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Pesquisa : D12.776.157.530.400.150.850 [Categoria DeCS]
Referências encontradas : 277 [refinar]
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[PMID]:28395140
[Au] Autor:Qu C; Ding M; Zhu Y; Lu Y; Du J; Miller M; Tian J; Zhu J; Xu J; Wen M; Er-Bu A; Wang J; Xiao Y; Wu M; McManus OB; Li M; Wu J; Luo HR; Cao Z; Shen B; Wang H; Zhu MX; Hong X
[Ad] Endereço:State Key Laboratory of Virology, Key Laboratory of Combinatorial Biosynthesis and Drug Discovery (MOE) and Hubei Province Engineering and Technology Research Center for Fluorinated Pharmaceuticals, Wuhan University School of Pharmaceutical Sciences , Wuhan, Hubei Province 430071, China.
[Ti] Título:Pyrazolopyrimidines as Potent Stimulators for Transient Receptor Potential Canonical 3/6/7 Channels.
[So] Source:J Med Chem;60(11):4680-4692, 2017 Jun 08.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transient receptor potential canonical 3/6/7 (TRPC3/6/7) are highly homologous receptor-operated nonselective cation channels. Despite their physiological significance, very few selective and potent agonists are available for functional examination of these channels. Using a cell-based high throughput screening approach, a lead compound with the pyrazolopyrimidine skeleton was identified as a TRPC6 agonist. Synthetic schemes for the lead and its analogues were established, and structural-activity relationship studies were carried out. A series of potent and direct agonists of TRPC3/6/7 channels were identified, and among them, 4m-4p have a potency order of TRPC3 > C7 > C6, with 4n being the most potent with an EC of <20 nM on TRPC3. Importantly, these compounds exhibited no stimulatory activity on related TRP channels. The potent and selective compounds described here should be suitable for evaluation of the roles of TRPC channels in the physiology and pathogenesis of diseases, including glomerulosclerosis and cancer.
[Mh] Termos MeSH primário: Pirazóis/química
Pirimidinas/farmacologia
Canais de Cátion TRPC/agonistas
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Pirimidinas/química
Relação Estrutura-Atividade
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyrazoles); 0 (Pyrimidines); 0 (TRPC Cation Channels); 0 (TRPC3 cation channel); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 0 (TRPC7 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00304


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[PMID]:28210627
[Au] Autor:Takada H; Yonekawa J; Matsumoto M; Furuya K; Sokabe M
[Ad] Endereço:Department of Physiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Nagoya 466-8550, Japan; Pixy Central Research Institute, 3-7-1 Kamitsuchidananaka, Ayase, Kanagawa 252-1113, Japan.
[Ti] Título:Hyperforin/HP- -Cyclodextrin Enhances Mechanosensitive Ca Signaling in HaCaT Keratinocytes and in Atopic Skin Ex Vivo Which Accelerates Wound Healing.
[So] Source:Biomed Res Int;2017:8701801, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cutaneous wound healing is accelerated by mechanical stretching, and treatment with hyperforin, a major component of a traditional herbal medicine and a known TRPC6 activator, further enhances the acceleration. We recently revealed that this was due to the enhancement of ATP-Ca signaling in keratinocytes by hyperforin treatment. However, the low aqueous solubility and easy photodegradation impede the topical application of hyperforin for therapeutic purposes. We designed a compound hydroxypropyl- -cyclodextrin- (HP- -CD-) tetracapped hyperforin, which had increased aqueous solubility and improved photoprotection. We assessed the physiological effects of hyperforin/HP- -CD on wound healing in HaCaT keratinocytes using live imaging to observe the ATP release and the intracellular Ca increase. In response to stretching (20%), ATP was released only from the foremost cells at the wound edge; it then diffused to the cells behind the wound edge and activated the P2Y receptors, which caused propagating Ca waves via TRPC6. This process might facilitate wound closure, because the Ca response and wound healing were inhibited in parallel by various inhibitors of ATP-Ca signaling. We also applied hyperforin/HP- -CD on an ex vivo skin model of atopic dermatitis and found that hyperforin/HP- -CD treatment for 24 h improved the stretch-induced Ca responses and oscillations which failed in atopic skin.
[Mh] Termos MeSH primário: Dermatite Atópica/tratamento farmacológico
Pele/efeitos dos fármacos
Estresse Mecânico
Canais de Cátion TRPC/biossíntese
Cicatrização/efeitos dos fármacos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Sinalização do Cálcio/efeitos dos fármacos
Células Cultivadas
Ciclodextrinas/administração & dosagem
Dermatite Atópica/patologia
Técnicas de Silenciamento de Genes
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Floroglucinol/administração & dosagem
Floroglucinol/análogos & derivados
Receptores Purinérgicos P2Y/genética
Receptores Purinérgicos P2Y/metabolismo
Pele/lesões
Pele/metabolismo
Canais de Cátion TRPC/genética
Canal de Cátion TRPC6
Terpenos/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclodextrins); 0 (Receptors, Purinergic P2Y); 0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 0 (Terpenes); 8L70Q75FXE (Adenosine Triphosphate); DHD7FFG6YS (Phloroglucinol); RM741E34FP (hyperforin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170218
[St] Status:MEDLINE
[do] DOI:10.1155/2017/8701801


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[PMID]:28110963
[Au] Autor:Thiel G; Rössler OG
[Ad] Endereço:Department of Medical Biochemistry and Molecular Biology, Saarland University Medical Faculty, D-66421 Homburg, Germany. Electronic address: gerald.thiel@uks.eu.
[Ti] Título:Hyperforin activates gene transcription involving transient receptor potential C6 channels.
[So] Source:Biochem Pharmacol;129:96-107, 2017 Apr 01.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hypericum perforatum is one of the most prominent medical plants. Hyperforin, a main ingredient of H. perforatum, has been shown to activate transient receptor potential canonical C6 (TRPC6) channels. Alternatively, it has been proposed that hyperforin functions as a protonophore in a TRPC6-independent manner. Here, we show that hyperforin stimulation activates the transcription factor AP-1 in HEK293 cells expressing TRPC6 (T6.11 cells), but did not substantially change the AP-1 activity in HEK293 cells lacking TRPC6. We identified the AP-1 binding site as a hyperforin-responsive element. AP-1 is composed of the transcription factors c-Jun and c-Fos, or other members of the c-Jun and c-Fos families of proteins. Hyperforin stimulation increased c-Jun and c-Fos promoter activities in T6.11 cells and induced an upregulation of c-Jun and c-Fos biosynthesis. The analysis of the c-Fos promoter revealed that the cAMP-response element also functions as a hyperforin-responsive element. Hyperforin-induced upregulation of AP-1 in T6.11 cells was attenuated by preincubation of the cells with either pregnenolone or progesterone, indicating that gene regulation via TRPC6 is under control of hormones or hormonal precursors. The signal transduction of hyperforin-induced AP-1 gene transcription required an influx of Ca ions into the cells, the activation of MAP kinases, and the activation of the transcription factors c-Jun and ternary complex factor. We conclude that hyperforin regulates gene transcription via activation of TRPC6 channels, involving stimulus-regulated protein kinases and stimulus-responsive transcription factors. The fact that hyperforin regulates gene transcription may explain many of the intracellular alterations induced by this compound.
[Mh] Termos MeSH primário: Floroglucinol/análogos & derivados
Canais de Cátion TRPC/fisiologia
Terpenos/farmacologia
Transcrição Genética/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Floroglucinol/farmacologia
Transdução de Sinais
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 0 (Terpenes); DHD7FFG6YS (Phloroglucinol); RM741E34FP (hyperforin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE


  4 / 277 MEDLINE  
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[PMID]:27818466
[Au] Autor:Kurahara LH; Hiraishi K; Sumiyoshi M; Doi M; Hu Y; Aoyagi K; Jian Y; Inoue R
[Ad] Endereço:Department of Physiology, Fukuoka University School of Medicine, Fukuoka 814-0180, Japan.
[Ti] Título:Significant contribution of TRPC6 channel-mediated Ca influx to the pathogenesis of Crohn's disease fibrotic stenosis.
[So] Source:J Smooth Muscle Res;52(0):78-92, 2016.
[Is] ISSN:1884-8796
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Intestinal fibrosis is an intractable complication of Crohn's disease (CD), and, when occurring excessively, causes severe intestinal obstruction that often necessitates surgical resection. The fibrosis is characterized by an imbalance in the turnover of extracellular matrix (ECM) components, where intestinal fibroblasts/myofibroblasts play active roles in ECM production, fibrogenesis and tissue remodeling, which eventually leads to the formation of stenotic lesions. There is however a great paucity of knowledge about how intestinal fibrosis initiates and progresses, which hampers the development of effective pharmacotherapies against CD. Recently, we explored the potential implications of transient receptor potential (TRP) channels in the pathogenesis of intestinal fibrosis, since they are known to act as cellular stress sensors/transducers affecting intracellular Ca homeostasis/dynamics, and are involved in a broad spectrum of cell pathophysiology including inflammation and tissue remodeling. In this review, we will place a particular emphasis on the intestinal fibroblast/myofibroblast TRPC6 channel to discuss its modulatory effects on fibrotic responses and therapeutic potential for anti-fibrotic treatment against CD-related stenosis.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Doença de Crohn/etiologia
Obstrução Intestinal/etiologia
Intestinos/patologia
Canais de Cátion TRPC/fisiologia
[Mh] Termos MeSH secundário: Doença de Crohn/tratamento farmacológico
Doença de Crohn/patologia
Matriz Extracelular/metabolismo
Fibroblastos/fisiologia
Fibrose
Seres Humanos
Intestinos/citologia
Terapia de Alvo Molecular
Miofibroblastos/fisiologia
Transdução de Sinais/fisiologia
Canal de Cátion TRPC6
Fator de Crescimento Transformador beta1/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 0 (Transforming Growth Factor beta1); SY7Q814VUP (Calcium)
[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:161108
[St] Status:MEDLINE


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[PMID]:27506849
[Au] Autor:Albarrán L; López JJ; Gómez LJ; Salido GM; Rosado JA
[Ad] Endereço:Department of Physiology (Cellular Physiology Research Group), University of Extremadura, Cáceres 10003, Spain.
[Ti] Título:SARAF modulates TRPC1, but not TRPC6, channel function in a STIM1-independent manner.
[So] Source:Biochem J;473(20):3581-3595, 2016 Oct 15.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Canonical transient receptor potential-1 (TRPC1) is an almost ubiquitously expressed channel that plays a relevant role in cell function. As other TRPC members, TRPC1 forms receptor-operated cation channels that exhibit both STIM1-dependent and store-independent behaviour. The STIM1 inhibitor SARAF (for store-operated Ca entry (SOCE)-associated regulatory factor) modulates SOCE by interaction with the STIM1 region responsible for Orai1 activation (SOAR). Furthermore, SARAF modulates Ca entry through the arachidonate-regulated Ca (ARC) channels, consisting of Orai1 and Orai3 heteropentamers and plasma membrane-resident STIM1. While a role for STIM1-Orai1-mediated signals has been demonstrated, the possible role of SARAF in TRPC1 function remains unknown. Here, we provide evidence for the interaction of SARAF with TRPC1, independently of STIM1 both in STIM1-deficient NG115-401L cells and SH-SY5Y cells endogenously expressing STIM1. Silencing of SARAF expression in STIM1-deficient cells demonstrated that SARAF plays a negative regulatory role in TRPC1-mediated Ca entry. The interaction of SARAF with TRPC1 in STIM1-deficient cells, as well as with the TRPC1 pool not associated with STIM1 in STIM1-expressing cells was enhanced by stimulation with the physiological agonist ATP. In contrast with TRPC1, we found that the interaction between SARAF and TRPC6 was constitutive rather than inducible by agonist stimulation. Furthermore, we found that SARAF expression silencing was without effect on Ca entry evoked by agonists in TRPC6 overexpressing cells, as well as in Ca influx evoked by the TRPC6 activator Hyp9. These findings provide evidence for a new regulator of TRPC1 channel function and highlight the relevance of SARAF in intracellular Ca homeostasis.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Proteínas de Membrana/metabolismo
Proteínas de Neoplasias/metabolismo
Molécula 1 de Interação Estromal/metabolismo
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Transporte Biológico/genética
Transporte Biológico/fisiologia
Western Blotting
Linhagem Celular Tumoral
Seres Humanos
Imunoprecipitação
Proteínas de Membrana/genética
Proteínas de Neoplasias/genética
Ligação Proteica/genética
Ligação Proteica/fisiologia
Molécula 1 de Interação Estromal/genética
Canais de Cátion TRPC/genética
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (STIM1 protein, human); 0 (Stromal Interaction Molecule 1); 0 (TMEM66 protein, human); 0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 0 (transient receptor potential cation channel, subfamily C, member 1); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160811
[St] Status:MEDLINE


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[PMID]:27161231
[Au] Autor:Bouron A; Chauvet S; Dryer S; Rosado JA
[Ad] Endereço:Université Grenoble Alpes, 38000, Grenoble, France. alexandre.bouron@cea.fr.
[Ti] Título:Second Messenger-Operated Calcium Entry Through TRPC6.
[So] Source:Adv Exp Med Biol;898:201-49, 2016.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canonical transient receptor potential 6 (TRPC6) proteins assemble into heteromultimeric structures forming non-selective cation channels. In addition, many TRPC6-interacting proteins have been identified like some enzymes, channels, pumps, cytoskeleton-associated proteins, immunophilins, or cholesterol-binding proteins, indicating that TRPC6 are engaged into macromolecular complexes. Depending on the cell type and the experimental conditions used, TRPC6 activity has been reported to be controlled by diverse modalities. For instance, the second messenger diacylglycerol, store-depletion, the plant extract hyperforin or H2O2 have all been shown to trigger the opening of TRPC6 channels. A well-characterized consequence of TRPC6 activation is the elevation of the cytosolic concentration of Ca(2+). This latter response can reflect the entry of Ca(2+) through open TRPC6 channels but it can also be due to the Na(+)/Ca(2+) exchanger (operating in its reverse mode) or voltage-gated Ca(2+) channels (recruited in response to a TRPC6-mediated depolarization). Although TRPC6 controls a diverse array of biological functions in many tissues and cell types, its pathophysiological functions are far from being fully understood. This chapter covers some key features of TRPC6, with a special emphasis on their biological significance in kidney and blood cells.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Sistemas do Segundo Mensageiro
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Transporte de Íons
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-26974-0_10


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[PMID]:27125747
[Au] Autor:Xie J; Wu YL; Huang CL
[Ad] Endereço:University of Texas Southwestern Medical Center, Dallas, TX, United States.
[Ti] Título:Deficiency of Soluble α-Klotho as an Independent Cause of Uremic Cardiomyopathy.
[So] Source:Vitam Horm;101:311-30, 2016.
[Is] ISSN:0083-6729
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease (CVD) is the major cause of mortality for patients with chronic kidney disease (CKD). Cardiac hypertrophy, occurring in up to 95% patients with CKD (also known as uremic cardiomyopathy), increases their risk for cardiovascular death. Many CKD-specific risk factors of uremic cardiomyopathy have been recognized, such as secondary hyperparathyroidism, indoxyl sulfate (IS)/p-cresyl, and vitamin D deficiency. However, several randomized controlled trials have recently shown that these risk factors have little impact on the mortality of CVD. Klotho is a type 1 membrane protein predominantly produced in the kidney, and CKD is known to be a Klotho-deficient state. Because of its important role in FGF23 and phosphate metabolism, Klotho is believed to affect cardiac growth and function indirectly through FGF23 and phosphate. Recent studies showed that soluble Klotho protects the heart against stress-induced cardiac hypertrophy by inhibiting TRPC6 channel-mediated abnormal Ca(2+) signaling in the heart, and the decreased level of circulating soluble Klotho in CKD is an important cause of uremic cardiomyopathy independent of FGF23 and phosphate. These new evidence suggested that Klotho is an independent contributing factor for uremic cardiomyopathy and a possible new target for treatment of this disease.
[Mh] Termos MeSH primário: Cardiomiopatias/etiologia
Glucuronidase/deficiência
Uremia/etiologia
[Mh] Termos MeSH secundário: Animais
Cardiomegalia
Cardiomiopatias/epidemiologia
Fatores de Crescimento de Fibroblastos/fisiologia
Seres Humanos
Hiperparatireoidismo
Doenças Metabólicas/complicações
Minerais/metabolismo
Fosfatos/metabolismo
Insuficiência Renal Crônica/metabolismo
Canais de Cátion TRPC
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Minerals); 0 (Phosphates); 0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 0 (fibroblast growth factor 23); 62031-54-3 (Fibroblast Growth Factors); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160430
[St] Status:MEDLINE


  8 / 277 MEDLINE  
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[PMID]:27011063
[Au] Autor:Wen L; Liang C; Chen E; Chen W; Liang F; Zhi X; Wei T; Xue F; Li G; Yang Q; Gong W; Feng X; Bai X; Liang T
[Ad] Endereço:Department of General Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, PR China.
[Ti] Título:Regulation of Multi-drug Resistance in hepatocellular carcinoma cells is TRPC6/Calcium Dependent.
[So] Source:Sci Rep;6:23269, 2016 Mar 24.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is notoriously refractory to chemotherapy because of its tendency to develop multi-drug resistance (MDR), whose various underlying mechanisms make it difficult to target. The calcium signalling pathway is associated with many cellular biological activities, and is also a critical player in cancer. However, its role in modulating tumour MDR remains unclear. In this study, stimulation by doxorubicin, hypoxia and ionizing radiation was used to induce MDR in HCC cells. A sustained aggregation of intracellular calcium was observed upon these stimuli, while inhibition of calcium signalling enhanced the cells' sensitivity to various drugs by attenuating epithelial-mesenchymal transition (EMT), Hif1-α signalling and DNA damage repair. The effect of calcium signalling is mediated via transient receptor potential canonical 6 (TRPC6), a subtype of calcium-permeable channel. An in vivo xenograft model of HCC further confirmed that inhibiting TRPC6 enhanced the efficacy of doxorubicin. In addition, we deduced that STAT3 activation is a downstream signalling pathway in MDR. Collectively, this study demonstrated that the various mechanisms regulating MDR in HCC cells are calcium dependent through the TRPC6/calcium/STAT3 pathway. We propose that targeting TRPC6 in HCC may be a novel antineoplastic strategy, especially combined with chemotherapy.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Carcinoma Hepatocelular/patologia
Neoplasias Hepáticas/patologia
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/metabolismo
Linhagem Celular Tumoral
Resistência a Múltiplos Medicamentos
Resistência a Medicamentos Antineoplásicos
Inativação Gênica
Seres Humanos
Neoplasias Hepáticas/metabolismo
Canais de Cátion TRPC/genética
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160325
[St] Status:MEDLINE
[do] DOI:10.1038/srep23269


  9 / 277 MEDLINE  
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[PMID]:26937558
[Au] Autor:Ma R; Chaudhari S; Li W
[Ad] Endereço:1 Institute for Cardiovascular and Metabolic Diseases, University of North Texas Health Science Center , Fort Worth, Texas.
[Ti] Título:Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.
[So] Source:Antioxid Redox Signal;25(13):732-748, 2016 Nov 01.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SIGNIFICANCE: Regulation of Ca signaling cascade by reactive oxygen species (ROS) is becoming increasingly evident and this regulation represents a key mechanism for control of many fundamental cellular functions. Canonical transient receptor potential (TRPC) 6, a member of Ca -conductive channel in the TRPC family, is widely expressed in kidney cells, including glomerular mesangial cells, podocytes, tubular epithelial cells, and vascular myocytes in renal microvasculature. Both overproduction of ROS and dysfunction of TRPC6 channel are involved in renal injury in animal models and human subjects. Although regulation of TRPC channel function by ROS has been well described in other tissues and cell types, such as vascular smooth muscle, this important cell regulatory mechanism has not been fully reviewed in kidney cells. Recent Advances: Accumulating evidence has shown that TRPC6 is a redox-sensitive channel, and modulation of TRPC6 Ca signaling by altering TRPC6 protein expression or TRPC6 channel activity in kidney cells is a downstream mechanism by which ROS induce renal damage. CRITICAL ISSUES: This review highlights how recent studies analyzing function and expression of TRPC6 channels in the kidney and their response to ROS improve our mechanistic understanding of oxidative stress-related kidney diseases. FUTURE DIRECTIONS: Although it is evident that ROS regulate TRPC6-mediated Ca signaling in several types of kidney cells, further study is needed to identify the underlying molecular mechanism. We hope that the newly identified ROS/TRPC6 pathway will pave the way to new, promising therapeutic strategies to target kidney diseases such as diabetic nephropathy. Antioxid. Redox Signal. 25, 732-748.
[Mh] Termos MeSH primário: Nefropatias/metabolismo
Rim/fisiologia
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Seres Humanos
Rim/patologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais
Canal de Cátion TRPC6
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160304
[St] Status:MEDLINE


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[PMID]:26913924
[Au] Autor:Shen B; He Y; Zhou S; Zhao H; Mei M; Wu X
[Ad] Endereço:Department of Kidney, Southwest Hospital, Third Military Medical University, Chongqing, China (mainland).
[Ti] Título:TRPC6 May Protect Renal Ischemia-Reperfusion Injury Through Inhibiting Necroptosis of Renal Tubular Epithelial Cells.
[So] Source:Med Sci Monit;22:633-41, 2016 Feb 25.
[Is] ISSN:1643-3750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND The aim of this study was to explore the potential role of TRPC6 in the pathophysiology of HK-2 cell injury following ischemia reperfusion (I/R). MATERIAL AND METHODS TRPC6 expression was analyzed by immunofluorescence staining. siRNA was transfected to knockout of TRPC6 in HK-2 cells, and in vitro I/R was then induced. Cell apoptosis and necrosis were determined by Annexin V-FITC/PI staining. Necroptosis was determined by necrostatin-1 and expressions of necroptosis-related proteins were evaluated. OAG, SKF96365, or KN-93 was further used to interfere with TRPC6 expression. RESULTS Cytoplasmic TRPC6 expression was demonstrated. I/R induced TRPC6 expression in normal or NC siRNA-transfected cells but not in TRPC6 siRNA-knockout ones. There was a progressive increase in apoptotic and necrotic cells with increasing reoxygenation time in all 3 groups, while necrosis in TRPC6 siRNA-transfected cells was comparatively higher than that of the other 2 groups (p<0.05). Expressions of necroptosis-related proteins were interfered with following I/R and these effects were enhanced by TRPC6 siRNA. Application of OAG, SKF96365, or KN93 further affected necroptosis following I/R. CONCLUSIONS This study described the expression and functional relevance of TRPC6 in the pathophysiology of HK-2 cell following I/R. Our results regarding the ability of TRPC6 to specifically interrupt necroptosis may shed new light on its role in prevention and control of ischemic kidney injury.
[Mh] Termos MeSH primário: Apoptose
Células Epiteliais/patologia
Isquemia/patologia
Túbulos Renais/irrigação sanguínea
Túbulos Renais/patologia
Substâncias Protetoras/metabolismo
Traumatismo por Reperfusão/prevenção & controle
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Benzilaminas/farmacologia
Western Blotting
Linhagem Celular
Forma Celular/efeitos dos fármacos
Regulação para Baixo/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Imunofluorescência
Seres Humanos
Imidazóis/farmacologia
Necrose
Oxigênio
RNA Interferente Pequeno/metabolismo
Traumatismo por Reperfusão/patologia
Sulfonamidas/farmacologia
Canal de Cátion TRPC6
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzylamines); 0 (Imidazoles); 0 (Protective Agents); 0 (RNA, Small Interfering); 0 (Sulfonamides); 0 (TRPC Cation Channels); 0 (TRPC6 Cation Channel); 0 (TRPC6 protein, human); 139298-40-1 (KN 93); I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole); S88TT14065 (Oxygen)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160226
[St] Status:MEDLINE



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