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[PMID]:27776507
[Au] Autor:Konstantinidou C; Taraviras S; Pachnis V
[Ad] Endereço:The Francis Crick Institute, Mill Hill Laboratory, The Ridgeway, Mill Hill, London, NW7 1AA, UK.
[Ti] Título:Geminin prevents DNA damage in vagal neural crest cells to ensure normal enteric neurogenesis.
[So] Source:BMC Biol;14(1):94, 2016 10 24.
[Is] ISSN:1741-7007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In vertebrate organisms, the neural crest (NC) gives rise to multipotential and highly migratory progenitors which are distributed throughout the embryo and generate, among other structures, the peripheral nervous system, including the intrinsic neuroglial networks of the gut, i.e. the enteric nervous system (ENS). The majority of enteric neurons and glia originate from vagal NC-derived progenitors which invade the foregut mesenchyme and migrate rostro-caudally to colonise the entire length of the gut. Although the migratory behaviour of NC cells has been studied extensively, it remains unclear how their properties and response to microenvironment change as they navigate through complex cellular terrains to reach their target embryonic sites. RESULTS: Using conditional gene inactivation in mice we demonstrate here that the cell cycle-dependent protein Geminin (Gem) is critical for the survival of ENS progenitors in a stage-dependent manner. Gem deletion in early ENS progenitors (prior to foregut invasion) resulted in cell-autonomous activation of DNA damage response and p53-dependent apoptosis, leading to severe intestinal aganglionosis. In contrast, ablation of Gem shortly after ENS progenitors had invaded the embryonic gut did not result in discernible survival or migratory deficits. In contrast to other developmental systems, we obtained no evidence for a role of Gem in commitment or differentiation of ENS lineages. The stage-dependent resistance of ENS progenitors to mutation-induced genotoxic stress was further supported by the enhanced survival of post gut invasion ENS lineages to γ-irradiation relative to their predecessors. CONCLUSIONS: Our experiments demonstrate that, in mammals, NC-derived ENS lineages are sensitive to genotoxic stress in a stage-specific manner. Following gut invasion, ENS progenitors are distinctly resistant to Gem ablation and irradiation in comparison to their pre-enteric counterparts. These studies suggest that the microenvironment of the embryonic gut protects ENS progenitors and their progeny from genotoxic stress.
[Mh] Termos MeSH primário: Dano ao DNA/efeitos dos fármacos
Sistema Nervoso Entérico/citologia
Geminina/farmacologia
Crista Neural/citologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Células Cultivadas
Sistema Nervoso Entérico/efeitos dos fármacos
Feminino
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Camundongos
Neurogênese/efeitos dos fármacos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Geminin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:28467926
[Au] Autor:Grasset E; Puel A; Charpentier J; Collet X; Christensen JE; Tercé F; Burcelin R
[Ad] Endereço:Institut National de la Santé et de la Recherche Médicale (INSERM), 31024 Toulouse, France; Université Paul Sabatier (UPS), Unité Mixte de Recherche (UMR) 1048, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Team 2: Intestinal Risk Factors, Diabetes, Dyslipidemia, Heart Failure, F-3
[Ti] Título:A Specific Gut Microbiota Dysbiosis of Type 2 Diabetic Mice Induces GLP-1 Resistance through an Enteric NO-Dependent and Gut-Brain Axis Mechanism.
[So] Source:Cell Metab;25(5):1075-1090.e5, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucagon-like peptide-1 (GLP-1)-based therapies control glycemia in type 2 diabetic (T2D) patients. However, in some patients the treatment must be discontinued, defining a state of GLP-1 resistance. In animal models we identified a specific set of ileum bacteria impairing the GLP-1-activated gut-brain axis for the control of insulin secretion and gastric emptying. Using prediction algorithms, we identified bacterial pathways related to amino acid metabolism and transport system modules associated to GLP-1 resistance. The conventionalization of germ-free mice demonstrated their role in enteric neuron biology and the gut-brain-periphery axis. Altogether, insulin secretion and gastric emptying require functional GLP-1 receptor and neuronal nitric oxide synthase in the enteric nervous system within a eubiotic gut microbiota environment. Our data open a novel route to improve GLP-1-based therapies.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Disbiose/metabolismo
Sistema Nervoso Entérico/metabolismo
Microbioma Gastrointestinal
Óxido Nítrico/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/patologia
Diabetes Mellitus Tipo 2/microbiologia
Diabetes Mellitus Tipo 2/patologia
Disbiose/microbiologia
Disbiose/patologia
Sistema Nervoso Entérico/microbiologia
Sistema Nervoso Entérico/patologia
Trato Gastrointestinal/metabolismo
Trato Gastrointestinal/microbiologia
Trato Gastrointestinal/patologia
Peptídeo 1 Semelhante ao Glucagon/metabolismo
Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 31C4KY9ESH (Nitric Oxide); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29196262
[Au] Autor:Nishida S; Yoshizaki H; Yasui Y; Kuwahara T; Kiyokawa E; Kohno M
[Ad] Endereço:Department of Pediatric Surgery, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku-gun, Ishikawa 920-0293, Japan.
[Ti] Título:Collagen VI suppresses fibronectin-induced enteric neural crest cell migration by downregulation of focal adhesion proteins.
[So] Source:Biochem Biophys Res Commun;495(1):1461-1467, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The enteric nervous system (ENS) is a network of neurons and glia that are derived from enteric neural crest cells (ENCCs) and essential for regulating peristaltic activity of the colon. ENCCs migrate along the gastrointestinal tract to form the ENS, and disruption of ENCC motility leads to ENS disorders, such as Hirschsprung's disease. Previous ENCC-transplant experiments show that ENCCs can invade into isolated mouse intestines by age E13.5, but not after E15.5. We hypothesized that altered age-specific micro-environments in the intestine are responsible for ENCC invasion/migration. Here, we compared gene expression in the intestine between at E11.5 and E15.5 and identified 1355 differentially expressed transcripts. Among these, we found that genes encoding extracellular matrix (ECM) proteins were enriched. Notably, collagen VI (ColVI) family members were upregulated in the E15.5 mouse intestine at the mRNA and protein levels, whereas fibronectin (FN) was downregulated; however, both proteins showed colocalization at E15.5. To understand the mechanisms of ColVI and FN in ENCC migration, we examined neurosphere or individual ENCC-adherence capabilities toward the ECM. ColVI suppressed FN-induced ENCC spreading/migration, whereas ColVI induced morphologically narrow ENCC spreading and weak stress-fiber formation as compared with those with FN. Additionally, in ENCCs cultured on plates containing ColVI, the expression and phosphorylation of p130 , a members of focal adhesion complexes, was reduced. These data indicated an inhibitory role of ColVI in ENCC migration and suggested that ColVI suppression in the intestine might represent a novel therapeutic strategy for aganglionic colonic diseases.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Colágeno Tipo VI/metabolismo
Sistema Nervoso Entérico/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Fibronectinas/metabolismo
Adesões Focais/metabolismo
Crista Neural/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Regulação para Baixo/fisiologia
Sistema Nervoso Entérico/citologia
Camundongos
Camundongos Endogâmicos C57BL
Crista Neural/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type VI); 0 (Extracellular Matrix Proteins); 0 (Fibronectins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


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[PMID]:28887374
[Au] Autor:Leclair-Visonneau L; Clairembault T; Coron E; Le Dily S; Vavasseur F; Dalichampt M; Péréon Y; Neunlist M; Derkinderen P
[Ad] Endereço:From Inserm (L.L.-V., T.C., E.C., M.N., P.D.), U1235, Nantes; University Nantes (L.L.-V., T.C., E.C., Y.P., M.N., P.D.); Inserm (L.L.-V., E.C., S.L.D., F.V., P.D.), CIC-04; CHU Nantes (L.L.-V., Y.P.), Department of Clinical Neurophysiology; CHU Nantes (T.C., E.C., F.V., M.N.), Institut des Maladies
[Ti] Título:REM sleep behavior disorder is related to enteric neuropathology in Parkinson disease.
[So] Source:Neurology;89(15):1612-1618, 2017 Oct 10.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine whether REM sleep behavior disorder (RBD) in Parkinson disease (PD) is associated with lesions and dysfunctions of the autonomic nervous system by evaluating enteric phosphorylated α-synuclein histopathology (PASH) and permeability. METHODS: A total of 45 patients with PD were included in this cross-sectional study. RBD was diagnosed on the basis of a standardized clinical interview and confirmed by polysomnography. For each patient, 5 biopsies were taken at the junction between the sigmoid and descending colon during the course of a rectosigmoidoscopy. For the detection of enteric PASH, 2 colonic biopsies were analyzed by immunohistochemistry with antibodies against phosphorylated α-synuclein and PGP9.5 in 43 patients (2 patients were excluded because only 1 biopsy was available). The paracellular permeability and transcellular permeability were evaluated by measuring sulfonic acid and horseradish peroxidase flux, respectively, in the 3 remaining biopsies mounted in Ussing chambers. RESULTS: Enteric PASH was more frequent in the subgroup of patients with PD with RBD compared to patients without RBD (18 of 28, 64.3%, vs 2 of 15, 13.3%, respectively, < 0.01). No differences were observed in intestinal permeability between patients with PD with and without RBD. CONCLUSIONS: Patients with PD and RBD have a greater frequency of synuclein pathology in the enteric nervous system, suggesting that RBD is associated with widespread synuclein neuropathology.
[Mh] Termos MeSH primário: Sistema Nervoso Entérico/patologia
Doença de Parkinson/complicações
Transtorno do Comportamento do Sono REM/etiologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Permeabilidade da Membrana Celular/fisiologia
Colonoscopia
Estudos Transversais
Sistema Nervoso Entérico/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Índice de Gravidade de Doença
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Synuclein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004496


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[PMID]:28840395
[Au] Autor:Soghomonyan S; Abdel-Rasoul M; Zuleta-Alarcon A; Grants I; Davila V; Yu J; Zhang C; Whitaker EE; Bergese SD; Stoicea N; Arsenescu R; Christofi FL
[Ad] Endereço:Department of Anesthesiology, The Wexner Medical Center, The Ohio State University, 420 West 12th Ave, Room 226, Columbus, OH, 43210, USA.
[Ti] Título:Clopidogrel IBS Patients Have Higher Incidence of Gastrointestinal Symptoms Influenced by Age and Gender.
[So] Source:Dig Dis Sci;62(10):2728-2743, 2017 Oct.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Clopidogrel is an irreversible antagonist of P2Y receptors (P2Y Rs) used as an antiplatelet drug to reduce risk of thrombosis. P2Y Rs are expressed in gastrointestinal (GI) tract where they might regulate GI function. AIM: To evaluate if blockade of P2Y Rs by clopidogrel is associated with higher incidence of GI symptoms in patients with irritable bowel syndrome (IBS). METHODS: A retrospective analysis of our institutional database was conducted for a 13-year period. IBS patients were identified, and their demographics, GI symptoms and clopidogrel therapy were collected. Logistic regression models were used to characterize symptoms in clopidogrel versus no-clopidogrel IBS-groups, adjusting for Age and Sex differences. An additional study characterized the P2Y R distribution in human gut. RESULTS: The search identified 7217 IBS patients (6761 no-clopidogrel/456 clopidogrel). There were a higher proportion of patients with GI symptoms on clopidogrel (68%) compared to controls (60%, p = 0.0011) that were Females (70 vs. 60%, p = 0.0003) not Males (61 vs. 60%; p = 0.8312). In Females, clopidogrel was associated with higher incidence of GI symptoms (Age adjusted; p < 0.0001) for pain, constipation, gastroparesis (p ≤ 0.0001) and psychogenic pain (p = 0.0006). Age or Sex (adjusted models) influenced one or more GI symptoms (i.e., pain, p < 0.0001; constipation, p < 0.0001/p = 0.008; diarrhea, flatulence, p = 0.01). P2Y R immunoreactivity was abundant in human ENS; glial-to-neuron ratio of P2Y Rs expressed in Females â‰« Males. CONCLUSIONS: Irreversible blockade of P2Y R by clopidogrel is associated with higher incidence of GI symptoms in Female IBS patients, although Age or Sex alone contributes to symptomatology. Prospective studies can determine clinical implications of P2Y Rs in IBS.
[Mh] Termos MeSH primário: Sistema Nervoso Entérico/efeitos dos fármacos
Intestinos/inervação
Síndrome do Intestino Irritável/epidemiologia
Inibidores da Agregação de Plaquetas/efeitos adversos
Antagonistas do Receptor Purinérgico P2Y/efeitos adversos
Ticlopidina/análogos & derivados
[Mh] Termos MeSH secundário: Dor Abdominal/induzido quimicamente
Dor Abdominal/epidemiologia
Adolescente
Adulto
Fatores Etários
Idoso
Constipação Intestinal/induzido quimicamente
Constipação Intestinal/epidemiologia
Bases de Dados Factuais
Diarreia/induzido quimicamente
Diarreia/epidemiologia
Registros Eletrônicos de Saúde
Sistema Nervoso Entérico/química
Sistema Nervoso Entérico/fisiopatologia
Feminino
Flatulência/induzido quimicamente
Flatulência/epidemiologia
Gastroparesia/induzido quimicamente
Gastroparesia/epidemiologia
Seres Humanos
Incidência
Síndrome do Intestino Irritável/diagnóstico
Síndrome do Intestino Irritável/fisiopatologia
Modelos Logísticos
Masculino
Meia-Idade
Análise Multivariada
Razão de Chances
Receptores Purinérgicos P2Y12/análise
Estudos Retrospectivos
Fatores de Risco
Fatores Sexuais
Ticlopidina/efeitos adversos
Fatores de Tempo
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (P2RY12 protein, human); 0 (Platelet Aggregation Inhibitors); 0 (Purinergic P2Y Receptor Antagonists); 0 (Receptors, Purinergic P2Y12); A74586SNO7 (clopidogrel); OM90ZUW7M1 (Ticlopidine)
[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:170826
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4707-7


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[PMID]:28732069
[Au] Autor:Brun P; Scarpa M; Marchiori C; Sarasin G; Caputi V; Porzionato A; Giron MC; Palù G; Castagliuolo I
[Ad] Endereço:Department of Molecular Medicine, University of Padova, Padova, Italy.
[Ti] Título:Saccharomyces boulardii CNCM I-745 supplementation reduces gastrointestinal dysfunction in an animal model of IBS.
[So] Source:PLoS One;12(7):e0181863, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We evaluated the effect of Saccharomyces boulardii CNCM I-745 on intestinal neuromuscular anomalies in an IBS-type mouse model of gastrointestinal motor dysfunctions elicited by Herpes Simplex Virus type 1 (HSV-1) exposure. METHODS: Mice were inoculated intranasally with HSV-1 (102 PFU) or vehicle at time 0 and 4 weeks later by the intragastric (IG) route (108 PFU). Six weeks after IG inoculum, mice were randomly allocated to receive oral gavage with either S. boulardii (107 CFU/day) or vehicle. After 4 weeks the following were determined: a) intestinal motility using fluorescein-isothiocyanate dextran distribution in the gut, fecal pellet expulsion, stool water content, and distal colonic transit of glass beads; b) integrity of the enteric nervous system (ENS) by immunohistochemistry on ileal whole-mount preparations and western blot of protein lysates from ileal longitudinal muscle and myenteric plexus; c) isometric muscle tension with electric field and pharmacological (carbachol) stimulation of ileal segments; and d) intestinal inflammation by levels of tumor necrosis factor α, interleukin(IL)-1ß, IL-10 and IL-4. RESULTS: S. boulardii CNCM I-745 improved HSV-1 induced intestinal dysmotility and alteration of intestinal transit observed ten weeks after IG inoculum of the virus. Also, the probiotic yeast ameliorated the structural alterations of the ENS induced by HSV-1 (i.e., reduced peripherin immunoreactivity and expression, increased glial S100ß protein immunoreactivity and neuronal nitric oxide synthase level, reduced substance P-positive fibers). Moreover, S. boulardii CNCM I-745 diminished the production of HSV-1 associated pro-inflammatory cytokines in the myenteric plexus and increased levels of anti-inflammatory interleukins. CONCLUSIONS: S. boulardii CNCM I-745 ameliorated gastrointestinal neuromuscular anomalies in a mouse model of gut dysfunctions typically observed with irritable bowel syndrome.
[Mh] Termos MeSH primário: Motilidade Gastrointestinal/efeitos dos fármacos
Síndrome do Intestino Irritável/microbiologia
Síndrome do Intestino Irritável/terapia
Probióticos/farmacologia
Saccharomyces boulardii/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Colo/metabolismo
Colo/microbiologia
Colo/virologia
Citocinas/metabolismo
Diarreia/metabolismo
Diarreia/microbiologia
Diarreia/virologia
Modelos Animais de Doenças
Sistema Nervoso Entérico/metabolismo
Sistema Nervoso Entérico/microbiologia
Sistema Nervoso Entérico/virologia
Herpes Simples/metabolismo
Herpes Simples/microbiologia
Herpes Simples/virologia
Herpesvirus Humano 1/patogenicidade
Íleo/metabolismo
Íleo/microbiologia
Íleo/virologia
Inflamação/metabolismo
Inflamação/microbiologia
Inflamação/virologia
Interleucina-10/metabolismo
Interleucina-1beta/metabolismo
Interleucina-4/metabolismo
Síndrome do Intestino Irritável/metabolismo
Síndrome do Intestino Irritável/virologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Músculos/metabolismo
Músculos/microbiologia
Músculos/virologia
Plexo Mientérico/metabolismo
Plexo Mientérico/microbiologia
Plexo Mientérico/virologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-1beta); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181863


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[PMID]:28711628
[Au] Autor:Rao M; Rastelli D; Dong L; Chiu S; Setlik W; Gershon MD; Corfas G
[Ad] Endereço:Department of Pediatrics, Columbia University Medical Center, New York, New York. Electronic address: mr3343@columbia.edu.
[Ti] Título:Enteric Glia Regulate Gastrointestinal Motility but Are Not Required for Maintenance of the Epithelium in Mice.
[So] Source:Gastroenterology;153(4):1068-1081.e7, 2017 Oct.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: When the glial fibrillary acidic protein (GFAP) promoter is used to express cellular toxins that eliminate glia in mice, intestinal epithelial permeability and proliferation increase; this led to the concept that glia are required for maintenance of the gastrointestinal epithelium. Many enteric glia, however, particularly in the mucosa, do not express GFAP. In contrast, virtually all enteric glia express proteolipid protein 1 (PLP1). We investigated whether elimination of PLP1-expressing cells compromises epithelial maintenance or gastrointestinal motility. METHODS: We generated mice that express tamoxifen-inducible Cre recombinase under control of the Plp1 promoter and carry the diptheria toxin subunit A (DTA) transgene in the Rosa26 locus (Plp1 ;Rosa26 mice). In these mice, PLP1-expressing glia are selectively eliminated without affecting neighboring cells. We measured epithelial barrier function and gastrointestinal motility in these mice and littermate controls, and analyzed epithelial cell proliferation and ultrastructure from their intestinal tissues. To compare our findings with those from previous studies, we also eliminated glia with ganciclovir in Gfap mice. RESULTS: Expression of DTA in PLP1-expressing cells selectively eliminated enteric glia from the small and large intestines, but caused no defects in epithelial proliferation, barrier integrity, or ultrastructure. In contrast, administration of ganciclovir to Gfap mice eliminated fewer glia but caused considerable non-glial toxicity and epithelial cell death. Elimination of PLP1-expressing cells did not reduce survival of neurons in the intestine, but altered gastrointestinal motility in female, but not male, mice. CONCLUSIONS: Using the Plp1 promoter to selectively eliminate glia in mice, we found that enteric glia are not required for maintenance of the intestinal epithelium, but are required for regulation of intestinal motility in females. Previous observations supporting the concept that maintenance of the intestinal epithelium requires enteric glia can be attributed to non-glial toxicity in Gfap mice and epithelial-cell expression of GFAP. Contrary to widespread notions, enteric glia are therefore not required for epithelial homeostasis. However, they regulate intestinal motility in a sex-dependent manner.
[Mh] Termos MeSH primário: Sistema Nervoso Entérico/fisiologia
Motilidade Gastrointestinal
Mucosa Intestinal/fisiologia
Intestinos/inervação
Neuroglia/fisiologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Toxina Diftérica/genética
Toxina Diftérica/metabolismo
Sistema Nervoso Entérico/metabolismo
Sistema Nervoso Entérico/ultraestrutura
Feminino
Ganciclovir/toxicidade
Genótipo
Proteína Glial Fibrilar Ácida/genética
Proteína Glial Fibrilar Ácida/metabolismo
Homeostase
Integrases/genética
Integrases/metabolismo
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Mucosa Intestinal/ultraestrutura
Intestinos/efeitos dos fármacos
Intestinos/metabolismo
Intestinos/ultraestrutura
Masculino
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteína Proteolipídica de Mielina/genética
Neuroglia/metabolismo
Neuroglia/ultraestrutura
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Fenótipo
Regiões Promotoras Genéticas
RNA não Traduzido/genética
Fatores Sexuais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diphtheria Toxin); 0 (Glial Fibrillary Acidic Protein); 0 (Gt(ROSA)26Sor non-coding RNA, mouse); 0 (Myelin Proteolipid Protein); 0 (Peptide Fragments); 0 (Plp1 protein, mouse); 0 (RNA, Untranslated); 0 (diphtheria toxin fragment A); 0 (glial fibrillary astrocytic protein, mouse); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases); P9G3CKZ4P5 (Ganciclovir)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


  8 / 2440 MEDLINE  
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[PMID]:28665193
[Au] Autor:Romanski KW
[Ad] Endereço:1 Department of Animal Physiology, Faculty of Veterinary Medicine, Wroclaw University of Environmental and Life Sciences , Wroclaw, Poland.
[Ti] Título:Importance of the enteric nervous system in the control of the migrating motility complex.
[So] Source:Physiol Int;104(2):97-129, 2017 Jun 01.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:The migrating motility complex (MMC), a cyclical phenomenon, represents rudimentary motility pattern in the gastrointestinal tract. The MMC is observed mostly in the stomach and gut of man and numerous animal species. It contains three or four phases, while its phase III is the most characteristic. The mechanisms controlling the pattern are unclear in part, although the neural control of the MMC seems crucial. The main goal of this article was to discuss the importance of intrinsic innervation of the gastrointestinal tract in MMC initiation, migration, and cessation to emphasize that various MMC-controlling mechanisms act through the enteric nervous system. Two main neural regions, central and peripheral, are able to initiate the MMC. However, central regulation of the MMC may require cooperation with the enteric nervous system. When central mechanisms are not active, the MMC can be initiated peripherally in any region of the small bowel. The enteric nervous system affects the MMC in response to the luminal stimuli which can contribute to the initiation and cessation of the cycle, and it may evoke irregular phasic contractions within the pattern. The hormonal regulators released from the endocrine cells may exert a modulatory effect upon the MMC mostly through the enteric nervous system. Their central action could also be considered. It can be concluded that the enteric nervous system is involved in the great majority of the MMC-controlling mechanisms.
[Mh] Termos MeSH primário: Sistema Nervoso Entérico/fisiologia
Células Enteroendócrinas/fisiologia
Trânsito Gastrointestinal/fisiologia
Modelos Neurológicos
Músculo Liso/fisiologia
Complexo Mioelétrico Migratório/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Endócrinas
Seres Humanos
Músculo Liso/inervação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1556/2060.104.2017.2.4


  9 / 2440 MEDLINE  
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[PMID]:28640080
[Au] Autor:Li H; Huang K; Wang H; Wang L; Yang M; Wang L; Lin R; Liu H; Gao J; Shuai X; Liu X; Tao K; Wang G; Wang Z
[Ad] Endereço:aDepartment of Gastrointestinal Surgery bInstitution of Cardiology, Union Hospital cDepartment of Medical Genetics, School of Basic Medicine and the Collaborative Innovation Center for Brain Science dCenter for Tissue Engineering and Regenerative Medicine eDepartment of Clinical Laboratory fDepartment of Pathology gDepartment of Radiology hDivision of Gastroenterology iCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Immature enteric ganglion cells were observed in a 13-year-old colon signet ring cell carcinoma patient: A case report and literature review.
[So] Source:Medicine (Baltimore);96(25):e7036, 2017 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: All the enteric ganglion cells are fully mature by 2 to 5 years of age in human. No one had reported the presentation of immature enteric ganglion cells in elder ones. Colorectal carcinoma is also rare in the adolescent population. The coincidence of these 2 rare events in a 13-year-old boy has never been reported elsewhere, which may suggest some linkage between them. PATIENT CONCERN: A 13-year-old boy presented with progressive abdominal pain and melena for 3 months. Computed tomography (CT) scan and endoscopic ultrasonography showed significant abnormality in the transverse colon characteristic of marked mural thickening. The biopsy results indicated signet ring cell carcinoma. DIAGNOSES: A 13-year-old male patient with advanced colon signet ring cell carcinoma. In addition, immature but not mature ganglion cells could be observed in almost all of the slices of the resected nontumorous area of the specimen. INTERVENTIONS: The transverse colon tumor was resected and the subsequent histopathological examination confirmed the diagnosis of primary colon signet ring cell carcinoma. Then the patient received adjuvant chemotherapy and biological target therapies subsequently. OUTCOMES: After 6 cycles of adjuvant chemotherapy and biological target therapies, metastasis was however detected within a year. LESSONS: In this case, a 13-year-old male patient with advanced colon signet ring cell carcinoma were presented. Unexpectedly, immature ganglion cells could be observed in almost all of the slices of the resected nontumorous area of the specimen. It is critical to raise medical awareness and improve the diagnosis and treatment of the signet ring cell carcinoma. This malignancy and the immature ganglion cells may be associated, possibly caused by some unidentified genetic defects. Genome sequencing, histopathological examination, and long-term follow-up of young patients with related diseases, would help further reveal the potential relationship between tumorigenesis and ganglion cells' immaturity, contributing to understanding the molecular mechanisms.
[Mh] Termos MeSH primário: Carcinoma de Células em Anel de Sinete/patologia
Neoplasias do Colo/patologia
Sistema Nervoso Entérico/patologia
Neurônios/patologia
[Mh] Termos MeSH secundário: Adolescente
Carcinoma de Células em Anel de Sinete/terapia
Neoplasias do Colo/terapia
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007036


  10 / 2440 MEDLINE  
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[PMID]:28636959
[Au] Autor:Yoo BB; Mazmanian SK
[Ad] Endereço:Division of Biology & Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. Electronic address: byoo@caltech.edu.
[Ti] Título:The Enteric Network: Interactions between the Immune and Nervous Systems of the Gut.
[So] Source:Immunity;46(6):910-926, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interactions between the nervous and immune systems enable the gut to respond to the variety of dietary products that it absorbs, the broad spectrum of pathogens that it encounters, and the diverse microbiome that it harbors. The enteric nervous system (ENS) senses and reacts to the dynamic ecosystem of the gastrointestinal (GI) tract by translating chemical cues from the environment into neuronal impulses that propagate throughout the gut and into other organs in the body, including the central nervous system (CNS). This review will describe the current understanding of the anatomy and physiology of the GI tract by focusing on the ENS and the mucosal immune system. We highlight emerging literature that the ENS is essential for important aspects of microbe-induced immune responses in the gut. Although most basic and applied research in neuroscience has focused on the brain, the proximity of the ENS to the immune system and its interface with the external environment suggest that novel paradigms for nervous system function await discovery.
[Mh] Termos MeSH primário: Sistema Nervoso Central/imunologia
Sistema Nervoso Entérico
Microbioma Gastrointestinal
Trato Gastrointestinal/fisiologia
Sistema Imunitário/imunologia
Imunidade nas Mucosas
Intestinos/imunologia
[Mh] Termos MeSH secundário: Animais
Exposição Ambiental
Trato Gastrointestinal/anatomia & histologia
Interações Hospedeiro-Patógeno
Seres Humanos
Neuroimunomodulação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE



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