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[PMID]:28813533
[Au] Autor:Hung CF; Hsiao CY; Hsieh WH; Li HJ; Tsai YJ; Lin CN; Chang HH; Wu NL
[Ad] Endereço:School of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
[Ti] Título:18ß-glycyrrhetinic acid derivative promotes proliferation, migration and aquaporin-3 expression in human dermal fibroblasts.
[So] Source:PLoS One;12(8):e0182981, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Licorice (Glycyrrhiza) species have been widely used as a traditional medicine and a natural sweetener in foods. The 18ß-glycyrrhetinic acid (18ß-GA) is a bioactive compound in licorice that exhibits potential anti-cancer, anti-inflammatory, and anti-microbial activities. Many synthesized derivatives of 18ß-GA have been reported to be cytotoxic and suggested for the treatment of malignant diseases. In this study, we explored the possible pharmacological roles of an 18ß-GA derivative in skin biology using primary human dermal fibroblasts and HaCaT keratinocytes as cell models. We found that this 18ß-GA derivative did not cause cell death, but significantly enhanced the proliferation of dermal fibroblasts and HaCaT keratinocytes. A scratch wound healing assay revealed that the 18ß-GA derivative promoted the migration of fibroblasts. Due to the important role of aquaporin-3 in cell migration and proliferation, we also investigated the expression of aquaporin-3 and found this compound up-regulated the expression of aquaporin-3 in dermal fibroblasts and HaCaT keratinocytes. In dermal fibroblasts, the 18ß-GA derivative induced the phosphorylation of Akt, ERK, and p38. The inhibitor of Akt predominantly suppressed the 18ß-GA derivative-induced expression of aquaporin-3. Collectively, this compound had a positive effect on the proliferation, migration, and aquaporin-3 expression of skin cells, implying its potential role in the treatment of skin diseases characterized by impaired wound healing or dermal defects.
[Mh] Termos MeSH primário: Aquaporina 3/genética
Derme/citologia
Derme/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Ácido Glicirretínico/análogos & derivados
[Mh] Termos MeSH secundário: Aquaporina 3/metabolismo
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Ácido Glicirretínico/química
Ácido Glicirretínico/farmacologia
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
1449-05-4 (18alpha-glycyrrhetinic acid); 158801-98-0 (Aquaporin 3); P540XA09DR (Glycyrrhetinic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182981


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[PMID]:28638886
[Au] Autor:Han X; Ji X; Zhao H; Zhang Y; Liu G; Wang Y; Zhao W; Wang S
[Ad] Endereço:College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.
[Ti] Título:MECHANISMS OF COIX SEED COMPOSITIONS IN THE TREATMENT OF SPLEEN DEFICIENCY AND WET DAMPNESS ZHENG.
[So] Source:Afr J Tradit Complement Altern Med;14(4):239-246, 2017.
[Is] ISSN:2505-0044
[Cp] País de publicação:Nigeria
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Coix seed has the functions of fortifying the spleen and inhibiting the dampness. However, it remains unclear which Coix seed compositions is responsible for these functions. Previous investigations have revealed that the main compositions of Coix seed are proteins, polysaccharides, oils and starches. The objectives of this study are to explore which is the most effective compositions in fortifying the spleen and examine how Coix seed works in regulating the water transport on the spleen deficiency and wet dampness (SDWD) rat model. MATERIALS AND METHODS: The rats used were divided into (i) control group, (ii) model group, (iii) decoction group, (iv) protein group, (v) polysaccharide group, (vi) oil group and (vii) starch group. The urine volume, the drinking volume and the water loading index in each group were calculated. Agilent 8*60K array was used for microarray-based gene expression analysis. The differential mRNAs related to the transport activity were screened. qRT-PCR was used to validate the mRNA microarray. RESULTS: The results demonstrated that all treatment groups could decrease the dampness of SDWD rats. mRNA microarray had significant effect on the protein group and the polysaccharide group in regulating the water transport, among which the most significant mRNA was Fabp6, Slc51a, Slc51b, Slc11a2, Slc4a10 and AQP3 respectively. CONCLUSION: The compositions of proteins and polysaccharides had the most significant effect in regulating the water transport of SDWD rat model. The contributing mRNA focused on Fabp, Slc and AQP family.
[Mh] Termos MeSH primário: Coix/química
Medicamentos de Ervas Chinesas/administração & dosagem
Baço/efeitos dos fármacos
Esplenopatias/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Aquaporina 3/genética
Aquaporina 3/metabolismo
Proteínas de Ligação a Ácido Graxo/genética
Proteínas de Ligação a Ácido Graxo/metabolismo
Feminino
Hormônios Gastrointestinais/genética
Hormônios Gastrointestinais/metabolismo
Seres Humanos
Masculino
Ratos
Ratos Wistar
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Sementes/química
Baço/metabolismo
Baço/fisiopatologia
Esplenopatias/genética
Esplenopatias/metabolismo
Esplenopatias/fisiopatologia
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aqp3 protein, rat); 0 (Drugs, Chinese Herbal); 0 (Fatty Acid-Binding Proteins); 0 (Gastrointestinal Hormones); 0 (Receptors, G-Protein-Coupled); 059QF0KO0R (Water); 117849-44-2 (fatty acid-binding protein 6); 158801-98-0 (Aquaporin 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.21010/ajtcam.v14i4.26


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[PMID]:28595905
[Au] Autor:Tardelli M; Claudel T; Bruschi FV; Moreno-Viedma V; Trauner M
[Ad] Endereço:Hans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology & Hepatology, Internal Medicine III, Medical University of Vienna, Austria.
[Ti] Título:Adiponectin regulates AQP3 via PPARα in human hepatic stellate cells.
[So] Source:Biochem Biophys Res Commun;490(1):51-54, 2017 Aug 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aquaporins (AQPs) are trans-membrane proteins which allow the movement of water and glycerol required by hepatic stellate cells (HSC) for triglyceride formation and lipid storage. Adiponectin (ADPQ) is a hormone produced by the adipose tissue, which is known to increase AQP3 expression. Since ADPQ receptor signals via the nuclear receptor PPAR we aimed to explore the role of this pathway in AQP3 regulation by ADPQ in HSC. AQP3 and CPT1α expression increased only after ADPQ but not rosiglitazone stimulation. In LX2 cells co-transfected with plasmids expressing PPARα or PPARγ coupled to a luciferase reporter gene, only PPARα increased luciferase activity after ADPQ stimulation. Collectively, our findings demonstrate that ADPQ increases AQP3 expression through PPARα-mediated signaling in HSC.
[Mh] Termos MeSH primário: Adiponectina/metabolismo
Aquaporina 3/metabolismo
Células Estreladas do Fígado/metabolismo
PPAR gama/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (AQP3 protein, human); 0 (Adiponectin); 0 (PPAR gamma); 158801-98-0 (Aquaporin 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE


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[PMID]:28546424
[Au] Autor:Hamed S; Ullmann Y; Egozi D; Keren A; Daod E; Anis O; Kabha H; Belokopytov M; Ashkar M; Shofti R; Zaretsky A; Schlesinger M; Teot L; Liu PY
[Ad] Endereço:Department of Research & Development, Remedor Biomed Ltd, Nazareth Illit, Israel saher@remedor.com.
[Ti] Título:Topical Erythropoietin Treatment Accelerates the Healing of Cutaneous Burn Wounds in Diabetic Pigs Through an Aquaporin-3-Dependent Mechanism.
[So] Source:Diabetes;66(8):2254-2265, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have previously reported that the topical application of erythropoietin (EPO) to cutaneous wounds in rats and mice with experimentally induced diabetes accelerates their healing by stimulating angiogenesis, reepithelialization, and collagen deposition, and by suppressing the inflammatory response and apoptosis. Aquaporins (AQPs) are integral membrane proteins whose function is to regulate intracellular fluid hemostasis by enabling the transport of water and glycerol. AQP3 is the AQP that is expressed in the skin where it facilitates cell migration and proliferation and re-epithelialization during wound healing. In this report, we provide the results of an investigation that examined the contribution of AQP3 to the mechanism of EPO action on the healing of burn wounds in the skin of pigs with experimentally induced type 1 diabetes. We found that topical EPO treatment of the burns accelerated their healing through an AQP3-dependent mechanism that activates angiogenesis, triggers collagen and hyaluronic acid synthesis and the formation of the extracellular matrix (ECM), and stimulates reepithelialization by keratinocytes. We also found that incorporating fibronectin, a crucial constituent of the ECM, into the topical EPO-containing gel, can potentiate the accelerating action of EPO on the healing of the burn injury.
[Mh] Termos MeSH primário: Indutores da Angiogênese/administração & dosagem
Aquaporina 3/metabolismo
Queimaduras/tratamento farmacológico
Eritropoetina/administração & dosagem
Cicatrização/efeitos dos fármacos
Cicatrização/genética
[Mh] Termos MeSH secundário: Administração Tópica
Animais
Queimaduras/genética
Colágeno/genética
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Tipo 1/genética
Matriz Extracelular/genética
Fibronectinas/administração & dosagem
Ácido Hialurônico/biossíntese
Queratinócitos/metabolismo
Neovascularização Fisiológica
Reepitelização/genética
Pele/metabolismo
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Fibronectins); 11096-26-7 (Erythropoietin); 158801-98-0 (Aquaporin 3); 9004-61-9 (Hyaluronic Acid); 9007-34-5 (Collagen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1205


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[PMID]:28526298
[Au] Autor:Choudhary V; Olala LO; Kagha K; Pan ZQ; Chen X; Yang R; Cline A; Helwa I; Marshall L; Kaddour-Djebbar I; McGee-Lawrence ME; Bollag WB
[Ad] Endereço:Charlie Norwood VA Medical Center, Augusta, Georgia, USA; Department of Physiology, Augusta University, Augusta, Georgia, USA; Department of Medicine (Dermatology), Augusta University, Augusta, Georgia, USA. Electronic address: vchoudhary@augusta.edu.
[Ti] Título:Regulation of the Glycerol Transporter, Aquaporin-3, by Histone Deacetylase-3 and p53 in Keratinocytes.
[So] Source:J Invest Dermatol;137(9):1935-1944, 2017 Sep.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aquaporin- (AQP) 3, a water and glycerol channel, plays an important role in epidermal function, with studies showing its involvement in keratinocyte proliferation, differentiation, and migration and in epidermal wound healing and barrier repair. Increasing speculation about the use of histone deacetylase (HDAC) inhibitors to treat skin diseases led us to investigate HDAC's role in the regulation of AQP3. The broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced AQP3 mRNA and protein expression in a dose- and time-dependent manner in normal keratinocytes. The SAHA-induced increase in AQP3 levels resulted in enhanced [ H]glycerol uptake in normal but not in AQP3-knockout keratinocytes, confirming that the expressed AQP3 was functional. Use of HDAC inhibitors with different specificities limited our exploration of the responsible HDAC member to HDAC1, HDAC2, or HDAC3. Cre-recombinase-mediated knockdown and overexpression of HDAC3 suggested a role for HDAC3 in suppressing AQP3 expression basally. Further investigation implicated p53 as a transcription factor involved in regulating HDAC inhibitor-induced AQP3 expression. Thus, our study supports the regulation of AQP3 expression by HDAC3 and p53. Because suberoylanilide hydroxamic acid is already approved to treat cutaneous T-cell lymphoma, it could potentially be used as a therapy for skin diseases like psoriasis, where AQP3 is abnormally expressed.
[Mh] Termos MeSH primário: Aquaporina 3/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Glicerol/metabolismo
Histona Desacetilases/farmacologia
Queratinócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Aquaporina 3/metabolismo
Transporte Biológico/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/fisiologia
Proliferação Celular/fisiologia
Células Cultivadas
Epiderme/metabolismo
Seres Humanos
Técnicas In Vitro
Queratinócitos/citologia
Camundongos
Camundongos Knockout
Sensibilidade e Especificidade
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53); 158801-98-0 (Aquaporin 3); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3); PDC6A3C0OX (Glycerol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170521
[St] Status:MEDLINE


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[PMID]:28515158
[Au] Autor:Helwa I; Choudhary V; Chen X; Kaddour-Djebbar I; Bollag WB
[Ad] Endereço:Charlie Norwood VA Medical Center (V.C., X.C., I.K.-D., W.B.B.), Augusta, Georgia; Department of Oral Biology (I.H., W.B.B.), Department of Physiology (V.C., X.C., I.K.-D., W.B.B.), and Department of Medicine (Dermatology) (W.B.B.), Medical College of Georgia, Augusta University, Augusta, Georgia.
[Ti] Título:Anti-Psoriatic Drug Monomethylfumarate Increases Nuclear Factor Erythroid 2-Related Factor 2 Levels and Induces Aquaporin-3 mRNA and Protein Expression.
[So] Source:J Pharmacol Exp Ther;362(2):243-253, 2017 Aug.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress contributes to inflammatory skin diseases, including psoriasis. Monomethylfumarate (MMF) is an antipsoriatic agent with a poorly understood mechanism of action. In other cell types MMF increases the expression of nuclear factor erythroid-derived 2-like 2 (Nrf2), a transcription factor that regulates cellular antioxidant responses, to reduce oxidative stress like that observed in inflammatory disorders such as multiple sclerosis. We tested the hypothesis that MMF enhances Nrf2 activity in keratinocytes, thereby improving their capacity to counteract environmental stresses. We used Western analysis, immunofluorescence, and real-time quantitative reverse-transcription polymerase chain reaction to examine the effect of MMF on the expression of Nrf2 and its targets. We also measured intracellular reactive oxygen species (ROS) levels following MMF treatment. Our data show that MMF increased total and nuclear Nrf2 levels in primary mouse keratinocytes and enhanced mRNA expression of several Nrf2-downstream effectors, including heme oxygenase-1 and peroxiredoxin-6. Moreover, MMF treatment attenuated the generation of ROS following hydrogen peroxide treatment. On the other hand, the expression and membranous localization of aquaporin-3 (AQP3), a glycerol channel implicated in keratinocyte differentiation, was stimulated by MMF, which also enhanced keratinocyte glycerol uptake. The Nrf2 activator sulforaphane also increased AQP3 levels, suggesting that AQP3 expression may be regulated by Nrf2. We show for the first time that MMF stimulates Nrf2 and AQP3 expression and function/activity in keratinocytes. This effect may account, in part, for the previously observed ability of MMF to inhibit proliferation and inflammatory mediator production and promote differentiation in keratinocytes and to treat psoriasis.
[Mh] Termos MeSH primário: Aquaporina 3/biossíntese
Fumaratos/farmacologia
Maleatos/farmacologia
Fator 2 Relacionado a NF-E2/biossíntese
Psoríase
RNA Mensageiro/biossíntese
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Aquaporina 3/agonistas
Aquaporina 3/genética
Sequência de Bases
Células Cultivadas
Expressão Gênica
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Camundongos
Fator 2 Relacionado a NF-E2/agonistas
RNA Mensageiro/agonistas
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aqp3 protein, mouse); 0 (Fumarates); 0 (Maleates); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (RNA, Messenger); 0RQ6CXO9KD (citraconic acid); 158801-98-0 (Aquaporin 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.116.239715


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[PMID]:28506994
[Au] Autor:Eskova A; Chauvigné F; Maischein HM; Ammelburg M; Cerdà J; Nüsslein-Volhard C; Irion U
[Ad] Endereço:Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.
[Ti] Título:Gain-of-function mutations in Aqp3a influence zebrafish pigment pattern formation through the tissue environment.
[So] Source:Development;144(11):2059-2069, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The development of the pigmentation pattern in zebrafish is a tightly regulated process that depends on both the self-organizing properties of pigment cells and extrinsic cues from other tissues. Many of the known mutations that alter the pattern act cell-autonomously in pigment cells, and our knowledge about external regulators is limited. Here, we describe novel zebrafish mutants, which encompass several dominant missense mutations in Aquaporin 3a (Aqp3a) that lead to broken stripes and short fins. A loss-of-function allele, generated by CRISPR-Cas9, has no phenotypic consequences, demonstrating that Aqp3a is dispensable for normal development. Strikingly, the pigment cells from dominant mutants are capable of forming a wild-type pattern when developing in a wild-type environment, but the surrounding tissues in the mutants influence pigment cell behaviour and interfere with the patterning process. The mutated amino acid residues in the dominant alleles line the pore surface of Aqp3a and influence pore permeability. These results demonstrate an important effect of the tissue environment on pigment cell behaviour and, thereby, on pattern formation.
[Mh] Termos MeSH primário: Aquaporina 3/genética
Mutação/genética
Pigmentação
Proteínas de Peixe-Zebra/genética
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Nadadeiras de Animais/anatomia & histologia
Nadadeiras de Animais/citologia
Animais
Aquaporina 3/química
Aquaporina 3/metabolismo
Cromatóforos/metabolismo
Genes Dominantes
Proteínas de Fluorescência Verde/metabolismo
Mutação de Sentido Incorreto/genética
Permeabilidade
Fenótipo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Proteínas de Peixe-Zebra/química
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Zebrafish Proteins); 0 (aquaporin 3, zebrafish); 147336-22-9 (Green Fluorescent Proteins); 158801-98-0 (Aquaporin 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1242/dev.143495


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[PMID]:28377226
[Au] Autor:Huang X; Huang L; Shao M
[Ad] Endereço:School of Life Sciences, Fudan University, Shanghai 200433, PR China.
[Ti] Título:Aquaporin 3 facilitates tumor growth in pancreatic cancer by modulating mTOR signaling.
[So] Source:Biochem Biophys Res Commun;486(4):1097-1102, 2017 May 13.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aquaporins (AQP) have been demonstrated to be dysregulated in many human cancers and is thought to be involved in pancreatic carcinogenesis and progression. However, the oncogenic roles and underlying mechanism of AQP in pancreatic ductal adenocarcinoma (PDAC) remain largely unknown. In this study, by data mining of TCGA dataset and CCLE database, we identified that AQP3 is the major AQP expressed in PDAC. Then, the microRNA-874, was demonstrated to be a key regulator of AQP3 expression in PDAC cells. Genetic silencing of AQP3 expression had pronounced effects on cell proliferation and apoptosis of the PDAC cell lines BXPC3 and HPAFII. Introduction of microRNA-874 suppressed cell proliferation and promoted cell apoptosis, whereas inhibition of microRNA-874 had the opposite effect. Mechanistically, by a large-scale proteomic analysis, we revealed that AQP3 was significantly associated the activity of mTOR signaling. Moreover, modulation of AQP3 or microRNA-874 altered mTOR activity as demonstrated by the phosphorylation level of mTOR and its downstream target S6. Taken together, our data, as a proof of principle, suggest that AQP3 can promote tumor growth of pancreatic cancer cells by activating the Mtor signaling pathway and provide a potential therapeutic target in the treatment of PDAC.
[Mh] Termos MeSH primário: Apoptose
Aquaporina 3/metabolismo
Proliferação Celular
MicroRNAs/metabolismo
Neoplasias Pancreáticas/patologia
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Ativação Enzimática
Regulação Neoplásica da Expressão Gênica
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP3 protein, human); 0 (MIRN874 microRNA, human); 0 (MicroRNAs); 158801-98-0 (Aquaporin 3); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE


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[PMID]:28258567
[Au] Autor:Xu M; Xiao M; Li S; Yang B
[Ad] Endereço:Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
[Ti] Título:Aquaporins in Nervous System.
[So] Source:Adv Exp Med Biol;969:81-103, 2017.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aquaporins (AQPs ) mediate water flux between the four distinct water compartments in the central nervous system (CNS). In the present chapter, we mainly focus on the expression and function of the 9 AQPs expressed in the CNS, which include five members of aquaporin subfamily: AQP1, AQP4, AQP5, AQP6, and AQP8; three members of aquaglyceroporin subfamily: AQP3, AQP7, and AQP9; and one member of superaquaporin subfamily: AQP11. In addition, AQP1, AQP2 and AQP4 expressed in the peripheral nervous system (PNS) are also reviewed. AQP4, the predominant water channel in the CNS, is involved both in the astrocyte swelling of cytotoxic edema and the resolution of vasogenic edema, and is of pivotal importance in the pathology of brain disorders such as neuromyelitis optica , brain tumors and Alzheimer's disease. Other AQPs are also involved in a variety of important physiological and pathological process in the brain. It has been suggested that AQPs could represent an important target in treatment of brain disorders like cerebral edema. Future investigations are necessary to elucidate the pathological significance of AQPs in the CNS.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Aquaporina 1/metabolismo
Aquaporina 3/metabolismo
Aquaporinas/metabolismo
Edema Encefálico/metabolismo
Neoplasias Encefálicas/metabolismo
Neuromielite Óptica/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/genética
Doença de Alzheimer/patologia
Animais
Aquaporina 1/genética
Aquaporina 3/genética
Aquaporinas/genética
Transporte Biológico
Edema Encefálico/genética
Edema Encefálico/patologia
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/patologia
Sistema Nervoso Central/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Neuromielite Óptica/genética
Neuromielite Óptica/patologia
Sistema Nervoso Periférico/metabolismo
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (AQP1 protein, human); 0 (AQP11 protein, human); 0 (AQP3 protein, human); 0 (Aquaporins); 0 (Protein Isoforms); 059QF0KO0R (Water); 146410-94-8 (Aquaporin 1); 158801-98-0 (Aquaporin 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170305
[St] Status:MEDLINE
[do] DOI:10.1007/978-94-024-1057-0_5


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[PMID]:28189680
[Au] Autor:Xiong G; Chen X; Zhang Q; Fang Y; Chen W; Li C; Zhang J
[Ad] Endereço:Department of Thoracic Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China.
[Ti] Título:RNA interference influenced the proliferation and invasion of XWLC-05 lung cancer cells through inhibiting aquaporin 3.
[So] Source:Biochem Biophys Res Commun;485(3):627-634, 2017 Apr 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The objective of this study was to construct a recombinant vector expressing siRNA targetedly inhibiting aquaporin 3 (AQP3), and to evaluate the effects of AQP3 inhibition on the proliferation and invasion of XWLC-05 human lung cancer cells. METHODS: We obtained human AQP3 sequence from the Genbank and established the recombinant vector expressing siRNA targeting AQP3. After the transfection of the recombinant vectors, the expression of AQP3 was determined by RT-PCR and western blot. The MTS assay, flow cytometry and Transwell assay were conducted to detect the proliferation, cell cycle process, apoptosis and invasion of XWLC-05 cells. Then the activity of metal matrix proteinase (MMP) 2 was determined by gelatin zymography. Tumor formation in vivo experiments were also conducted in nude mice. RESULTS: RNA interference (RNAi) of AQP3 substantially suppressed the XWLC-05 cell proliferation and invasion, blocked the cell cycle progressing and promoted cell apoptosis. In addition, the activity of MMP2 was remarkably attenuated in RNAi group. AQP3 RNAi did not affect the tumor formation rate in nude mice but reduced the tumor growth. CONCLUSION: The inhibition of AQP3 retarded the growth and invasiveness of XWLC-05 lung cancer cells and decreased the activity of MMP2.
[Mh] Termos MeSH primário: Aquaporina 3/genética
Ciclo Celular/genética
Proliferação Celular/genética
Neoplasias Pulmonares/genética
Interferência de RNA
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Aquaporina 3/metabolismo
Western Blotting
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/terapia
Metaloproteinase 2 da Matriz/metabolismo
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Terapêutica com RNAi/métodos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Carga Tumoral/genética
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
158801-98-0 (Aquaporin 3); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE



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