Base de dados : MEDLINE
Pesquisa : D12.644.276.200 [Categoria DeCS]
Referências encontradas : 320 [refinar]
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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


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[PMID]:29246200
[Au] Autor:Hu Q; Liu J; Wang Y; Wang J; Shi H; Sun Y; Wu X; Yang C; Teng J
[Ad] Endereço:Department of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
[Ti] Título:Delayed-onset of progressive pseudorheumatoid dysplasia in a Chinese adult with a novel compound WISP3 mutation: a case report.
[So] Source:BMC Med Genet;18(1):149, 2017 12 15.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Progressive pseudorheumatoid dysplasia (PPD) is a rare autosomal recessive genetic disease that is characterized by pain, stiffness and enlargement of multiple joints with an age of onset between 3 and 8 years old. Mutations in the WISP3 (Wnt1-inducible signal pathway) gene are known to be the cause of PPD. CASE PRESENTATION: We present a case of delayed-onset PPD in a Chinese man. The 35-year-old proband presented with an almost 20-year history of pain and limitations in mobility in multiple joints. Based on the clinical manifestations, the patient was diagnosed with PPD; however, there was no specific evidence to confirm this diagnosis. Through mutational analyses, two WIPS3 mutations in exon 4, including a novel frameshift mutation (c.670dupA) in the paternal allele and an already described nonsense mutation (c.756C > A, p.Cys252*) in the maternal allele, were identified in the proband. Thus, the patient was diagnosed with PPD. Furthermore, we found that the proband's son only carried one of the mutations (c.670dupA) and therefore determined that he would not be affected by PPD in the future. CONCLUSIONS: In this case, we successfully diagnosed the disease that the proband was affected precisely after the reunion of clinical diagnosis and genetic analysis. These findings demonstrate the clinical utility of genetic analysis to diagnose skeletal dysplasia and guide genetic counseling.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/genética
Artropatias/congênito
[Mh] Termos MeSH secundário: Adulto
Idade de Início
Grupo com Ancestrais do Continente Asiático
China
Análise Mutacional de DNA
Seres Humanos
Artropatias/genética
Artropatias/patologia
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (WISP3 protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171231
[Lr] Data última revisão:
171231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-017-0507-3


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[PMID]:28783045
[Au] Autor:Quiros M; Nishio H; Neumann PA; Siuda D; Brazil JC; Azcutia V; Hilgarth R; O'Leary MN; Garcia-Hernandez V; Leoni G; Feng M; Bernal G; Williams H; Dedhia PH; Gerner-Smidt C; Spence J; Parkos CA; Denning TL; Nusrat A
[Ad] Endereço:Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA.
[Ti] Título:Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling.
[So] Source:J Clin Invest;127(9):3510-3520, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In response to injury, epithelial cells migrate and proliferate to cover denuded mucosal surfaces and repair the barrier defect. This process is orchestrated by dynamic crosstalk between immune cells and the epithelium; however, the mechanisms involved remain incompletely understood. Here, we report that IL-10 was rapidly induced following intestinal mucosal injury and was required for optimal intestinal mucosal wound closure. Conditional deletion of IL-10 specifically in CD11c-expressing cells in vivo implicated macrophages as a critical innate immune contributor to IL-10-induced wound closure. Consistent with these findings, wound closure in T cell- and B cell-deficient Rag1-/- mice was unimpaired, demonstrating that adaptive immune cells are not absolutely required for this process. Further, following mucosal injury, macrophage-derived IL-10 resulted in epithelial cAMP response element-binding protein (CREB) activation and subsequent synthesis and secretion of the pro-repair WNT1-inducible signaling protein 1 (WISP-1). WISP-1 induced epithelial cell proliferation and wound closure by activating epithelial pro-proliferative pathways. These findings define the involvement of macrophages in regulating an IL-10/CREB/WISP-1 signaling axis, with broad implications in linking innate immune activation to mucosal wound repair.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/metabolismo
Interleucina-10/metabolismo
Macrófagos/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD11/metabolismo
Proliferação Celular
Colo/patologia
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Deleção de Genes
Regulação da Expressão Gênica
Seres Humanos
Inflamação
Mucosa Intestinal/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Transdução de Sinais
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (CD11 Antigens); 0 (CREB1 protein, human); 0 (Cyclic AMP Response Element-Binding Protein); 0 (IL10 protein, human); 0 (Proto-Oncogene Proteins); 0 (WISP1 protein, human); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


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[PMID]:28739741
[Au] Autor:Li L; Cui Y; Ji JF; Jiang WG
[Ad] Endereço:Beijing Cancer Hospital and Key Laboratory of Carcinogenesis and Translational Research, Department of Gastrointestinal Surgery, Peking University Cancer Hospital and Institute, Beijing, P.R. China.
[Ti] Título:Clinical Correlation Between WISP2 and ß-Catenin in Gastric Cancer.
[So] Source:Anticancer Res;37(8):4469-4473, 2017 08.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Evidence indicates that wingless-type MMTV integration site family, member 1 (WNT1)-inducible signaling pathway protein 2 (WISP2) may play an important role in the development of gastric cancer (GC) by regulating the WNT/ß-catenin signaling pathway. In the present study, we investigated whether there is correlation between WISP2 and ß-catenin proteins, and their association with clinicopathological features in GC. MATERIALS AND METHODS: Immunohistochemical staining was carried out on 119 paraffin-embedded gastric cancer tissues and 99 adjacent normal gastric tissues collected from patients with GC at the Beijing Cancer Hospital. Data were analyzed by Spearman rank correlation and Chi-square tests. RESULTS: Both WISP2 and ß-catenin were more highly expressed in GC tissues compared to adjacent normal tissues. Moreover, Spearman rank correlation analysis showed positive correlation between WISP2 and ß-catenin (R=0.2254, p=0.0137). Additionally, their co-expression was seen in a higher proportion of patients with GC at early stage or without metastasis. CONCLUSION: These findings suggest that the expression of WISP2 and ß-catenin might be a favorable biomarker for prediction and prognosis in the early stage of GC.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/metabolismo
Proteínas Repressoras/metabolismo
Neoplasias Gástricas/patologia
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Prognóstico
Neoplasias Gástricas/metabolismo
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (CTNNB1 protein, human); 0 (Repressor Proteins); 0 (WISP2 protein, human); 0 (beta Catenin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28618940
[Au] Autor:Jia S; Qu T; Feng M; Ji K; Li Z; Jiang W; Ji J
[Ad] Endereço:1 Laboratory of Surgery, The Affiliated Hospital, Inner Mongolia Medical University, Hohhot, China.
[Ti] Título:Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells.
[So] Source:Tumour Biol;39(6):1010428317699755, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Wnt1-inducible signaling pathway protein-1 is a cysteine-rich protein that belongs to the CCN family, which has been implicated in mediating the occurrence and progression through distinct molecular mechanisms in several tumor types. However, the association of Wnt1-inducible signaling pathway protein-1 with gastric cancer and the related molecular mechanisms remain to be elucidated. Therefore, this study aimed to clarify the biological role of Wnt1-inducible signaling pathway protein-1 in the proliferation, migration, and invasion in gastric cancer cells and further investigated the associated molecular mechanism on these biological functions. We first detected the expression level of Wnt1-inducible signaling pathway protein-1 in gastric cancer, and the reverse transcription polymerase chain reaction have shown that Wnt1-inducible signaling pathway protein-1 expression levels were upregulated in gastric cancer tissues. The expression of Wnt1-inducible signaling pathway protein-1 in gastric cancer cell lines was also detected by quantitative real-time polymerase chain reaction and Western blotting. Furthermore, two gastric cancer cell lines with high expression of Wnt1-inducible signaling pathway protein-1 were selected to explore the biological function of Wnt1-inducible signaling pathway protein-1 in gastric cancer. Function assays indicated that knockdown of Wnt1-inducible signaling pathway protein-1 suppressed cell proliferation, migration, and invasion in BGC-823 and AGS gastric cancer cells. Further investigation of mechanisms suggested that cyclinD1 was identified as one of Wnt1-inducible signaling pathway protein-1 related genes to accelerate proliferation in gastric cancer cells. In addition, one pathway of Wnt1-inducible signaling pathway protein-1 induced migration and invasion was mainly through the enhancement of epithelial-to-mesenchymal transition progression. Taken together, our findings presented the first evidence that Wnt1-inducible signaling pathway protein-1 was upregulated in gastric cancer and acted as an oncogene by promoting proliferation, migration, and invasion in gastric cancer cells.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Proteínas de Sinalização Intercelular CCN/biossíntese
Proliferação Celular/genética
Proteínas Proto-Oncogênicas/biossíntese
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/genética
Proteínas de Sinalização Intercelular CCN/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Transição Epitelial-Mesenquimal/genética
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Proteínas Proto-Oncogênicas/genética
Transdução de Sinais
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CCN Intercellular Signaling Proteins); 0 (Proto-Oncogene Proteins); 0 (WISP1 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317699755


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[PMID]:28426731
[Au] Autor:Lau HK; Wu ER; Chen MK; Hsieh MJ; Yang SF; Wang LY; Chou YE
[Ad] Endereço:Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
[Ti] Título:Effect of genetic variation in microRNA binding site in WNT1-inducible signaling pathway protein 1 gene on oral squamous cell carcinoma susceptibility.
[So] Source:PLoS One;12(4):e0176246, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oral squamous cell carcinoma (OSCC), which is the most common head and neck cancer, accounts for 1%-2% of all human malignancies and is characterized by poor prognosis and reduced survival rates. WNT1-inducible signaling pathway protein 1 (WISP1), a cysteine-rich protein belonging to the Cyr61, CTGF, Nov (CCN) family of matricellular proteins, has many developmental functions and may be involved in carcinogenesis. This study investigated WISP1 single-nucleotide polymorphisms (SNPs) to elucidate OSCC susceptibility and clinicopathologic characteristics. METHODOLOGY/PRINCIPAL FINDINGS: Real-time polymerase chain reaction was used to analyze 6 SNPs of WISP1 in 900 OSCC patients and 1200 cancer-free controls. The results showed that WISP1 rs2929970 polymorphism carriers with at least one G allele were susceptible to OSCC. Moreover, compared with smokers, non-smoker patients with higher frequencies of WISP1 rs2929970 (AG + GG) variants had a late stage (stages III and IV) and a large tumor size. In addition, OSCC patients who were betel quid chewers and carried WISP1 rs16893344 (CT + TT) variants had a low risk of lymph node metastasis. CONCLUSION: Our results demonstrate that a joint effect of WISP1 rs2929970 with smoking as well as WISP1 rs16893344 with betel nut chewing causally contributes to the occurrence of OSCC. WISP1 polymorphism may serve as a marker or a therapeutic target in OSCC.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/genética
Carcinoma de Células Escamosas/metabolismo
MicroRNAs/metabolismo
Neoplasias Bucais/metabolismo
Proteínas Proto-Oncogênicas/genética
[Mh] Termos MeSH secundário: Sítios de Ligação
Proteínas de Sinalização Intercelular CCN/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Proteínas Proto-Oncogênicas/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins); 0 (WISP1 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176246


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[PMID]:28406476
[Au] Autor:Tsai HC; Tzeng HE; Huang CY; Huang YL; Tsai CH; Wang SW; Wang PC; Chang AC; Fong YC; Tang CH
[Ad] Endereço:Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
[Ti] Título:WISP-1 positively regulates angiogenesis by controlling VEGF-A expression in human osteosarcoma.
[So] Source:Cell Death Dis;8(4):e2750, 2017 Apr 13.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In recent years, much research has focused on the role of angiogenesis in osteosarcoma, which occurs predominantly in adolescents and young adults. The vascular endothelial growth factor-A (VEGF-A) pathway is the key regulator of angiogenesis and in osteosarcoma. VEGF-A expression has been recognized as a prognostic marker in angiogenesis. Aberrant WNT1-inducible signaling pathway protein-1 (WISP-1) expression is associated with various cancers. However, the function of WISP-1 in osteosarcoma angiogenesis is poorly understood. We demonstrate a positive correlation between WISP-1 and VEGF-A expression in human osteosarcoma. Moreover, we show that WISP-1 promotes VEGF-A expression in human osteosarcoma cells, subsequently inducing human endothelial progenitor cell (EPC) migration and tube formation. The focal adhesion kinase (FAK), Jun amino-terminal kinase (JNK), and hypoxia-inducible factor (HIF)-1α signaling pathways were activated after WISP-1 stimulation, while FAK, JNK, and HIF-1α inhibitors or small interfering RNA (siRNA) abolished WISP-1-induced VEGF-A expression and angiogenesis. In vitro and in vivo studies revealed down-regulation of microRNA-381 (miR-381) in WISP-1-induced VEGF-A expression and angiogenesis. Our findings reveal that WISP-1 enhances VEGF-A expression and angiogenesis through the FAK/JNK/HIF-1α signaling pathways, as well as via down-regulation of miR-381 expression. WISP-1 may be a promising target in osteosarcoma angiogenesis.
[Mh] Termos MeSH primário: Neoplasias Ósseas
Proteínas de Sinalização Intercelular CCN/metabolismo
Regulação Neoplásica da Expressão Gênica
Neovascularização Patológica
Osteossarcoma
Proteínas Proto-Oncogênicas/metabolismo
Fator A de Crescimento do Endotélio Vascular/biossíntese
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Neoplasias Ósseas/irrigação sanguínea
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Linhagem Celular Tumoral
Embrião de Galinha
Células Endoteliais/metabolismo
Células Endoteliais/patologia
Feminino
Seres Humanos
Masculino
MicroRNAs/biossíntese
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
Osteossarcoma/irrigação sanguínea
Osteossarcoma/metabolismo
Osteossarcoma/patologia
RNA Neoplásico/biossíntese
Transdução de Sinais
Células-Tronco/metabolismo
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (MIRN381 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins); 0 (RNA, Neoplasm); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (WISP1 protein, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.421


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[PMID]:28167681
[Au] Autor:Zhang Y; Yu M; Dai M; Chen C; Tang Q; Jing W; Wang H; Tian W
[Ad] Endereço:State Key Laboratory of Oral Disease, West China School of Stomatology, Sichuan University, Chengdu 610041, China.
[Ti] Título:miR-450a-5p within rat adipose tissue exosome-like vesicles promotes adipogenic differentiation by targeting WISP2.
[So] Source:J Cell Sci;130(6):1158-1168, 2017 Mar 15.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adipose tissue is an active endocrine organ that can secrete a wide number of factors to regulate adipogenesis via paracrine signals. In addition to soluble proteins in adipose tissue, microRNAs (miRNAs) enriched in extracellular vesicles (EVs), such as exosomes or microvesicles, could modulate intercellular communications. In this study, we demonstrated that exosome-like vesicles derived from adipose tissue (Exo-AT) were internalized by adipose tissue-derived stem cells (ADSCs), and that these, in turn, induced adipogenesis. High-throughput sequencing showed that 45 miRNAs were enriched in Exo-AT, and 31.11% of them were associated with adipogenesis, compared with ADSC-derived exosome-like vesicles (Exo-ADSC). miR-450a-5p, one of the most abundant miRNAs in Exo-AT, was a proadipogenic miRNA. Further study demonstrated that miR-450a-5p promoted adipogenesis through repressing expression of WISP2 by targeting its 3' untranslated region. Additionally, Exo-AT could also downregulate the expression of WISP2, while miR-450a-5p inhibitor reversed this effect. Moreover, inhibition of miR-450a-5p impaired adipogenesis mediated by exosome-like vesicles. In conclusion, Exo-AT mediates adipogenic differentiation through a mechanism involving transfer of miR-450a-5p.
[Mh] Termos MeSH primário: Adipogenia
Tecido Adiposo/metabolismo
Proteínas de Sinalização Intercelular CCN/metabolismo
Exossomos/metabolismo
MicroRNAs/metabolismo
Proteínas Repressoras/metabolismo
[Mh] Termos MeSH secundário: Adipogenia/genética
Animais
Sequência de Bases
Endocitose
Exossomos/ultraestrutura
Perfilação da Expressão Gênica
MicroRNAs/genética
Modelos Biológicos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (MIRN450 microRNA, rat); 0 (MicroRNAs); 0 (Repressor Proteins); 0 (Wisp2 protein, rat)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.197764


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[PMID]:27878658
[Au] Autor:Jayakumar AR; Apeksha A; Norenberg MD
[Ad] Endereço:Laboratory of Neuropathology, Veterans Affairs Medical Center, Miami, FL, USA.
[Ti] Título:Role of Matricellular Proteins in Disorders of the Central Nervous System.
[So] Source:Neurochem Res;42(3):858-875, 2017 Mar.
[Is] ISSN:1573-6903
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Matricellular proteins (MCPs) are actively expressed non-structural proteins present in the extracellular matrix, which rapidly turnover and possess regulatory roles, as well as mediate cell-cell interactions. MCPs characteristically contain binding sites for other extracellular proteins, cell surface receptors, growth factors, cytokines and proteases, that provide structural support for surrounding cells. MCPs are present in most organs, including brain, and play a major role in cell-cell interactions and tissue repair. Among the MCPs found in brain include thrombospondin-1/2, secreted protein acidic and rich in cysteine family (SPARC), including Hevin/SC1, Tenascin C and CYR61/Connective Tissue Growth Factor/Nov family of proteins, glypicans, galectins, plasminogen activator inhibitor (PAI-1), autotaxin, fibulin and perisostin. This review summarizes the potential role of MCPs in the pathogenesis of major neurological disorders, including Alzheimer's disease, amyotrophic lateral sclerosis, ischemia, trauma, hepatic encephalopathy, Down's syndrome, autism, multiple sclerosis, brain neoplasms, Parkinson's disease and epilepsy. Potential therapeutic opportunities of MCP's for these disorders are also considered in this review.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Central/metabolismo
Proteínas da Matriz Extracelular/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Sinalização Intercelular CCN/metabolismo
Doenças do Sistema Nervoso Central/tratamento farmacológico
Glipicanas/metabolismo
Seres Humanos
Osteonectina/metabolismo
Tenascina/metabolismo
Trombospondinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (Extracellular Matrix Proteins); 0 (Glypicans); 0 (Osteonectin); 0 (Tenascin); 0 (Thrombospondins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.1007/s11064-016-2088-5


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[PMID]:27863006
[Au] Autor:Liu JL; Kaddour N; Chowdhury S; Li Q; Gao ZH
[Ad] Endereço:Fraser Laboratories, Department of Medicine, The Research Institute of McGill University Health Centre, Montreal, Canada.
[Ti] Título:Role of CCN5 (WNT1 inducible signaling pathway protein 2) in pancreatic islets.
[So] Source:J Diabetes;9(5):462-474, 2017 May.
[Is] ISSN:1753-0407
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:In search of direct targets of insulin-like growth factor (IGF)-1 action, we discovered CCN5 (WNT1 inducible signaling pathway protein 2 [WISP2]) as a novel protein expressed in pancreatic ß-cells. As a member of the "CCN" ( C ysteine-rich angiogenic inducer 61 [Cyr61], C onnective tissue growth factor [CTGF in humans], and N ephroblastoma overexpressed [Nov; in chickens]) family, the expression of CCN5/WISP2 is stimulated by IGF-1 together with Wnt signaling. When overexpressed in insulinoma cells, CCN5 promotes cell proliferation and cell survival against streptozotocin-induced cell death. The cell proliferation effect seems to be caused by AKT phosphorylation and increased cyclin D1 levels. These properties resemble those of CCN2/CTGF, another isoform of the CCN family, although CCN5 is the only one within the family of six proteins that lacks the C-terminal repeat. Treatment of primary mouse islets with recombinant CCN5 protein produced similar effects to those of gene transfection, indicating that either as a matricellular protein or a secreted growth factor, CCN5 stimulates ß-cell proliferation and regeneration in a paracrine fashion. This review also discusses the regulation of CCN5/WISP2 by estrogen and its involvement in angiogenesis and tumorigenesis.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/metabolismo
Fator de Crescimento Insulin-Like I/farmacologia
Ilhotas Pancreáticas/efeitos dos fármacos
Proteínas Repressoras/metabolismo
Via de Sinalização Wnt/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proteínas de Sinalização Intercelular CCN/genética
Linhagem Celular Tumoral
Proliferação Celular/genética
Sobrevivência Celular/genética
Seres Humanos
Ilhotas Pancreáticas/metabolismo
Camundongos
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (Repressor Proteins); 0 (WISP2 protein, human); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1111/1753-0407.12507



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