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[PMID]:29287726
[Au] Autor:Kim Y; Yang H; Min JK; Park YJ; Jeong SH; Jang SW; Shim S
[Ad] Endereço:Department of Biochemistry, Chungbuk National University, Cheongju, Republic of Korea.
[Ti] Título:CCN3 secretion is regulated by palmitoylation via ZDHHC22.
[So] Source:Biochem Biophys Res Commun;495(4):2573-2578, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Normal extracellular secretion of nephroblastoma overexpressed (NOV, also known as CCN3) is important for the adhesion, migration, and differentiation of cells. In previous studies, we have shown that the intracellular accumulation of CCN3 inhibits the growth of prominent neurons. Increased intracellular CCN3 can be induced through various processes, such as transcription, detoxification, and posttranslational modification. In general, posttranslational modifications are very important for protein secretion. However, it is unclear whether posttranslational modification is necessary for CCN3 secretion. In this study, we have conducted mutational analysis of CCN3 to demonstrate that its thrombospondin type-1 (TSP1) domain is important for CCN3 secretion and intracellular function. Point mutation analysis confirmed that CCN3 secretion was inhibited by cysteine (C)241 mutation, and overexpression of CCN3-C241A inhibited neuronal axonal growth in vivo. Furthermore, we demonstrated that palmitoylation is important for the extracellular secretion of CCN3 and that zinc finger DHHC-type containing 22 (ZDHHC22), a palmityoltransferase, can interact with CCN3. Taken together, our results suggest that palmitoylation by ZDHHC22 at C241 in the CCN3 TSP1 domain may be required for the secretion of CCN3. Aberrant palmitoylation induces intracellular accumulation of CCN3, inhibiting neuronal axon growth.
[Mh] Termos MeSH primário: Carnitina O-Palmitoiltransferase/química
Carnitina O-Palmitoiltransferase/metabolismo
Lipoilação/fisiologia
Proteínas de Membrana/química
Proteínas de Membrana/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/química
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Células HEK293
Seres Humanos
Camundongos
Camundongos Endogâmicos ICR
Neurônios/química
Neurônios/citologia
Ligação Proteica
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; PATIENT EDUCATION HANDOUT; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); EC 2.3.1.- (ZDHHC22 protein, human); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  2 / 182 MEDLINE  
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[PMID]:29235329
[Au] Autor:Minchenko OH; Kharkova AP; Minchenko DO; Karbovskyi LL
[Ti] Título:Expression of IGFBP6, IGFBP7, NOV, CYR61, WISP1 and WISP2 genes in U87 glioma cells in glutamine deprivation condition.
[So] Source:Ukr Biochem J;88(3):66-77, 2016 May-Jun.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We have studied gene expression of insulin-like growth factor binding proteins in U87 glioma cells upon glutamine deprivation depending on the inhibition of IRE1 (inositol requiring enzyme-1), a central mediator of endoplasmic reticulum stress. We have shown that exposure of control glioma cells upon glutamine deprivation leads to down-regulation of NOV/IGFBP9, WISP1 and WISP2 gene expressions and up-regulation of CYR61/IGFBP10 gene expression at the mRNA level. At the same time, the expression of IGFBP6 and IGFBP7 genes in control glioma cells was resistant to glutamine deprivation. It was also shown that the inhibition of IRE1 modifies the effect of glutamine deprivation on the expression of all studied genes. Thus, the inhibition of IRE1 signaling enzyme enhances the effect of glutamine deprivation on the expression of CYR61 and WISP1 genes and suppresses effect of the deprivation on WISP2 gene expression in glioma cells. Moreover, the inhibition of IRE1 introduces sensitivity of the expression of IGFBP6 and IGFBP7 genes to glutamine deprivation and removes this sensitivity to NOV gene. We have also demonstrated that the expression of all studied genes in glioma cells growing with glutamine is regulated by IRE1 signaling enzyme, because the inhibition of IRE1 significantly down-regulates IGFBP6 and NOV genes and up-regulates IGFBP7, CYR61, WISP1, and WISP2 genes as compared to control glioma cells. The present study demonstrates that glutamine deprivation condition affects most studied IGFBP and WISP gene expressions in relation to IRE1 signaling enzyme function and possibly contributes to slower glioma cell proliferation upon inhibition of IRE1.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Glutamina/deficiência
Proteína 6 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Neuroglia/enzimologia
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
[Mh] Termos MeSH secundário: Proteínas de Sinalização Intercelular CCN/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Proteína Rica em Cisteína 61/genética
Proteína Rica em Cisteína 61/metabolismo
Endorribonucleases/deficiência
Seres Humanos
Proteína 6 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/genética
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Neuroglia/patologia
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (CYR61 protein, human); 0 (Cysteine-Rich Protein 61); 0 (Insulin-Like Growth Factor Binding Protein 6); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); 0 (Proto-Oncogene Proteins); 0 (Repressor Proteins); 0 (WISP1 protein, human); 0 (WISP2 protein, human); 0 (insulin-like growth factor binding protein-related protein 1); 0RH81L854J (Glutamine); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.1.- (Endoribonucleases)
[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:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.03.066


  3 / 182 MEDLINE  
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[PMID]:28887577
[Au] Autor:Kii I; Ito H
[Ad] Endereço:Common Facilities Unit, Integrated Research Group, Compass to Healthy Life Research Complex Program, RIKEN Cluster for Science and Technology Hub, 6-7-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan. isao.kii@riken.jp.
[Ti] Título:Periostin and its interacting proteins in the construction of extracellular architectures.
[So] Source:Cell Mol Life Sci;74(23):4269-4277, 2017 Dec.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Periostin is a matricellular protein that is composed of a multi-domain structure with an amino-terminal EMI domain, a tandem repeat of four FAS 1 domains, and a carboxyl-terminal domain. These distinct domains have been demonstrated to bind to many proteins including extracellular matrix proteins (Collagen type I and V, fibronectin, tenascin, and laminin), matricellular proteins (CCN3 and ßig-h3), and enzymes that catalyze covalent crosslinking between extracellular matrix proteins (lysyl oxidase and BMP-1). Adjacent binding sites on periostin have been suggested to put the interacting proteins in close proximity, promoting intermolecular interactions between each protein, and leading to their assembly into extracellular architectures. These extracellular architectures determine the mechanochemical properties of connective tissues, in which periostin plays an important role in physiological homeostasis and disease progression. In this review, we introduce the proteins that interact with periostin, and discuss how the multi-domain structure of periostin functions as a scaffold for the assembly of interacting proteins, and how it underlies construction of highly sophisticated extracellular architectures.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/genética
Tecido Conjuntivo/metabolismo
Domínios e Motivos de Interação entre Proteínas
Mapeamento de Interação de Proteínas
[Mh] Termos MeSH secundário: Proteína Morfogenética Óssea 1/genética
Proteína Morfogenética Óssea 1/metabolismo
Moléculas de Adesão Celular/metabolismo
Colágeno/genética
Colágeno/metabolismo
Tecido Conjuntivo/anatomia & histologia
Fibronectinas/genética
Fibronectinas/metabolismo
Expressão Gênica
Seres Humanos
Laminina/genética
Laminina/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/genética
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Ligação Proteica
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Proteoglicanas/metabolismo
Transdução de Sinais
Tenascina/genética
Tenascina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Fibronectins); 0 (LAMC2 protein, human); 0 (Laminin); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); 0 (POSTN protein, human); 0 (Protein Isoforms); 0 (Proteoglycans); 0 (Tenascin); 9007-34-5 (Collagen); EC 3.4.24.19 (BMP1 protein, human); EC 3.4.24.19 (Bone Morphogenetic Protein 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2644-4


  4 / 182 MEDLINE  
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[PMID]:28584056
[Au] Autor:Xu ER; Blythe EE; Fischer G; Hyvönen M
[Ad] Endereço:From the Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom.
[Ti] Título:Structural analyses of von Willebrand factor C domains of collagen 2A and CCN3 reveal an alternative mode of binding to bone morphogenetic protein-2.
[So] Source:J Biol Chem;292(30):12516-12527, 2017 Jul 28.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic proteins (BMPs) are secreted growth factors that promote differentiation processes in embryogenesis and tissue development. Regulation of BMP signaling involves binding to a variety of extracellular proteins, among which are many von Willebrand factor C (vWC) domain-containing proteins. Although the crystal structure of the complex of crossveinless-2 (CV-2) vWC1 and BMP-2 previously revealed one mode of the vWC/BMP-binding mechanism, other vWC domains may bind to BMP differently. Here, using X-ray crystallography, we present for the first time structures of the vWC domains of two proteins thought to interact with BMP-2: collagen IIA and matricellular protein CCN3. We found that these two vWC domains share a similar N-terminal fold that differs greatly from that in CV-2 vWC, which comprises its BMP-2-binding site. We analyzed the ability of these vWC domains to directly bind to BMP-2 and detected an interaction only between the collagen IIa vWC and BMP-2. Guided by the collagen IIa vWC domain crystal structure and conservation of surface residues among orthologous domains, we mapped the BMP-binding epitope on the subdomain 1 of the vWC domain. This binding site is different from that previously observed in the complex between CV-2 vWC and BMP-2, revealing an alternative mode of interaction between vWC domains and BMPs.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/metabolismo
Colágeno/química
Colágeno/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/química
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Fator de von Willebrand/química
[Mh] Termos MeSH secundário: Sítios de Ligação
Proteína Morfogenética Óssea 2/química
Células Cultivadas
Seres Humanos
Modelos Moleculares
Ligação Proteica
Domínios Proteicos
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); 0 (von Willebrand Factor); 9007-34-5 (Collagen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.788992


  5 / 182 MEDLINE  
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[PMID]:28576832
[Au] Autor:Cao J; Singh SP; McClung JA; Joseph G; Vanella L; Barbagallo I; Jiang H; Falck JR; Arad M; Shapiro JI; Abraham NG
[Ad] Endereço:Departments of Medicine and Pharmacology, New York Medical College, Valhalla, New York.
[Ti] Título:EET intervention on Wnt1, NOV, and HO-1 signaling prevents obesity-induced cardiomyopathy in obese mice.
[So] Source:Am J Physiol Heart Circ Physiol;313(2):H368-H380, 2017 Aug 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have previously reported that epoxyeicosatrienoic acid (EET) has multiple beneficial effects on vascular function; in addition to its antiapoptotic action, it increases insulin sensitivity and inhibits inflammation. To uncover the signaling mechanisms by which EET reduces cardiomyopathy, we hypothesized that EET infusion might ameliorate obesity-induced cardiomyopathy by improving heme oxygenase (HO)-1, Wnt1, thermogenic gene levels, and mitochondrial integrity in cardiac tissues and improved pericardial fat phenotype. EET reduced levels of fasting blood glucose and proinflammatory adipokines, including nephroblastoma overexpressed (NOV) signaling, while increasing echocardiographic fractional shortening and O consumption. Of interest, we also noted a marked improvement in mitochondrial integrity, thermogenic genes, and Wnt 1 and HO-1 signaling mechanisms. Knockout of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in EET-treated mice resulted in a reversal of these beneficial effects including a decrease in myocardial Wnt1 and HO-1 expression and an increase in NOV. To further elucidate the effects of EET on pericardial adipose tissues, we observed EET treatment increases in adiponectin, PGC-1α, phospho-AMP-activated protein kinase, insulin receptor phosphorylation, and thermogenic genes, resulting in a "browning" pericardial adipose phenotype under high-fat diets. Collectively, these experiments demonstrate that an EET agonist increased Wnt1 and HO-1 signaling while decreasing NOV pathways and the progression of cardiomyopathy. Furthermore, this report presents a portal into potential therapeutic approaches for the treatment of heart failure and metabolic syndrome. The mechanism by which EET acts on obesity-induced cardiomyopathy is unknown. Here, we describe a previously unrecognized function of EET infusion that inhibits nephroblastoma overexpressed (NOV) levels and activates Wnt1, hence identifying NOV inhibition and enhanced Wnt1 expression as novel pharmacological targets for the prevention and treatment of cardiomyopathy and heart failure.Listen to this article's corresponding podcast at http://ajpheart.physiology.org/content/early/2017/05/31/ajpheart.00093.2017.
[Mh] Termos MeSH primário: Tecido Adiposo/efeitos dos fármacos
Cardiomiopatias/prevenção & controle
Eicosanoides/farmacologia
Heme Oxigenase-1/metabolismo
Proteínas de Membrana/metabolismo
Miócitos Cardíacos/efeitos dos fármacos
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Obesidade/tratamento farmacológico
Via de Sinalização Wnt/efeitos dos fármacos
Proteína Wnt1/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipocinas/metabolismo
Tecido Adiposo/enzimologia
Tecido Adiposo/fisiopatologia
Animais
Biomarcadores/sangue
Glicemia/efeitos dos fármacos
Glicemia/metabolismo
Pressão Sanguínea
Cardiomiopatias/enzimologia
Cardiomiopatias/etiologia
Cardiomiopatias/fisiopatologia
Modelos Animais de Doenças
Mediadores da Inflamação/metabolismo
Camundongos
Camundongos Knockout
Mitocôndrias Cardíacas/efeitos dos fármacos
Mitocôndrias Cardíacas/enzimologia
Miócitos Cardíacos/enzimologia
Obesidade/complicações
Obesidade/enzimologia
Obesidade/fisiopatologia
Consumo de Oxigênio
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/deficiência
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
Remodelação Ventricular
Ganho de Peso/efeitos dos fármacos
Proteínas Wnt/metabolismo
beta Catenina
[Pt] Tipo de publicação:JOURNAL ARTICLE; WEBCASTS
[Nm] Nome de substância:
0 (Adipokines); 0 (Biomarkers); 0 (Blood Glucose); 0 (CTNNB1 protein, mouse); 0 (Eicosanoids); 0 (Inflammation Mediators); 0 (Membrane Proteins); 0 (Nephroblastoma Overexpressed Protein); 0 (Nov protein, mouse); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, mouse); 0 (Wnt Proteins); 0 (Wnt1 Protein); 0 (Wnt1 protein, mouse); 0 (Wnt5b protein, mouse); 0 (beta Catenin); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00093.2017


  6 / 182 MEDLINE  
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[PMID]:28527710
[Au] Autor:Shi H; Zhang C; Pasupuleti V; Hu X; Prosdocimo DA; Wu W; Qing Y; Wu S; Mohammad H; Gerson SL; Perbal B; Klenotic PA; Dong N; Lin Z
[Ad] Endereço:Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Cardiovascular Research Institute, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio; Harrington Heart and Vascular Ins
[Ti] Título:CCN3 Regulates Macrophage Foam Cell Formation and Atherosclerosis.
[So] Source:Am J Pathol;187(6):1230-1237, 2017 Jun.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies implicate the Cyr61, CTGF, Nov (CCN) matricellular signaling protein family as emerging players in vascular biology, with NOV (alias CCN3) as an important regulator of vascular homeostasis. Herein, we examined the role of CCN3 in the pathogenesis of atherosclerosis. In response to a 15-week high-fat diet feeding, CCN3-deficient mice on the atherosclerosis-prone Apoe background developed increased aortic lipid-rich plaques compared to control Apoe mice, a result that was observed in the absence of alterations in plasma lipid content. To address the cellular contributor(s) responsible for the atherosclerotic phenotype, we performed bone marrow transplantation experiments. Transplantation of Apoe; Ccn3 double-knockout bone marrow into Apoe mice resulted in an increase of atherosclerotic plaque burden, whereas transplantation of Apoe marrow to Apoe; Ccn3 double-knockout mice caused a reduction of atherosclerosis. These results indicate that CCN3 deficiency, specifically in the bone marrow, plays a major role in the development of atherosclerosis. Mechanistically, cell-based studies in isolated peritoneal macrophages demonstrated that CCN3 deficiency leads to an increase of lipid uptake and foam cell formation, an effect potentially attributed to the increased expression of scavenger receptors CD36 and SRA1, key factors involved in lipoprotein uptake. These results suggest that bone marrow-derived CCN3 is an essential regulator of atherosclerosis and point to a novel role of CCN3 in modulating lipid accumulation within macrophages.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Células Espumosas/metabolismo
Macrófagos Peritoneais/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/fisiologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Aorta/metabolismo
Aorta/patologia
Aterosclerose/etiologia
Aterosclerose/patologia
Aterosclerose/prevenção & controle
Medula Óssea/metabolismo
Transplante de Medula Óssea
Antígenos CD36/metabolismo
Células Cultivadas
Dieta Hiperlipídica/efeitos adversos
Progressão da Doença
Células Espumosas/patologia
Metabolismo dos Lipídeos/fisiologia
Macrófagos Peritoneais/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteína Sobre-Expressa em Nefroblastoma/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (CD36 Antigens); 0 (Nephroblastoma Overexpressed Protein); 0 (Nov protein, mouse); 0 (Sra-1 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170522
[St] Status:MEDLINE


  7 / 182 MEDLINE  
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[PMID]:28288125
[Au] Autor:Dombrowski Y; O'Hagan T; Dittmer M; Penalva R; Mayoral SR; Bankhead P; Fleville S; Eleftheriadis G; Zhao C; Naughton M; Hassan R; Moffat J; Falconer J; Boyd A; Hamilton P; Allen IV; Kissenpfennig A; Moynagh PN; Evergren E; Perbal B; Williams AC; Ingram RJ; Chan JR; Franklin RJM; Fitzgerald DC
[Ad] Endereço:Centre for Experimental Medicine, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, Northern Ireland, UK.
[Ti] Título:Regulatory T cells promote myelin regeneration in the central nervous system.
[So] Source:Nat Neurosci;20(5):674-680, 2017 May.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regeneration of CNS myelin involves differentiation of oligodendrocytes from oligodendrocyte progenitor cells. In multiple sclerosis, remyelination can fail despite abundant oligodendrocyte progenitor cells, suggesting impairment of oligodendrocyte differentiation. T cells infiltrate the CNS in multiple sclerosis, yet little is known about T cell functions in remyelination. We report that regulatory T cells (T ) promote oligodendrocyte differentiation and (re)myelination. T -deficient mice exhibited substantially impaired remyelination and oligodendrocyte differentiation, which was rescued by adoptive transfer of T . In brain slice cultures, T accelerated developmental myelination and remyelination, even in the absence of overt inflammation. T directly promoted oligodendrocyte progenitor cell differentiation and myelination in vitro. We identified CCN3 as a T -derived mediator of oligodendrocyte differentiation and myelination in vitro. These findings reveal a new regenerative function of T in the CNS, distinct from immunomodulation. Although the cells were originally named 'T ' to reflect immunoregulatory roles, this also captures emerging, regenerative T functions.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Bainha de Mielina/fisiologia
Regeneração/fisiologia
Linfócitos T Reguladores/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/ultraestrutura
Diferenciação Celular/fisiologia
Feminino
Masculino
Camundongos
Proteína Sobre-Expressa em Nefroblastoma/fisiologia
Oligodendroglia/fisiologia
Células-Tronco/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nephroblastoma Overexpressed Protein); 0 (Nov protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4528


  8 / 182 MEDLINE  
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[PMID]:27815387
[Au] Autor:Fong KW; Zhao JC; Kim J; Li S; Yang YA; Song B; Rittie L; Hu M; Yang X; Perbal B; Yu J
[Ad] Endereço:Division of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
[Ti] Título:Polycomb-Mediated Disruption of an Androgen Receptor Feedback Loop Drives Castration-Resistant Prostate Cancer.
[So] Source:Cancer Res;77(2):412-422, 2017 Jan 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The lethal phenotype of castration-resistant prostate cancer (CRPC) is generally caused by augmented signaling from the androgen receptor (AR). Here, we report that the AR-repressed gene CCN3/NOV inhibits AR signaling and acts in a negative feedback loop to block AR function. Mechanistically, a cytoplasmic form of CCN3 interacted with the AR N-terminal domain to sequester AR in the cytoplasm of prostate cancer cells, thereby reducing AR transcriptional activity and inhibiting cell growth. However, constitutive repression of CCN3 by the Polycomb group protein EZH2 disrupted this negative feedback loop in both CRPC and enzalutamide-resistant prostate cancer cells. Notably, restoring CCN3 was sufficient to effectively reduce CPRC cell proliferation in vitro and to abolish xenograft tumor growth in vivo Taken together, our findings establish CCN3 as a pivotal regulator of AR signaling and prostate cancer progression and suggest a functional intersection between Polycomb and AR signaling in CRPC. Cancer Res; 77(2); 412-22. ©2016 AACR.
[Mh] Termos MeSH primário: Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Neoplasias de Próstata Resistentes à Castração/patologia
Receptores Androgênicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Imunoprecipitação da Cromatina
Retroalimentação Fisiológica/fisiologia
Xenoenxertos
Seres Humanos
Imunoprecipitação
Masculino
Camundongos
Reação em Cadeia da Polimerase
Neoplasias de Próstata Resistentes à Castração/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, human); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); 0 (Receptors, Androgen); EC 2.1.1.43 (EZH2 protein, human); EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-1949


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[PMID]:28002484
[Au] Autor:Marti HP; Jeffs A; Scherer A; Leader J; Leader C; Bedford J; Walker R
[Ad] Endereço:Department of Clinical Medicine, University of Bergen, Bergen, Norway and Haukeland University Hospital, Bergen, Norway.
[Ti] Título:Renal Fibrosis mRNA Classifier: Validation in Experimental Lithium-Induced Interstitial Fibrosis in the Rat Kidney.
[So] Source:PLoS One;11(12):e0168240, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accurate diagnosis of fibrosis is of paramount clinical importance. A human fibrosis classifier based on metzincins and related genes (MARGS) was described previously. In this investigation, expression changes of MARGS genes were explored and evaluated to examine whether the MARGS-based algorithm has any diagnostic value in a rat model of lithium nephropathy. Male Wistar rats (n = 12) were divided into 2 groups (n = 6). One group was given a diet containing lithium (40 mmol/kg food for 7 days, followed by 60mmol/kg food for the rest of the experimental period), while a control group (n = 6) was fed a normal diet. After six months, animals were sacrificed and the renal cortex and medulla of both kidneys removed for analysis. Gene expression changes were analysed using 24 GeneChip® Affymetrix Rat Exon 1.0 ST arrays. Statistically relevant genes (p-value<0.05, fold change>1.5, t-test) were further examined. Matrix metalloproteinase-2 (MMP2), CD44, and nephroblastoma overexpressed gene (NOV) were overexpressed in the medulla and cortex of lithium-fed rats compared to the control group. TGFß2 was overrepresented in the cortex of lithium-fed animals 1.5-fold, and 1.3-fold in the medulla of the same animals. In Gene Set Enrichment Analysis (GSEA), both the medulla and cortex of lithium-fed animals showed an enrichment of the MARGS, TGFß network, and extracellular matrix (ECM) gene sets, while the cortex expression signature was enriched in additional fibrosis-related-genes and the medulla was also enriched in immune response pathways. Importantly, the MARGS-based fibrosis classifier was able to classify all samples correctly. Immunohistochemistry and qPCR confirmed the up-regulation of NOV, CD44, and TGFß2. The MARGS classifier represents a cross-organ and cross-species classifier of fibrotic conditions and may help to design a test to diagnose and to monitor fibrosis. The results also provide evidence for a common pathway in the pathogenesis of fibrosis.
[Mh] Termos MeSH primário: Fibrose/diagnóstico
Fibrose/fisiopatologia
Rim/metabolismo
Lítio/toxicidade
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Animais
Receptores de Hialuronatos/genética
Receptores de Hialuronatos/metabolismo
Imuno-Histoquímica
Rim/efeitos dos fármacos
Rim/patologia
Masculino
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/genética
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta2/genética
Fator de Crescimento Transformador beta2/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hyaluronan Receptors); 0 (Nephroblastoma Overexpressed Protein); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta2); 9FN79X2M3F (Lithium); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[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:161222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0168240


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[PMID]:27750106
[Au] Autor:Awolaran O; Brooks SA; Lavender V
[Ad] Endereço:Department of Applied Health and Professional Development, Oxford Brookes University, Gipsy Lane, Headington, Oxford, OX3 0BP, UK.
[Ti] Título:Breast cancer osteomimicry and its role in bone specific metastasis; an integrative, systematic review of preclinical evidence.
[So] Source:Breast;30:156-171, 2016 Dec.
[Is] ISSN:1532-3080
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Metastasis accounts for most of the deaths from breast cancer and the preference of invasive breast cancer metastasising to bone has been widely reported. However, the biological basis of breast cancer osteotropism is not fully understood. This paper provides, for the first time, an integrative, systematic review of evidence of molecular factors that have functional roles in the homing of metastatic breast cancer to the bone. Pubmed, Web of Science and EBSCOhost were searched using keywords and synonyms for molecular, metastasis, breast cancer and bone to identify articles published between January 2004 and August 2016. 4491 potentially relevant citations were retrieved. 63 articles met the inclusion criteria, which were primary studies reporting evidence of molecular factors that have functional roles in predisposing breast cancer bone metastasis in vivo. 12 of those 63 articles that additionally met quality criteria were included in the review. Extracted data were tabulated and key findings that indicated biological mechanisms involved in breast cancer metastasis to bone were synthesised. 15 proteins expressed by breast cancer cells were identified as factors that mediate breast cancer bone metastasis: ICAM-1, cadherin-11, osteoactivin, bone sialoprotein, CCN3, IL-11, CCL2, CITED2, CXCR4, CTGF, OPN, CX CR1, TWIST1, adrenomedullin and Enpp1. Upregulation or overexpression of one or more of them by breast cancer cells resulted in increased breast cancer metastasis to bone in vivo, except for CCL2 where bone-metastatic cells showed a reduced expression of this factor. All factors identified, here expressed by breast cancer cells, are proteins that are normally expressed in the bone microenvironment and linked to physiologic bone functions. All have a functional role in one of more of the following: cell proliferation and differentiation, bone mineralization and remodelling, cell adhesion and/or chemokine signalling. Six of them (cadherin-11, ICAM-1, OPN, CX CR1, CCN3 and osteoactivin) have a reported function in cell adhesion and another eight (CCN3, osteoactivin, Enpp1, IL-11, CTGF, TWIST1, adrenomedullin and CITED2) are reported to be involved in cell proliferation and differentiation. This review collates and synthesises published evidence to increase our understanding of the biology of breast cancer osteomimicry in the development of bone metastasis. Findings of this review suggest that changes in expression of proteins in breast cancer cells that confer osteomimicry facilitate homing to bone to enable the development of bone metastasis.
[Mh] Termos MeSH primário: Neoplasias Ósseas/secundário
Neoplasias da Mama/patologia
[Mh] Termos MeSH secundário: Adrenomedulina/metabolismo
Animais
Neoplasias Ósseas/metabolismo
Neoplasias da Mama/metabolismo
Receptor 1 de Quimiocina CX3C
Caderinas/metabolismo
Linhagem Celular Tumoral
Quimiocina CCL2/metabolismo
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Seres Humanos
Sialoproteína de Ligação à Integrina/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-11/metabolismo
Glicoproteínas de Membrana/metabolismo
Metástase Neoplásica
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Osteopontina/metabolismo
Diester Fosfórico Hidrolases/metabolismo
Pirofosfatases/metabolismo
Receptores CXCR4/metabolismo
Receptores de Quimiocinas/metabolismo
Proteínas Repressoras/metabolismo
Transativadores/metabolismo
Proteína 1 Relacionada a Twist/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CITED2 protein, human); 0 (CTGF protein, human); 0 (CX3C Chemokine Receptor 1); 0 (CX3CR1 protein, human); 0 (CXCR4 protein, human); 0 (Cadherins); 0 (Chemokine CCL2); 0 (GPNMB protein, human); 0 (Integrin-Binding Sialoprotein); 0 (Interleukin-11); 0 (Membrane Glycoproteins); 0 (Nephroblastoma Overexpressed Protein); 0 (Receptors, CXCR4); 0 (Receptors, Chemokine); 0 (Repressor Proteins); 0 (Trans-Activators); 0 (Twist-Related Protein 1); 106441-73-0 (Osteopontin); 126547-89-5 (Intercellular Adhesion Molecule-1); 139568-91-5 (Connective Tissue Growth Factor); 148498-78-6 (Adrenomedullin); 156621-71-5 (osteoblast cadherin); EC 3.1.4.- (Phosphoric Diester Hydrolases); EC 3.1.4.1 (ectonucleotide pyrophosphatase phosphodiesterase 1); EC 3.6.1.- (Pyrophosphatases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE



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