de Sódio/metabolismo
Hipertensão/metabolismo
Cloreto de Sódio na Dieta/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/uso terapêutico
Complexos Endossomais de Distribuição Requeridos para Transporte/genética
Seres Humanos
Hipertensão/tratamento farmacológico
Ubiquitina-Proteína Ligases Nedd4
Proteínas Cotransportadoras de Sódio-Fosfato/metabolismo
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Endosomal Sorting Complexes Required for Transport); 0 (Epithelial Sodium Channels); 0 (Sodium Chloride, Dietary); 0 (Sodium-Phosphate Cotransporter Proteins); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, human); EC 2.3.2.26 (Nedd4L protein, human); EC 2.3.2.26 (Nedd4l protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150121
[St] Status:MEDLINE
[do] DOI:10.1097/MNH.0000000000000097


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[PMID]:25452235
[Au] Autor:Inden M
[Ad] Endereço:Laboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University.
[Ti] Título:[The causative gene of Parkinsonism and its medical treatment strategy].
[So] Source:Yakugaku Zasshi;134(12):1253-8, 2014.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Parkinsonism is a neurological syndrome characterized by tremor, hypokinesia, rigidity, and postural instability. The neurodegenerative condition of Parkinson's disease (PD) is the most common cause of parkinsonism. PD is classified as sporadic PD and familial PD. Whereas idiopathic PD is caused by a number of complex factors, familial PD is a result of mutations in PD-associated genes. Unraveling the mechanisms surrounding familial PD will offer pivotal clues in understanding etiology of not only familial PD but also sporadic PD. We have demonstrated neuroprotective effects with particular focus on DJ-1. On the other hand, idiopathic basal ganglia calcification, also known as Fahr disease (FD) is another condition characterized by parkinsonism. In 2012, solute carrier family 20A2 (SLC20A2) was identified as the causative gene for familial FD. Our analysis of patient samples revealed a novel mutation in SLC20A2. Type-III sodium-dependent phosphate transporter 2 (PiT-2), the protein encoded by SLC20A2, plays an important role in phosphate homeostasis. However, PiT-2's role in the pathology of FD remains largely unclear. We have established induced pluripotent stem (iPS) cells from FD patients and are investigating their usefulness in drug development. Here, we present some of our latest research findings.
[Mh] Termos MeSH primário: Doença de Parkinson/genética
[Mh] Termos MeSH secundário: Loci Gênicos
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Doença de Parkinson/terapia
Proteínas Cotransportadoras de Sódio-Fosfato/genética
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (SLC20A2 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:141202
[Lr] Data última revisão:
141202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141203
[St] Status:MEDLINE



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