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Pesquisa : D12.644.360.325.150.100.200 [Categoria DeCS]
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[PMID]:28346224
[Au] Autor:Nugent AA; Park JG; Wei Y; Tenney AP; Gilette NM; DeLisle MM; Chan WM; Cheng L; Engle EC
[Ti] Título:Mutant α2-chimaerin signals via bidirectional ephrin pathways in Duane retraction syndrome.
[So] Source:J Clin Invest;127(5):1664-1682, 2017 May 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Duane retraction syndrome (DRS) is the most common form of congenital paralytic strabismus in humans and can result from α2-chimaerin (CHN1) missense mutations. We report a knockin α2-chimaerin mouse (Chn1KI/KI) that models DRS. Whole embryo imaging of Chn1KI/KI mice revealed stalled abducens nerve growth and selective trochlear and first cervical spinal nerve guidance abnormalities. Stalled abducens nerve bundles did not reach the orbit, resulting in secondary aberrant misinnervation of the lateral rectus muscle by the oculomotor nerve. By contrast, Chn1KO/KO mice did not have DRS, and embryos displayed abducens nerve wandering distinct from the Chn1KI/KI phenotype. Murine embryos lacking EPH receptor A4 (Epha4KO/KO), which is upstream of α2-chimaerin in corticospinal neurons, exhibited similar abducens wandering that paralleled previously reported gait alterations in Chn1KO/KO and Epha4KO/KO adult mice. Findings from Chn1KI/KI Epha4KO/KO mice demonstrated that mutant α2-chimaerin and EphA4 have different genetic interactions in distinct motor neuron pools: abducens neurons use bidirectional ephrin signaling via mutant α2-chimaerin to direct growth, while cervical spinal neurons use only ephrin forward signaling, and trochlear neurons do not use ephrin signaling. These findings reveal a role for ephrin bidirectional signaling upstream of mutant α2-chimaerin in DRS, which may contribute to the selective vulnerability of abducens motor neurons in this disorder.
[Mh] Termos MeSH primário: Quimerina 1/metabolismo
Síndrome da Retração Ocular/metabolismo
Embrião de Mamíferos/metabolismo
Neurônios Motores/metabolismo
Receptor EphA4/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Córtex Cerebral/metabolismo
Córtex Cerebral/patologia
Quimerina 1/genética
Síndrome da Retração Ocular/genética
Seres Humanos
Camundongos
Camundongos Knockout
Neurônios Motores/patologia
Receptor EphA4/genética
Medula Espinal/metabolismo
Medula Espinal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chimerin 1); EC 2.7.10.1 (Receptor, EphA4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE


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[PMID]:27072986
[Au] Autor:Couch G; Redman JE; Wernisch L; Newton R; Malhotra S; Dawsey SM; Lao-Sirieix P; Fitzgerald RC
[Ad] Endereço:MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom.
[Ti] Título:The Discovery and Validation of Biomarkers for the Diagnosis of Esophageal Squamous Dysplasia and Squamous Cell Carcinoma.
[So] Source:Cancer Prev Res (Phila);9(7):558-66, 2016 Jul.
[Is] ISSN:1940-6215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 5-year survival rate of esophageal cancer is less than 10% in developing countries, where more than 90% of these cancers are esophageal squamous cell carcinomas (ESCC). Endoscopic screening is undertaken in high incidence areas. Biomarker analysis could reduce the subjectivity associated with histologic assessment of dysplasia and thus improve diagnostic accuracy. The aims of this study were therefore to identify biomarkers for esophageal squamous dysplasia and carcinoma. A publicly available dataset was used to identify genes with differential expression in ESCC compared with normal esophagus. Each gene was ranked by a support vector machine separation score. Expression profiles were examined, before validation by qPCR and IHC. We found that 800 genes were overexpressed in ESCC compared with normal esophagus (P < 10(-5)). Of the top 50 genes, 33 were expressed in ESCC epithelium and not in normal esophagus epithelium or stroma using the Protein Atlas website. These were taken to qPCR validation, and 20 genes were significantly overexpressed in ESCC compared with normal esophagus (P < 0.05). TNFAIP3 and CHN1 showed differential expression with IHC. TNFAIP3 expression increased gradually through normal esophagus, mild, moderate and severe dysplasia, and SCC (P < 0.0001). CHN1 staining was rarely present in the top third of normal esophagus epithelium and extended progressively towards the surface in mild, moderate, and severe dysplasia, and SCC (P < 0.0001). Two novel promising biomarkers for ESCC were identified, TNFAIP3 and CHN1. CHN1 and TNFAIP3 may improve diagnostic accuracy of screening methods for ESCC. Cancer Prev Res; 9(7); 558-66. ©2016 AACR.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Carcinoma de Células Escamosas/diagnóstico
Quimerina 1/biossíntese
Neoplasias Esofágicas/diagnóstico
Lesões Pré-Cancerosas/diagnóstico
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/biossíntese
[Mh] Termos MeSH secundário: Perfilação da Expressão Gênica
Seres Humanos
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Chimerin 1); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160414
[St] Status:MEDLINE
[do] DOI:10.1158/1940-6207.CAPR-15-0379


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[PMID]:26642701
[Au] Autor:Zhuang X; Sun F; Li L; Jiang D; Li X; Sun A; Pan Z; Lou N; Zhang L; Lou F
[Ti] Título:Therapeutic Effect of Metformin on Chemerin in Non-Obese Patients with Non-Alcoholic Fatty Liver Disease (NAFLD).
[So] Source:Clin Lab;61(10):1409-14, 2015.
[Is] ISSN:1433-6510
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chemerin is an important risk factor of insulin resistance. Non-alcoholic fatty liver has typical characteristics of insulin resistance. The aim of this study was to explore the potential role of chemerin in NAFLD. METHODS: 45 subjects included 22 control subjects (A group) and 23 subjects diagnosed with non-alcoholic fatty liver disease (B group) participated in the study. 23 patients in the NAFLD group received oral daily metformin at a dose of 20 mg/kg/day for 24 weeks follow-up. Chemerin and insulin resistance markers were determined at baseline and 24 weeks. RESULTS: The levels of WHR, BMI, FINS, HOMA-IR, TG, ALT, AST, and Chemerin in B group were significantly higher than A group. After 24 weeks of metformin treatment, the levels of WHR, AST, ALT, TG, chemerin and HOMA-IR were significantly reduced (p < 0.05) and other indexes were not changed significantly. Correlation analysis indicated that serum chemerin concentrations were positively correlated with BMI, WHR, HOMA-IR, FINS, TG, ALT, and AST levels. Logistic regression analysis showed chemerin, TG, and ALT were independent variables associated with NAFLD. CONCLUSIONS: These findings showed a significant increase of chemerin level in NAFLD patients. Metformin treatment can improve NAFLD and decrease the level of chemerin. Chemerin, TG, and ALT were independent variables associated with NAFLD.
[Mh] Termos MeSH primário: Quimerina 1/metabolismo
Metformina/uso terapêutico
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Oral
Adulto
Biomarcadores/metabolismo
Pressão Sanguínea
Sinergismo Farmacológico
Feminino
Seres Humanos
Hipoglicemiantes/uso terapêutico
Insulina/química
Resistência à Insulina
Modelos Logísticos
Masculino
Meia-Idade
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chimerin 1); 0 (Hypoglycemic Agents); 0 (Insulin); 9100L32L2N (Metformin)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:151208
[Lr] Data última revisão:
151208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151209
[St] Status:MEDLINE


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[PMID]:26446225
[Au] Autor:Iwata R; Matsukawa H; Yasuda K; Mizuno H; Itohara S; Iwasato T
[Ad] Endereço:Division of Neurogenetics, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan, Department of Genetics, Sokendai, Mishima, Shizuoka 411-8540, Japan, and tiwasato@nig.ac.jp riwata@nig.ac.jp.
[Ti] Título:Developmental RacGAP α2-Chimaerin Signaling Is a Determinant of the Morphological Features of Dendritic Spines in Adulthood.
[So] Source:J Neurosci;35(40):13728-44, 2015 Oct 07.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Morphological characteristics of dendritic spines form the basis of cognitive ability. However, molecular mechanisms involved in fine-tuning of spine morphology during development are not fully understood. Moreover, it is unclear whether, and to what extent, these developmental mechanisms determine the normal adult spine morphological features. Here, we provide evidence that α2-isoform of Rac-specific GTPase-activating protein α-chimaerin (α2-chimaerin) is involved in spine morphological refinement during late postnatal period, and furthermore show that this developmental α2-chimaerin function affects adult spine morphologies. We used a series of mice with global and conditional knock-out of α-chimaerin isoforms (α1-chimaerin and α2-chimaerin). α2-Chimaerin disruption, but not α1-chimaerin disruption, in the mouse results in an increased size (and density) of spines in the hippocampus. In contrast, overexpression of α2-chimaerin in developing hippocampal neurons induces a decrease of spine size. Disruption of α2-chimaerin suppressed EphA-mediated spine morphogenesis in cultured developing hippocampal neurons. α2-Chimaerin disruption that begins during the juvenile stage results in an increased size of spines in the hippocampus. Meanwhile, spine morphologies are unaltered when α2-chimaerin is deleted only in adulthood. Consistent with these spine morphological results, disruption of α2-chimaerin beginning in the juvenile stage led to an increase in contextual fear learning in adulthood; whereas contextual learning was recently shown to be unaffected when α2-chimaerin was deleted only in adulthood. Together, these results suggest that α2-chimaerin signaling in developmental stages contributes to determination of the morphological features of adult spines and establishment of normal cognitive ability. SIGNIFICANCE STATEMENT: Recent studies of neurodevelopmental disorders in humans and their animal models have led to an attractive hypothesis that spine morphogenesis during development forms the basis of adult cognition. In particular, the roles of Rac and its regulators, such as Rac-specific GTPase-activating proteins (RacGAPs) and Rac guanine nucleotide exchange factors, are a topic of focus in spine morphogenesis and cognitive ability. Using a series of mice with global and conditional knock-out (KO) of RacGAP α-chimaerin isoforms (α1-chimaerin and α2-chimaerin), we provide compelling evidence demonstrating that α2-chimaerin is involved in spine morphological refinement during late postnatal development and that this developmental α2-chimaerin function affects adult spine morphologies. Furthermore, our results clearly showed that α2-chimaerin signaling during late postnatal development contributes to normal cognitive ability in adult mice.
[Mh] Termos MeSH primário: Quimerina 1/metabolismo
Espinhas Dendríticas/fisiologia
Proteínas Ativadoras de GTPase/metabolismo
Regulação da Expressão Gênica no Desenvolvimento/genética
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/genética
Fatores Etários
Animais
Animais Recém-Nascidos
Quimerina 1/genética
Condicionamento (Psicologia)/fisiologia
Efrina-A3/metabolismo
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/genética
Medo
Proteínas Ativadoras de GTPase/genética
Hipocampo/citologia
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Masculino
Camundongos
Camundongos Transgênicos
Neurônios/ultraestrutura
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chimerin 1); 0 (Ephrin-A3); 0 (GTPase-Activating Proteins); 0 (Luminescent Proteins)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:151008
[Lr] Data última revisão:
151008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151009
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0419-15.2015


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[PMID]:25676811
[Au] Autor:Kato T; Konishi Y; Shimohama S; Beach TG; Akatsu H; Tooyama I
[Ad] Endereço:Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu 520-2192, Japan.
[Ti] Título:Alpha1-chimaerin, a Rac1 GTPase-activating protein, is expressed at reduced mRNA levels in the brain of Alzheimer's disease patients.
[So] Source:Neurosci Lett;591:19-24, 2015 Mar 30.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Alpha1-chimaerin is a GTPase-activating protein (GAP) for Rac1, a member of the Rho small GTPase family, whose action leads to the inactivation of Rac1. Rac1 activity is upregulated in Alzheimer's disease, but little is known about the role of α1-chimaerin. In this study, we investigated the expression and localization of α1-chimaerin mRNA in postmortem human brains from patients with Alzheimer's disease and control subjects. In situ hybridization studies demonstrated that α1-chimaerin was expressed by neurons in the neo-cortex of the temporal lobe and the hippocampus of both controls and Alzheimer's disease cases, with the signal intensity dramatically decreased in patients with Alzheimer's disease. Real-time PCR analysis confirmed a significant reduction of α1-chimaerin mRNA expression in the temporal cortex of Alzheimer's disease cases. In contrast, α2-chimaerin mRNA levels showed no significant difference between the groups. The present study showed reduced α1-chimaerin expression in the brain of Alzheimer's disease cases, suggesting a role in the upregulation of Rac1 activity during the disease process.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Encéfalo/metabolismo
Quimerina 1/metabolismo
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Estudos de Casos e Controles
Quimerina 1/genética
Feminino
Hipocampo/metabolismo
Seres Humanos
Masculino
Meia-Idade
Células Piramidais/metabolismo
Lobo Temporal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chimerin 1); 0 (RNA, Messenger)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150214
[St] Status:MEDLINE


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[PMID]:25673830
[Au] Autor:Kao TJ; Nicholl GC; Johansen JA; Kania A; Beg AA
[Ad] Endereço:Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7 Canada, Graduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology and Center for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan, and.
[Ti] Título:α2-chimaerin is required for Eph receptor-class-specific spinal motor axon guidance and coordinate activation of antagonistic muscles.
[So] Source:J Neurosci;35(6):2344-57, 2015 Feb 11.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Axonal guidance involves extrinsic molecular cues that bind growth cone receptors and signal to the cytoskeleton through divergent pathways. Some signaling intermediates are deployed downstream of molecularly distinct axon guidance receptor families, but the scope of this overlap is unclear, as is the impact of embryonic axon guidance fidelity on adult nervous system function. Here, we demonstrate that the Rho-GTPase-activating protein α2-chimaerin is specifically required for EphA and not EphB receptor signaling in mouse and chick spinal motor axons. Reflecting this specificity, the loss of α2-chimaerin function disrupts the limb trajectory of extensor-muscle-innervating motor axons the guidance of which depends on EphA signaling. These embryonic defects affect coordinated contraction of antagonistic flexor-extensor muscles in the adult, indicating that accurate embryonic motor axon guidance is critical for optimal neuromuscular function. Together, our observations provide the first functional evidence of an Eph receptor-class-specific intracellular signaling protein that is required for appropriate neuromuscular connectivity.
[Mh] Termos MeSH primário: Axônios/fisiologia
Quimerina 1/genética
Quimerina 1/fisiologia
Neurônios Motores/fisiologia
Músculo Esquelético/inervação
Músculo Esquelético/fisiologia
Receptores da Família Eph/fisiologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/fisiologia
Embrião de Galinha
Marcha/fisiologia
Masculino
Camundongos
Atividade Motora/fisiologia
Contração Muscular/fisiologia
Equilíbrio Postural/fisiologia
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chimerin 1); EC 2.7.10.1 (Receptors, Eph Family); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:150212
[Lr] Data última revisão:
150212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150213
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.4151-14.2015


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[PMID]:25331612
[Au] Autor:Hwang JM; Seong MW; Kim JH; Park SS
[Ad] Endereço:Department of Ophthalmology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
[Ti] Título:Absence of CHN1 in two patients with a bilateral absence of cranial nerves IV and VI.
[So] Source:Graefes Arch Clin Exp Ophthalmol;253(3):491-2, 2015 Mar.
[Is] ISSN:1435-702X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Nervo Abducente/anormalidades
Quimerina 1/genética
Síndrome da Retração Ocular/genética
Doenças do Nervo Troclear/congênito
Nervo Troclear/anormalidades
[Mh] Termos MeSH secundário: Blefaroptose/diagnóstico
Blefaroptose/genética
Pré-Escolar
Análise Mutacional de DNA
Síndrome da Retração Ocular/diagnóstico
Exotropia/diagnóstico
Exotropia/genética
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Reação em Cadeia da Polimerase
Doenças do Nervo Troclear/diagnóstico
Doenças do Nervo Troclear/genética
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Chimerin 1)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141022
[St] Status:MEDLINE
[do] DOI:10.1007/s00417-014-2828-7


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[PMID]:25159148
[Au] Autor:Iwata R; Ohi K; Kobayashi Y; Masuda A; Iwama M; Yasuda Y; Yamamori H; Tanaka M; Hashimoto R; Itohara S; Iwasato T
[Ad] Endereço:Division of Neurogenetics, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan; Department of Genetics, The Graduate University for Advanced Studies (SOKENDAI), Mishima, Shizuoka 411-8540, Japan.
[Ti] Título:RacGAP α2-chimaerin function in development adjusts cognitive ability in adulthood.
[So] Source:Cell Rep;8(5):1257-64, 2014 Sep 11.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major concern in neuroscience is how cognitive ability in adulthood is affected and regulated by developmental mechanisms. The molecular bases of cognitive development are not well understood. We provide evidence for the involvement of the α2 isoform of Rac-specific guanosine triphosphatase (GTPase)-activating protein (RacGAP) α-chimaerin (chimerin) in this process. We generated and analyzed mice with global and conditional knockouts of α-chimaerin and its isoforms (α1-chimaerin and α2-chimaerin) and found that α-chimaerin plays a wide variety of roles in brain function and that the roles of α1-chimaerin and α2-chimaerin are distinct. Deletion of α2-chimaerin, but not α1-chimaerin, beginning during early development results in an increase in contextual fear learning in adult mice, whereas learning is not altered when α2-chimaerin is deleted only in adulthood. Our findings suggest that α2-chimaerin acts during development to establish normal cognitive ability in adulthood.
[Mh] Termos MeSH primário: Encéfalo/crescimento & desenvolvimento
Quimerina 1/metabolismo
Cognição
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/fisiologia
Quimerina 1/genética
Condicionamento Clássico
Medo
Camundongos
Camundongos Endogâmicos C57BL
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chimerin 1); 0 (Protein Isoforms)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:140913
[Lr] Data última revisão:
140913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140828
[St] Status:MEDLINE


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[PMID]:24727542
[Au] Autor:Lin Y; Yang X; Yue W; Xu X; Li B; Zou L; He R
[Ad] Endereço:Department of Immunology, School of Basic Medical Sciences, Shanghai, China.
[Ti] Título:Chemerin aggravates DSS-induced colitis by suppressing M2 macrophage polarization.
[So] Source:Cell Mol Immunol;11(4):355-66, 2014 Jul.
[Is] ISSN:2042-0226
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Chemerin is present in various inflammatory sites and is closely involved in tissue inflammation. Recent studies have demonstrated that chemerin treatment can cause either anti-inflammatory or pro-inflammatory effects according to the disease model being investigated. Elevated circulating chemerin was recently found in patients with inflammatory bowel disease (IBD); however, the role of chemerin in intestinal inflammation remains unknown. In this study, we demonstrated that the administration of exogenous chemerin (aa17-156) aggravated the severity of dextran sulfate sodium (DSS)-induced colitis, which was characterized by higher clinical scores, extensive mucosal damage and significantly increased local and systemic production of pro-inflammatory cytokines, including IL-6, TNF-α and interferon (IFN-γ). Interestingly, chemerin did not appear to influence the magnitudes of inflammatory infiltrates in the colons, but did result in significantly decreased colonic expression of M2 macrophage-associated genes, including Arginase 1 (Arg-1), Ym1, FIZZ1 and IL-10, following DSS exposure, suggesting an impaired M2 macrophage skewing in vivo. Furthermore, an in vitro experiment showed that the addition of chemerin directly suppressed M2 macrophage-associated gene expression and STAT6 phosphorylation in IL-4-stimulated macrophages. Significantly elevated chemerin levels were found in colons from DSS-exposed mice and from ulcerative colitis (UC) patients and appeared to positively correlate with disease severity. Moreover, the in vivo administration of neutralizing anti-chemerin antibody significantly improved intestinal inflammation following DSS exposure. Taken together, our findings reveal a pro-inflammatory role for chemerin in DSS-induced colitis and the ability of chemerin to suppress the anti-inflammatory M2 macrophage response. Our study also suggests that upregulated chemerin in inflamed colons may contribute to the pathogenesis of IBD.
[Mh] Termos MeSH primário: Quimerina 1/administração & dosagem
Colite Ulcerativa/imunologia
Colite/imunologia
Colo/imunologia
Macrófagos/imunologia
Fragmentos de Peptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Arginase/genética
Arginase/metabolismo
Diferenciação Celular/genética
Células Cultivadas
Colite/induzido quimicamente
Citocinas/metabolismo
Sulfato de Dextrana/imunologia
Modelos Animais de Doenças
Progressão da Doença
Regulação para Baixo
Feminino
Seres Humanos
Mediadores da Inflamação/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Lectinas/genética
Lectinas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Fator de Transcrição STAT6/metabolismo
beta-N-Acetil-Hexosaminidases/genética
beta-N-Acetil-Hexosaminidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chimerin 1); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Intercellular Signaling Peptides and Proteins); 0 (Lectins); 0 (Peptide Fragments); 0 (Retnla protein, mouse); 0 (STAT6 Transcription Factor); 9042-14-2 (Dextran Sulfate); EC 3.2.1.52 (Chi3l3 protein, mouse); EC 3.2.1.52 (beta-N-Acetylhexosaminidases); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:150806
[Lr] Data última revisão:
150806
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140415
[St] Status:MEDLINE
[do] DOI:10.1038/cmi.2014.15


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[PMID]:24675530
[Au] Autor:Sekiya R; Maeda M; Yuan H; Asano E; Hyodo T; Hasegawa H; Ito S; Shibata K; Hamaguchi M; Kikkawa F; Kajiyama H; Senga T
[Ad] Endereço:Department of Obstetrics and Gynecology and Division of Cancer Biology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
[Ti] Título:PLAGL2 regulates actin cytoskeletal architecture and cell migration.
[So] Source:Carcinogenesis;35(9):1993-2001, 2014 Sep.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pleomorphic adenoma gene like-2 (PLAGL2), a member of the PLAG gene family, is a C2H2 zinc finger transcriptional factor that is involved in cellular transformation and apoptosis. In this report, we show that PLAGL2 is associated with the organization of stress fibers and with small guanosine triphosphatase (GTPase) activity. Depletion of PLAGL2 in two different ovarian cancer cell lines, ES-2 and HEY, induced activation of RhoA, whereas activity of Rac1 was suppressed. Organization of actin stress fibers and focal adhesions was significantly promoted by PLAGL2 knockdown in a RhoA-dependent manner. Conversely, exogenous expression of PLAGL2 in MDA-MB-231 cells, a breast cancer cell line, resulted in the activation of Rac1 and the inactivation of RhoA. In addition, PLAGL2 expression induced lamellipodia formation and disruption of stress fiber formation. Finally, we show that CHN1 expression is essential for Rac1 inactivation in PLAGL2-depleted cells. Our results demonstrate a crucial role of PLAGL2 in actin dynamics and give further insight into the role of PLAGL2 in cellular transformation and apoptosis.
[Mh] Termos MeSH primário: Movimento Celular
Proteínas de Ligação a DNA/fisiologia
Proteínas de Ligação a RNA/fisiologia
Fibras de Estresse/metabolismo
Fatores de Transcrição/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Quimerina 1/metabolismo
Seres Humanos
Pseudópodes/metabolismo
Pseudópodes/patologia
Fibras de Estresse/patologia
Proteínas rac1 de Ligação ao GTP/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chimerin 1); 0 (DNA-Binding Proteins); 0 (PLAGL2 protein, human); 0 (RAC1 protein, human); 0 (RNA-Binding Proteins); 0 (Transcription Factors); 124671-05-2 (RHOA protein, human); EC 3.6.5.2 (rac1 GTP-Binding Protein); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:140828
[Lr] Data última revisão:
140828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140329
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgu081



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