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[PMID]:29300865
[Au] Autor:Fan J; Wang K; Zirkin B; Papadopoulos V
[Ad] Endereço:Research Institute of the McGill University Health Centre and Department of Medicine, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
[Ti] Título:CRISPR/Cas9‒Mediated Tspo Gene Mutations Lead to Reduced Mitochondrial Membrane Potential and Steroid Formation in MA-10 Mouse Tumor Leydig Cells.
[So] Source:Endocrinology;159(2):1130-1146, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The outer mitochondrial membrane translocator protein (TSPO) binds cholesterol with high affinity and is involved in mediating its delivery into mitochondria, the rate-limiting step in hormone-induced steroidogenesis. Specific ligand binding to TSPO has been shown to initiate steroid formation. However, recent studies of the genetic deletion of Tspo have provided conflicting results. Here, we address and extend previous studies by examining the effects of Tspo-specific mutations on steroid formation in hormone- and cyclic adenosine monophosphate (cAMP)-responsive MA-10 cells, using the CRISPR/Cas9 system. Two mutant subcell lines, nG1 and G2G, each carrying a Tspo exon2-specific genome modification, and two control subcell lines, G1 and HH, each carrying a wild-type Tspo, were produced. In response to dibutyryl cAMP, the nG1 and G2G cells produced progesterone at levels significantly lower than those produced by the corresponding control cells G1 and HH. Neutral lipid homeostasis, which provides free cholesterol for steroid biosynthesis, was altered significantly in the Tspo mutant cells. Interestingly, the mitochondrial membrane potential (ΔΨm) of the Tspo mutant cells was significantly reduced compared with that of the control cells, likely because of TSPO interactions with the voltage-dependent anion channel and tubulin at the outer mitochondrial membrane. Steroidogenic acute regulatory protein (STAR) expression was induced in nG1 cells, suggesting that reduced TSPO affected STAR synthesis and/or processing. Taken together, these results provide further evidence for the critical role of TSPO in steroid biosynthesis and suggest that it may function at least in part via its regulation of ΔΨm and effects on STAR.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Hormônios Esteroides Gonadais/biossíntese
Células Intersticiais do Testículo/metabolismo
Potencial da Membrana Mitocondrial/genética
Mutagênese Sítio-Dirigida
Mutação
Receptores de GABA/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Tumor de Células de Leydig/genética
Tumor de Células de Leydig/metabolismo
Tumor de Células de Leydig/patologia
Masculino
Camundongos
Mutagênese Sítio-Dirigida/métodos
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Esteroides/biossíntese
Neoplasias Testiculares/genética
Neoplasias Testiculares/metabolismo
Neoplasias Testiculares/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bzrp protein, mouse); 0 (Gonadal Steroid Hormones); 0 (Phosphoproteins); 0 (Receptors, GABA); 0 (Steroids); 0 (steroidogenic acute regulatory protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03065


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[PMID]:29283228
[Au] Autor:Bazyan AS
[Ti] Título:Integration the Highest Function of Brain as the Basis of Cognition.
[So] Source:Usp Fiziol Nauk;47(3):17-29, 2016 Jul-Sep.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Based on the process needs, motivations and emotions, are describing molecular, cellular and systemic mechanisms of goal-direction motivated behavior. Goal-direction behavior is impossible without the orientation in space and forming a cognitive map. This process implements the hippocampus, via the neocortical connections. The hippocampus is linked to the amygdala, which is involved in the implementation of emotional behavior and organizing emotionally intense cognitive map or context of the environment.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/fisiologia
Cognição/fisiologia
Emoções/fisiologia
Hipocampo/fisiologia
Rede Nervosa/fisiologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/anatomia & histologia
Mapeamento Encefálico
Corpo Estriado/anatomia & histologia
Corpo Estriado/fisiologia
Hipocampo/anatomia & histologia
Seres Humanos
Motivação/fisiologia
Neocórtex/anatomia & histologia
Neocórtex/fisiologia
Rede Nervosa/anatomia & histologia
Plasticidade Neuronal/fisiologia
Receptores Dopaminérgicos/fisiologia
Receptores de GABA/fisiologia
Receptores de Glutamato Metabotrópico/fisiologia
Transdução de Sinais
Tálamo/anatomia & histologia
Tálamo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Dopamine); 0 (Receptors, GABA); 0 (Receptors, Metabotropic Glutamate)
[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:171229
[St] Status:MEDLINE


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[PMID]:29253887
[Au] Autor:Jensen R
[Ad] Endereço:Research Service, VA Boston Healthcare System, Boston, Massachusetts, United States of America.
[Ti] Título:Effects of GABACR and mGluR1 antagonists on contrast response functions of Sprague-Dawley and P23H rat retinal ganglion cells.
[So] Source:PLoS One;12(12):e0189980, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The GABACR antagonist TPMPA and the mGluR1 antagonist JNJ16259685 have been shown previously to alter the sensitivity of retinal ganglion cells (RGCs) in the Sprague-Dawley (SD) rat and P23H rat (animal model of retinitis pigmentosa) to brief flashes of light. In order to better understand the effects of these antagonists on the visual responses of SD and P23H rat RGCs, I examined the responses of RGCs to a drifting sinusoidal grating of various contrasts. Multielectrode array recordings were made from RGCs to a drifting sinusoidal grating of a spatial frequency of 1 cycle/mm and a temporal frequency of 2 cycles/s. In both SD and P23H rat retinas, contrast response functions were found to have a variable shape across cells. Some cells showed saturation of responses at high contrast levels while others did not. Whereas 49% of SD rat RGCs exhibited response saturation, only 14% of P23H rat RGCs showed response saturation. TPMPA decreased the responses of saturating SD rat RGCs to low (6% to 13%) grating contrasts but increased the response to the highest contrast (83%) tested. JNJ16259685 did not significantly affect the contrast response functions of either saturating or non-saturating SD rat RGCs. In contrast, both TPMPA and JNJ16259685 increased the responses of saturating and non-saturating P23H rat RGCs to all grating contrasts. Neither TPMPA nor JNJ16259685 affected the contrast thresholds of SD rat RGCs, but both antagonists lowered the contrast thresholds of P23H rat RGCs. Overall, the findings show that GABACR and mGluR1 antagonists have differential effects on the contrast response functions of SD and P23H rat RGCs. Notably, these receptor antagonists increase the responsiveness of P23H rat RGCs to both low and high contrast visual stimuli.
[Mh] Termos MeSH primário: Receptores de GABA/metabolismo
Receptores de Glutamato Metabotrópico/antagonistas & inibidores
Células Ganglionares da Retina/metabolismo
Retinite Pigmentosa/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Calibragem
Modelos Animais de Doenças
Eletrodos
Eletrofisiologia
Feminino
Homozigoto
Masculino
Ratos
Ratos Sprague-Dawley
Receptores de Glutamato Metabotrópico/metabolismo
Retina/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-C receptor); 0 (Receptors, GABA); 0 (Receptors, Metabotropic Glutamate); 0 (metabotropic glutamate receptor type 1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189980


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[PMID]:29053775
[Au] Autor:Datta G; Colasanti A; Rabiner EA; Gunn RN; Malik O; Ciccarelli O; Nicholas R; Van Vlierberghe E; Van Hecke W; Searle G; Santos-Ribeiro A; Matthews PM
[Ad] Endereço:Division of Brain Sciences, Imperial College London, UK.
[Ti] Título:Neuroinflammation and its relationship to changes in brain volume and white matter lesions in multiple sclerosis.
[So] Source:Brain;140(11):2927-2938, 2017 Nov 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Brain magnetic resonance imaging is an important tool in the diagnosis and monitoring of multiple sclerosis patients. However, magnetic resonance imaging alone provides limited information for predicting an individual patient's disability progression. In part, this is because magnetic resonance imaging lacks sensitivity and specificity for detecting chronic diffuse and multi-focal inflammation mediated by activated microglia/macrophages. The aim of this study was to test for an association between 18 kDa translocator protein brain positron emission tomography signal, which arises largely from microglial activation, and measures of subsequent disease progression in multiple sclerosis patients. Twenty-one patients with multiple sclerosis (seven with secondary progressive disease and 14 with a relapsing remitting disease course) underwent T1- and T2-weighted and magnetization transfer magnetic resonance imaging at baseline and after 1 year. Positron emission tomography scanning with the translocator protein radioligand 11C-PBR28 was performed at baseline. Brain tissue and lesion volumes were segmented from the T1- and T2-weighted magnetic resonance imaging and relative 11C-PBR28 uptake in the normal-appearing white matter was estimated as a distribution volume ratio with respect to a caudate pseudo-reference region. Normal-appearing white matter distribution volume ratio at baseline was correlated with enlarging T2-hyperintense lesion volumes over the subsequent year (ρ = 0.59, P = 0.01). A post hoc analysis showed that this association reflected behaviour in the subgroup of relapsing remitting patients (ρ = 0.74, P = 0.008). By contrast, in the subgroup of secondary progressive patients, microglial activation at baseline was correlated with later progression of brain atrophy (ρ = 0.86, P = 0.04). A regression model including the baseline normal-appearing white matter distribution volume ratio, T2 lesion volume and normal-appearing white matter magnetization transfer ratio for all of the patients combined explained over 90% of the variance in enlarging lesion volume over the subsequent 1 year. Glial activation in white matter assessed by translocator protein PET significantly improves predictions of white matter lesion enlargement in relapsing remitting patients and is associated with greater brain atrophy in secondary progressive disease over a period of short term follow-up.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Inflamação/diagnóstico por imagem
Esclerose Múltipla Crônica Progressiva/diagnóstico por imagem
Esclerose Múltipla Recidivante-Remitente/diagnóstico por imagem
Substância Branca/diagnóstico por imagem
[Mh] Termos MeSH secundário: Acetamidas
Adulto
Atrofia
Encéfalo/patologia
Radioisótopos de Carbono
Feminino
Seres Humanos
Processamento de Imagem Assistida por Computador
Imagem por Ressonância Magnética
Masculino
Microglia
Meia-Idade
Tamanho do Órgão
Tomografia por Emissão de Pósitrons
Piridinas
Receptores de GABA
Substância Branca/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Carbon Radioisotopes); 0 (N-(2-methoxybenzyl)-N-(4-phenoxypyridin-3-yl)acetamide); 0 (Pyridines); 0 (Receptors, GABA); 0 (TSPO protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx228


  5 / 3484 MEDLINE  
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[PMID]:28968465
[Au] Autor:Narayan N; Mandhair H; Smyth E; Dakin SG; Kiriakidis S; Wells L; Owen D; Sabokbar A; Taylor P
[Ad] Endereço:Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Headington, Oxford, United Kingdom.
[Ti] Título:The macrophage marker translocator protein (TSPO) is down-regulated on pro-inflammatory 'M1' human macrophages.
[So] Source:PLoS One;12(10):e0185767, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The translocator protein (TSPO) is a mitochondrial membrane protein, of as yet uncertain function. Its purported high expression on activated macrophages, has lent utility to TSPO targeted molecular imaging in the form of positron emission tomography (PET), as a means to detect and quantify inflammation in vivo. However, existing literature regarding TSPO expression on human activated macrophages is lacking, mostly deriving from brain tissue studies, including studies of brain malignancy, and inflammatory diseases such as multiple sclerosis. Here, we utilized three human sources of monocyte derived macrophages (MDM), from THP-1 monocytes, healthy peripheral blood monocytes and synovial fluid monocytes from patients with rheumatoid arthritis, to undertake a detailed investigation of TSPO expression in activated macrophages. In this work, we demonstrate a consistent down-regulation of TSPO mRNA and protein in macrophages activated to a pro-inflammatory, or 'M1' phenotype. Conversely, stimulation of macrophages to an M2 phenotype with IL-4, dexamethasone or TGF-ß1 did not alter TSPO expression, regardless of MDM source. The reasons for this are uncertain, but our study findings add some supporting evidence for recent investigations concluding that TSPO may be involved in negative regulation of inflammatory responses in macrophages.
[Mh] Termos MeSH primário: Regulação para Baixo
Inflamação/metabolismo
Macrófagos/metabolismo
Receptores de GABA/metabolismo
[Mh] Termos MeSH secundário: Artrite Reumatoide/metabolismo
Linhagem Celular
Seres Humanos
Interferon gama/farmacologia
Interleucina-4/farmacologia
Lipopolissacarídeos/farmacologia
Monócitos/metabolismo
Tomografia por Emissão de Pósitrons
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores de GABA/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (RNA, Messenger); 0 (Receptors, GABA); 0 (TSPO protein, human); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185767


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[PMID]:28954853
[Au] Autor:Pelkey KA; Chittajallu R; Craig MT; Tricoire L; Wester JC; McBain CJ
[Ad] Endereço:Porter Neuroscience Center, Eunice Kennedy-Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland; Institute of Biomedical and Clinical Sciences, University of Exeter Medical School, Hatherly Laboratories, University of Exeter, Exeter, Uni
[Ti] Título:Hippocampal GABAergic Inhibitory Interneurons.
[So] Source:Physiol Rev;97(4):1619-1747, 2017 Oct 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the hippocampus GABAergic local circuit inhibitory interneurons represent only ~10-15% of the total neuronal population; however, their remarkable anatomical and physiological diversity allows them to regulate virtually all aspects of cellular and circuit function. Here we provide an overview of the current state of the field of interneuron research, focusing largely on the hippocampus. We discuss recent advances related to the various cell types, including their development and maturation, expression of subtype-specific voltage- and ligand-gated channels, and their roles in network oscillations. We also discuss recent technological advances and approaches that have permitted high-resolution, subtype-specific examination of their roles in numerous neural circuit disorders and the emerging therapeutic strategies to ameliorate such pathophysiological conditions. The ultimate goal of this review is not only to provide a touchstone for the current state of the field, but to help pave the way for future research by highlighting where gaps in our knowledge exist and how a complete appreciation of their roles will aid in future therapeutic strategies.
[Mh] Termos MeSH primário: Neurônios GABAérgicos/metabolismo
Hipocampo/metabolismo
Interneurônios/metabolismo
Inibição Neural
Transmissão Sináptica
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Animais
Doenças do Sistema Nervoso Central/metabolismo
Doenças do Sistema Nervoso Central/patologia
Doenças do Sistema Nervoso Central/fisiopatologia
Neurônios GABAérgicos/patologia
Hipocampo/patologia
Hipocampo/fisiopatologia
Seres Humanos
Interneurônios/patologia
Rede Nervosa/metabolismo
Rede Nervosa/patologia
Rede Nervosa/fisiopatologia
Receptores de GABA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, GABA); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00007.2017


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[PMID]:28942923
[Au] Autor:Paul A; Crow M; Raudales R; He M; Gillis J; Huang ZJ
[Ad] Endereço:Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
[Ti] Título:Transcriptional Architecture of Synaptic Communication Delineates GABAergic Neuron Identity.
[So] Source:Cell;171(3):522-539.e20, 2017 Oct 19.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding the organizational logic of neural circuits requires deciphering the biological basis of neuronal diversity and identity, but there is no consensus on how neuron types should be defined. We analyzed single-cell transcriptomes of a set of anatomically and physiologically characterized cortical GABAergic neurons and conducted a computational genomic screen for transcriptional profiles that distinguish them from one another. We discovered that cardinal GABAergic neuron types are delineated by a transcriptional architecture that encodes their synaptic communication patterns. This architecture comprises 6 categories of ∼40 gene families, including cell-adhesion molecules, transmitter-modulator receptors, ion channels, signaling proteins, neuropeptides and vesicular release components, and transcription factors. Combinatorial expression of select members across families shapes a multi-layered molecular scaffold along the cell membrane that may customize synaptic connectivity patterns and input-output signaling properties. This molecular genetic framework of neuronal identity integrates cell phenotypes along multiple axes and provides a foundation for discovering and classifying neuron types.
[Mh] Termos MeSH primário: Neurônios GABAérgicos/citologia
Perfilação da Expressão Gênica
Análise de Célula Única
[Mh] Termos MeSH secundário: Animais
Moléculas de Adesão Celular Neuronais/metabolismo
Matriz Extracelular/metabolismo
Neurônios GABAérgicos/metabolismo
Camundongos
Receptores de GABA/metabolismo
Receptores Ionotrópicos de Glutamato/metabolismo
Transdução de Sinais
Sinapses
Transcrição Genética
Zinco/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules, Neuronal); 0 (Receptors, GABA); 0 (Receptors, Ionotropic Glutamate); 56-12-2 (gamma-Aminobutyric Acid); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


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[PMID]:28858490
[Au] Autor:Milite C; Barresi E; Da Pozzo E; Costa B; Viviano M; Porta A; Messere A; Sbardella G; Da Settimo F; Novellino E; Cosconati S; Castellano S; Taliani S; Martini C
[Ad] Endereço:Dipartimento di Farmacia, Università di Salerno , Via Giovanni Paolo II 132, 84084 Fisciano, Salerno, Italy.
[Ti] Título:Exploiting the 4-Phenylquinazoline Scaffold for the Development of High Affinity Fluorescent Probes for the Translocator Protein (TSPO).
[So] Source:J Med Chem;60(18):7897-7909, 2017 Sep 28.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The quinazoline class was exploited to search for a new translocator protein (TSPO) fluorescent probe endowed with improved affinity and residence time (RT). Computational studies on an "in-house" collection of quinazoline derivatives, featuring highly steric demanding groups at the amide nitrogen, suggested that, despite their molecular extension, these ligands are still easily lodged in the TSPO binding site. Binding assays supported this hypothesis, highlighting a low nanomolar/subnanomolar affinity of these ligands, together with a higher RT of the representative compound 11 with respect to our previously reported indole-based fluorescent probe. Thanks to the amenability of the amide nitrogen atom to be substituted with bulky groups, we developed quinazoline-based imaging tools by fluorescently labeling the scaffold at this position. Probes with relevant TSPO affinity, favorable spectroscopic properties, and improved RT were identified. The results from fluorescence microscopy showed that these probes specifically labeled the TSPO at the mitochondrial level in the U343 cell line.
[Mh] Termos MeSH primário: Corantes Fluorescentes/química
Quinazolinas/química
Receptores de GABA/análise
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
Ligantes
Microscopia de Fluorescência
Mitocôndrias/química
Imagem Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Ligands); 0 (Quinazolines); 0 (Receptors, GABA); 0 (TSPO protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b01031


  9 / 3484 MEDLINE  
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[PMID]:28771957
[Au] Autor:Iacobazzi RM; Lopalco A; Cutrignelli A; Laquintana V; Lopedota A; Franco M; Denora N
[Ad] Endereço:Istituto Tumori IRCCS Giovanni Paolo II, Viale O. Flacco 65, 70124, Bari, Italy.
[Ti] Título:Bridging Pharmaceutical Chemistry with Drug and Nanoparticle Targeting to Investigate the Role of the 18-kDa Translocator Protein TSPO.
[So] Source:ChemMedChem;12(16):1261-1274, 2017 Aug 22.
[Is] ISSN:1860-7187
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:An interesting mitochondrial biomarker is the 18-kDa mitochondrial translocator protein (TSPO). Decades of study have shown that this protein plays an important role in a wide range of cellular functions, including opening of the mitochondrial permeability transition pore as well as programmed cell death and proliferation. Variations in TSPO expression have been correlated to different diseases, from tumors to endocrine and neurological disorders. TSPO has therefore become an appealing target for both early diagnosis and selective mitochondrial drug delivery. The number of structurally different TSPO ligands examined has increased over time, highlighting the scientific community's growing understanding of the roles of TSPO in normal and pathological conditions. However, only few TSPO ligands are characterized by the presence of groups that are potentially derivatizable; therefore only few such ligands are well suited for the preparation of targeted prodrugs or nanocarriers able to deliver therapeutics and/or diagnostic agents to mitochondria. This review provides an overview of the very few examples of drug delivery systems characterized by moieties that target TSPO.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Nanopartículas/química
Receptores de GABA/metabolismo
[Mh] Termos MeSH secundário: Amidas/química
Amidas/metabolismo
Animais
Azepinas/química
Azepinas/metabolismo
Portadores de Fármacos/química
Seres Humanos
Ligantes
Pró-Fármacos/química
Pró-Fármacos/metabolismo
Ligação Proteica
Pirimidinas/química
Pirimidinas/metabolismo
Receptores de GABA/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Amides); 0 (Azepines); 0 (Drug Carriers); 0 (Ligands); 0 (Prodrugs); 0 (Pyrimidines); 0 (Receptors, GABA)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1002/cmdc.201700322


  10 / 3484 MEDLINE  
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[PMID]:28667430
[Au] Autor:Aggarwal S; Ahuja V; Paul J
[Ad] Endereço:School of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
[Ti] Título:Attenuated GABAergic Signaling in Intestinal Epithelium Contributes to Pathogenesis of Ulcerative Colitis.
[So] Source:Dig Dis Sci;62(10):2768-2779, 2017 Oct.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Neuromediators produced by enteric nervous system regulate inflammatory processes via interacting with enteric immune system. Role of γ-aminobutyric acid (GABA), which is also a neuromediator, has been implicated in autoimmune diseases like multiple sclerosis, type 1 diabetes, and rheumatoid arthritis, where they modulate the immune responses. However, its role in ulcerative colitis (UC) has not been defined. AIMS: This study was carried out to investigate the role of GABA and its signaling components in pathogenesis of UC. METHODS: Peripheral blood, colon mucosal biopsy, and fecal specimens were collected from UC and control groups. Quantification of GABA was done using ELISA. Expression of GABAergic signal system components was analyzed through RT-PCR analysis. Enumeration of GABA-producing bacteria was done by qPCR analysis. Activity of p38 MAPK and expression of proinflammatory cytokines were determined by immunohistochemistry and RT-PCR analysis, respectively. RESULTS: GABA levels were significantly reduced in patients with UC as compared to control group when measured in serum and colon biopsy. Altered expression of GABAergic signal system was observed in UC patients. Reduced abundance of selected GABA-producing bacteria was detected in stool samples of UC patients as compared to control. p38 MAPK activity and expression of its downstream effector cytokines were found to be increased in UC patients as compared to control. CONCLUSIONS: Reduced levels of GABA were observed in patients with UC, and this leads to hyperactivation of p38 MAPK and overexpression of downstream effector cytokines suggesting a role of GABA in pathogenesis of UC.
[Mh] Termos MeSH primário: Colite Ulcerativa/metabolismo
Colo/química
Mucosa Intestinal/química
Receptores de GABA/análise
Ácido gama-Aminobutírico/análise
[Mh] Termos MeSH secundário: Adulto
Bactérias/química
Bactérias/genética
Biópsia
Estudos de Casos e Controles
Colite Ulcerativa/microbiologia
Colite Ulcerativa/patologia
Colo/microbiologia
Colo/patologia
Citocinas/análise
Citocinas/genética
Regulação para Baixo
Fezes/química
Fezes/microbiologia
Feminino
Seres Humanos
Mediadores da Inflamação/análise
Mucosa Intestinal/microbiologia
Mucosa Intestinal/patologia
Masculino
Meia-Idade
Receptores de GABA/genética
Transdução de Sinais
Adulto Jovem
Proteínas Quinases p38 Ativadas por Mitógeno/análise
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Receptors, GABA); 56-12-2 (gamma-Aminobutyric Acid); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4662-3



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