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Pesquisa : D12.776.543.750.705.408.100.300 [Categoria DeCS]
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[PMID]:29262349
[Au] Autor:Fu B; Zhou Y; Ni X; Tong X; Xu X; Dong Z; Sun R; Tian Z; Wei H
[Ad] Endereço:Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Te
[Ti] Título:Natural Killer Cells Promote Fetal Development through the Secretion of Growth-Promoting Factors.
[So] Source:Immunity;47(6):1100-1113.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are present in large populations at the maternal-fetal interface during early pregnancy. However, the role of NK cells in fetal growth is unclear. Here, we have identified a CD49a Eomes subset of NK cells that secreted growth-promoting factors (GPFs), including pleiotrophin and osteoglycin, in both humans and mice. The crosstalk between HLA-G and ILT2 served as a stimulus for GPF-secreting function of this NK cell subset. Decreases in this GPF-secreting NK cell subset impaired fetal development, resulting in fetal growth restriction. The transcription factor Nfil3, but not T-bet, affected the function and the number of this decidual NK cell subset. Adoptive transfer of induced CD49a Eomes NK cells reversed impaired fetal growth and rebuilt an appropriate local microenvironment. These findings reveal properties of NK cells in promoting fetal growth. In addition, this research proposes approaches for therapeutic administration of NK cells in order to reverse restricted nourishments within the uterine microenvironment during early pregnancy.
[Mh] Termos MeSH primário: Aborto Habitual/imunologia
Transferência Adotiva
Proteínas de Transporte/secreção
Citocinas/secreção
Desenvolvimento Fetal/imunologia
Retardo do Crescimento Fetal/prevenção & controle
Peptídeos e Proteínas de Sinalização Intercelular/secreção
Células Matadoras Naturais/transplante
[Mh] Termos MeSH secundário: Aborto Habitual/genética
Aborto Habitual/patologia
Adulto
Animais
Antígenos CD/genética
Antígenos CD/imunologia
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/imunologia
Proteínas de Transporte/genética
Proteínas de Transporte/imunologia
Microambiente Celular
Citocinas/genética
Citocinas/imunologia
Decídua/imunologia
Decídua/patologia
Feminino
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/imunologia
Retardo do Crescimento Fetal/patologia
Feto
Regulação da Expressão Gênica no Desenvolvimento
Antígenos HLA-G/genética
Antígenos HLA-G/imunologia
Seres Humanos
Integrina alfa1/genética
Integrina alfa1/imunologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/imunologia
Células Matadoras Naturais/citologia
Células Matadoras Naturais/imunologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/genética
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Gravidez
Transdução de Sinais
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Carrier Proteins); 0 (Cytokines); 0 (EOMES protein, human); 0 (HLA-G Antigens); 0 (Integrin alpha1); 0 (Intercellular Signaling Peptides and Proteins); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (NFIL3 protein, human); 0 (OGN protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 134034-50-7 (pleiotrophin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28792982
[Au] Autor:Martrus G; Kautz T; Lunemann S; Richert L; Glau L; Salzberger W; Goebels H; Langeneckert A; Hess L; Poch T; Schramm C; Oldhafer KJ; Koch M; Tolosa E; Nashan B; Altfeld M
[Ad] Endereço:Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.
[Ti] Título:Proliferative capacity exhibited by human liver-resident CD49a+CD25+ NK cells.
[So] Source:PLoS One;12(8):e0182532, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The recruitment and retention of Natural Killer (NK) cells in the liver are thought to play an important role during hepatotropic infections and liver cirrhosis. The aims of this study were to determine differences between liver-derived and peripheral blood-derived NK cells in the context of liver inflammation and cirrhosis. We conducted a prospective dual-center cross-sectional study in patients undergoing liver transplantation or tumor-free liver resections, in which both liver tissue and peripheral blood samples were obtained from each consenting study participants. Intrahepatic lymphocytes and PBMCs were stained, fixed and analyzed by flow cytometry. Our results showed that, within cirrhotic liver samples, intrahepatic NK cells were particularly enriched for CD49a+ NK cells when compared to tumor-free liver resection samples. CD49a+ liver-derived NK cells included populations of cells expressing CD25, CD34 and CXCR3. Moreover, CD49a+CD25+ liver-derived NK cells exhibited high proliferative capacity in vitro in response to low doses of IL-2. Our study identified a specific subset of CD49a+CD25+ NK cells in cirrhotic livers bearing functional features of proliferation.
[Mh] Termos MeSH primário: Proliferação Celular/fisiologia
Integrina alfa1/fisiologia
Subunidade alfa de Receptor de Interleucina-2/fisiologia
Células Matadoras Naturais/fisiologia
Fígado/citologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD34/fisiologia
Estudos Transversais
Feminino
Citometria de Fluxo
Seres Humanos
Células Matadoras Naturais/imunologia
Fígado/imunologia
Fígado/fisiologia
Transplante de Fígado
Masculino
Meia-Idade
Estudos Prospectivos
Receptores CXCR3/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (CXCR3 protein, human); 0 (IL2RA protein, human); 0 (Integrin alpha1); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182532


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[PMID]:28264467
[Au] Autor:Liu X; Tian H; Li H; Ge C; Zhao F; Yao M; Li J
[Ad] Endereço:State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, 25/Ln 2200, Xietu Road, Shanghai 200032, China. liuxiaoqin106484@163.com.
[Ti] Título:Derivate Isocorydine (d-ICD) Suppresses Migration and Invasion of Hepatocellular Carcinoma Cell by Downregulating ITGA1 Expression.
[So] Source:Int J Mol Sci;18(3), 2017 Feb 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In our previous studies, we found that isocorydine (ICD) could be a potential antitumor agent in hepatocellular carcinoma (HCC). Derivate isocorydine (d-ICD), a more effective antitumor agent, has been demonstrated to inhibit proliferation and drug resistance in HCC. In order to investigate the potential role of d-ICD on HCC cell migration and its possible mechanism, wound healing assay, trans-well invasion assay, western blot analysis, and qRT-PCR were performed to study the migration and invasion ability of HCC cells as well as relevant molecular alteration following d-ICD treatment. Results indicated that the migration and invasion ability of HCC cells were suppressed when cultured with d-ICD. Meanwhile, the expression level of was markedly reduced. Furthermore, we found that promotes HCC cell migration and invasion in vitro, and that can partly reverse the effect of d-ICD-induced migration and invasion suppression in HCC cells. In addition, dual luciferase reporter assay and chromatin immunoprecipitation assay were used to study the expression regulation of , and found that directly upregulates expression and d-ICD inhibits expression. Taken together, these results reveal that d-ICD inhibits HCC cell migration and invasion may partly by downregulating / expression.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Aporfinas/farmacologia
Movimento Celular/efeitos dos fármacos
Expressão Gênica
Integrina alfa1/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/metabolismo
Linhagem Celular Tumoral
Fator de Transcrição E2F1/metabolismo
Inativação Gênica
Seres Humanos
Neoplasias Hepáticas/metabolismo
MicroRNAs/genética
Regiões Promotoras Genéticas
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Aporphines); 0 (E2F1 Transcription Factor); 0 (Integrin alpha1); 0 (MicroRNAs); 3B5E87JEOX (isocorydine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE


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[PMID]:28214226
[Au] Autor:Cheuk S; Schlums H; Gallais Sérézal I; Martini E; Chiang SC; Marquardt N; Gibbs A; Detlofsson E; Introini A; Forkel M; Höög C; Tjernlund A; Michaëlsson J; Folkersen L; Mjösberg J; Blomqvist L; Ehrström M; Ståhle M; Bryceson YT; Eidsmo L
[Ad] Endereço:Department of Medicine Solna, Karolinska Institutet, Stockholm 171 77, Sweden.
[Ti] Título:CD49a Expression Defines Tissue-Resident CD8 T Cells Poised for Cytotoxic Function in Human Skin.
[So] Source:Immunity;46(2):287-300, 2017 Feb 21.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident memory T (Trm) cells form a heterogeneous population that provides localized protection against pathogens. Here, we identify CD49a as a marker that differentiates CD8 Trm cells on a compartmental and functional basis. In human skin epithelia, CD8 CD49a Trm cells produced interferon-γ, whereas CD8 CD49a Trm cells produced interleukin-17 (IL-17). In addition, CD8 CD49a Trm cells from healthy skin rapidly induced the expression of the effector molecules perforin and granzyme B when stimulated with IL-15, thereby promoting a strong cytotoxic response. In skin from patients with vitiligo, where melanocytes are eradicated locally, CD8 CD49a Trm cells that constitutively expressed perforin and granzyme B accumulated both in the epidermis and dermis. Conversely, CD8 CD49a Trm cells from psoriasis lesions predominantly generated IL-17 responses that promote local inflammation in this skin disease. Overall, CD49a expression delineates CD8 Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Citotoxicidade Imunológica/imunologia
Integrina alfa1/imunologia
Pele/imunologia
Subpopulações de Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Separação Celular
Citometria de Fluxo
Seres Humanos
Memória Imunológica/imunologia
Integrina alfa1/biossíntese
Ativação Linfocitária/imunologia
Microscopia Confocal
Psoríase/imunologia
Vitiligo/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170219
[St] Status:MEDLINE


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[PMID]:28031334
[Au] Autor:Li T; Wang J; Wang Y; Chen Y; Wei H; Sun R; Tian Z
[Ad] Endereço:The Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China; and.
[Ti] Título:Respiratory Influenza Virus Infection Induces Memory-like Liver NK Cells in Mice.
[So] Source:J Immunol;198(3):1242-1252, 2017 Feb 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although NK cells are classified as innate immune cells, recent studies have demonstrated the transformation of NK cells into long-lived memory cells that contribute to secondary immune responses in certain mouse models. However, whether NK cells mount an Ag-specific memory response to acute influenza virus infection has not yet been examined. Here, we show that, consistent with previous studies, lung NK cells play an important role in controlling viral proliferation after primary influenza virus infection. However, although lung NK cells display a memory phenotype at the late stage of infection, these cells do not protect mice against secondary influenza virus infection. Interestingly, liver NK cells from influenza virus-infected mice possess a memory phenotype and protect mice against secondary influenza virus infection. Memory-like liver NK cells display a CD49a DX5 phenotype, and the adoptive transfer of purified liver CD49a DX5 NK cells into naive mice followed by viral infection results in protective immunity and decreased viral titer. Moreover, we demonstrate that primary inactivated influenza virus induces memory NK cells residing in the liver of Rag1 mice. Collectively, these data suggest that liver CD49a DX5 NK cells remember encountered Ag from influenza virus after primary infection and are more protective upon subsequent infection.
[Mh] Termos MeSH primário: Memória Imunológica
Células Matadoras Naturais/imunologia
Fígado/imunologia
Infecções por Orthomyxoviridae/imunologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Homeodomínio/fisiologia
Integrina alfa1/análise
Pulmão/imunologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Integrin alpha1); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1502186


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[PMID]:27493244
[Au] Autor:Krueger PD; Narayanan S; Surette FA; Brown MG; Sung SJ; Hahn YS
[Ad] Endereço:Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, USA.
[Ti] Título:Murine liver-resident group 1 innate lymphoid cells regulate optimal priming of anti-viral CD8+ T cells.
[So] Source:J Leukoc Biol;101(1):329-338, 2017 Jan.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The liver contains 2 transcriptionally distinct group 1 ILC subsets: CD49a ILC1s and CD49b NK cells. However, little is known about how group 1 ILCs contribute to hepatic immune responses. Therefore, we characterized murine liver-resident group 1 ILCs and found that CD49a ILC1s express high levels of the inhibitory receptor NKG2A and localize near DCs in perivascular spaces surrounding the portal triads. Upon hepatic viral infection, NKG2A signaling in group 1 ILCs, especially in CD49a ILC1s, inhibits CXCL9 expression required for robust accumulation of IFN-γ CD49b NK cells. As a consequence, NKG2A mice showed increased numbers of IFN-γ-producing NK cells that preferentially activate liver CD103 DCs, leading to the sustained proliferation of adoptively transferred, virus-specific CD8 T cells. Collectively, these data suggest that group 1 ILCs play a role in maintaining the liver as a tolerogenic site by limiting the recruitment of peripheral NK cells during the early phase of viral infection. Furthermore, our findings implicate that the inhibition of NKG2A signaling on group 1 ILCs may be a novel vaccine strategy to induce robust CD8 T cell responses against persistent liver pathogens.
[Mh] Termos MeSH primário: Antivirais/imunologia
Linfócitos T CD8-Positivos/imunologia
Apresentação Cruzada/imunologia
Imunidade Inata
Fígado/citologia
Linfócitos/citologia
[Mh] Termos MeSH secundário: Adenoviridae/metabolismo
Animais
Antígenos CD/metabolismo
Linfócitos T CD8-Positivos/efeitos dos fármacos
Contagem de Células
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Quimiocina CXCL9/biossíntese
Fatores Quimiotáticos/farmacologia
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Epitopos/imunologia
Feminino
Imunidade Inata/efeitos dos fármacos
Cadeias alfa de Integrinas/metabolismo
Integrina alfa1/metabolismo
Interferon gama/metabolismo
Células Matadoras Naturais/imunologia
Linfócitos/efeitos dos fármacos
Masculino
Camundongos
Subfamília C de Receptores Semelhantes a Lectina de Células NK/deficiência
Subfamília C de Receptores Semelhantes a Lectina de Células NK/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antiviral Agents); 0 (Chemokine CXCL9); 0 (Chemotactic Factors); 0 (Epitopes); 0 (Integrin alpha Chains); 0 (Integrin alpha1); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (alpha E integrins); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160806
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3A0516-225R


  7 / 252 MEDLINE  
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[PMID]:27909848
[Au] Autor:Peng H; Tian Z
[Ad] Endereço:Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China. huipeng@mail.ustc.edu.cn.
[Ti] Título:Tissue-resident natural killer cells in the livers.
[So] Source:Sci China Life Sci;59(12):1218-1223, 2016 Dec.
[Is] ISSN:1869-1889
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Nature killer (NK) cells are important lymphocytes of the innate immune system, well known for their pivotal roles in immune surveillance and defense against tumor and virus-infected cells. Current studies have revealed that NK cells are not a homogeneous population, but instead consist of distinct subsets with diverse characteristics. As an organ with predominant innate immunity, the liver is enriched with NK cells, among which two distinct NK cell subsets have recently been identified: conventional NK (cNK) cells and tissue-resident NK (trNK) cells. Liver trNK cells are markedly different from cNK cells in many aspects, representing a new lineage of innate lymphoid cell (ILC) family. Here, we summarize the phenotypic and functional features of liver trNK cells, and review current knowledge regarding developmental pathway of liver trNK cells. We also overview recent advances in human liver trNK cells and discuss the striking shared hallmarks of trNK cells in different tissues.
[Mh] Termos MeSH primário: Linhagem da Célula/imunologia
Imunidade Inata/imunologia
Células Matadoras Naturais/imunologia
Fígado/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/imunologia
Seres Humanos
Integrina alfa1/imunologia
Integrina alfa1/metabolismo
Células Matadoras Naturais/metabolismo
Modelos Imunológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Integrin alpha1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161203
[St] Status:MEDLINE


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[PMID]:27670593
[Au] Autor:Zhang LH; Shin JH; Haggadone MD; Sunwoo JB
[Ad] Endereço:Division of Head and Neck Surgery, Department of Otolaryngology, Program in Immunology, Stanford Cancer Institute and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305.
[Ti] Título:The aryl hydrocarbon receptor is required for the maintenance of liver-resident natural killer cells.
[So] Source:J Exp Med;213(11):2249-2257, 2016 Oct 17.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A tissue-resident population of natural killer cells (NK cells) in the liver has recently been described to have the unique capacity to confer immunological memory in the form of hapten-specific contact hypersensitivity independent of T and B cells. Factors regulating the development and maintenance of these liver-resident NK cells are poorly understood. The aryl hydrocarbon receptor (AhR) is a transcription factor modulated by exogenous and endogenous ligands that is important in the homeostasis of immune cells at barrier sites, such as the skin and gut. In this study, we show that liver-resident NK (NK1.1 CD3 ) cells, defined as CD49a TRAIL CXCR6 DX5 cells in the mouse liver, constitutively express AhR. In AhR mice, there is a significant reduction in the proportion and absolute number of these cells, which results from a cell-intrinsic dependence on AhR. This deficiency in liver-resident NK cells appears to be the result of higher turnover and increased susceptibility to cytokine-induced cell death. Finally, we show that this deficiency has functional implications in vivo. Upon hapten exposure, AhR mice are not able to mount an NK cell memory response to hapten rechallenge. Together, these data demonstrate the requirement of AhR for the maintenance of CD49a TRAIL CXCR6 DX5 liver-resident NK cells and their hapten memory function.
[Mh] Termos MeSH primário: Células Matadoras Naturais/metabolismo
Fígado/citologia
Receptores de Hidrocarboneto Arílico/metabolismo
[Mh] Termos MeSH secundário: Animais
Dermatite de Contato/imunologia
Dermatite de Contato/patologia
Homeostase
Integrina alfa1/metabolismo
Integrina alfa2/metabolismo
Camundongos Endogâmicos C57BL
Receptores de Hidrocarboneto Arílico/deficiência
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha1); 0 (Integrin alpha2); 0 (Receptors, Aryl Hydrocarbon); 0 (TNF-Related Apoptosis-Inducing Ligand)
[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:160928
[St] Status:MEDLINE


  9 / 252 MEDLINE  
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[PMID]:27484337
[Au] Autor:Gao G; He J; Nong L; Xie H; Huang Y; Xu N; Zhou D
[Ad] Endereço:Department of Orthopedics, Changzhou Second Hospital Affiliated to Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
[Ti] Título:Periodic mechanical stress induces the extracellular matrix expression and migration of rat nucleus pulposus cells by upregulating the expression of intergrin α1 and phosphorylation of downstream phospholipase Cγ1.
[So] Source:Mol Med Rep;14(3):2457-64, 2016 Sep.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Intervertebral disk degeneration (IDD) is a major cause of low back pain and an important socioeconomic burden. Degradation of the extracellular matrix (ECM) of nucleus pulposus (NP) cells in the interverterbal disk is important for IDD. Stress of a suitable frequency and amplitude promotes the synthesis of the ECM of NP cells, however, the associated mechanisms remain to be fully elucidated The present study aimed to investigate the effect of integrin α1 on the migration and ECM synthesis of NP cells under soft periodic mechanical stress. Rat NP cells were isolated and plated onto slides, and were then treated with or without the use of a periodic mechanical stress system. The expression levels of integrin α1, α5 and αv, ECM collagen 2A1 (Col2A1) and aggrecan, and the phosphorylation of phospholipase C­Î³1 (PLCγ1) were measured using reverse transcription­quantitative polymerase chain reaction and western blot analyses. Cell migration was assayed using a scratch experiment. The results showed that exposure to periodic mechanical stress significantly induced the mRNA expression levels of Col2A1 and aggrecan, cell migration, mRNA expression of integrin α1 and phosphorylation of PLC­Î³1 of the NP, compared with the control (P<0.05). Inhibition of the PLCγ1 protein by U73122 significantly decreased the ECM expression under periodic mechanical stress (P<0.05). Small interfering RNA­mediated integrin α1 gene knockdown suppressed the mRNA expression levels of Col2A1 and aggrecan, and suppressed the migration and phosphorylation of PLCγ1 of the NP cells under periodic mechanical stress, compared with the control (P<0.05). In conclusion, periodic mechanical stress induced ECM expression and the migration of NP cells via upregulating the expression of integrin α1 and the phosphorylation of downstream PLCγ1. These findings provide novel information to aid the understanding of the pathogenesis and development of IDD.
[Mh] Termos MeSH primário: Matriz Extracelular/metabolismo
Integrina alfa1/metabolismo
Núcleo Pulposo/citologia
Núcleo Pulposo/metabolismo
Fosfolipase C gama/metabolismo
Estresse Mecânico
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Colágeno Tipo II/genética
Colágeno Tipo II/metabolismo
Expressão Gênica
Integrina alfa1/genética
Degeneração do Disco Intervertebral/genética
Degeneração do Disco Intervertebral/metabolismo
Degeneração do Disco Intervertebral/patologia
Masculino
Fosforilação
Interferência de RNA
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type II); 0 (Integrin alpha1); 0 (RNA, Messenger); 0 (RNA, Small Interfering); EC 3.1.4.3 (Phospholipase C gamma); EC 3.1.4.3 (phospholipase Cgamma1, rat)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5549


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[PMID]:27392662
[Au] Autor:Vagace JM; Cardesa R; Corbacho A; Vázquez T; de la Maya MD; Gonzalez FA; Nieto JB; Urrutia E; Gómez MJ; Pascual T; Aguinaco MR; Gervasini G
[Ad] Endereço:Service of Hematology, Infanta Cristina University Hospital, Badajoz, Spain.
[Ti] Título:Etiopathological mechanisms and clinical characteristics of hyperhemolysis syndrome in Spanish patients with thalassemia.
[So] Source:Ann Hematol;95(9):1419-27, 2016 Sep.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Hyperhemolysis syndrome (HHS) is characterized by severe intravascular hemolysis with a decrease in the reticulocyte count, which is triggered and aggravated by transfusion and cannot be explained by standard immunohematological studies. A nationwide study was conducted in order to retrospectively identify thalassemia patients with HHS in Spain in order to assess pre-disposing mechanisms for this syndrome. For this, the expression of adhesion (CD49, CD36) and complement-related molecules (C3a, CD59) and the levels of reticulocyte apoptosis and macrophage activation were measured in 4 thalassemia patients with HHS, 14 patients without HHS, and 10 healthy subjects. Five of the six thalassemia patients had δß-thalassemia. The patients were not alloimmunized prior to the syndrome, which was developed after the first transfusion in all but one case. Patients with δß-thalassemia did not respond to corticoids or immunoglobulins; only splenectomy was successful. The expression of CD49 (α4ß1 integrin) was far higher in patients who had experienced HHS (85.07 ± 18.46 vs. 46.28 ± 24.31; p < 0.01), and the difference remained significant after correcting by the number of molecules analyzed (Bonferroni p < 0.05). In our population, δß-thalassemia was the most common hemoglobinopathy in patients with HHS. Furthermore, the risk to develop this syndrome may be associated with an increased expression of α4ß1 integrin.
[Mh] Termos MeSH primário: Transfusão de Sangue/métodos
Hemólise/fisiologia
Talassemia/fisiopatologia
Talassemia/terapia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Apoptose
Antígenos CD36/sangue
Antígenos CD59/sangue
Complemento C3a/análise
Feminino
Citometria de Fluxo
Seres Humanos
Integrina alfa1/sangue
Ativação de Macrófagos
Masculino
Meia-Idade
Reticulócitos/metabolismo
Estudos Retrospectivos
Fatores de Risco
Espanha
Síndrome
Talassemia/sangue
Adulto Jovem
Talassemia beta/sangue
Talassemia beta/fisiopatologia
Talassemia beta/terapia
Talassemia delta/sangue
Talassemia delta/fisiopatologia
Talassemia delta/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (CD59 Antigens); 0 (Integrin alpha1); 101754-01-2 (CD59 protein, human); 80295-42-7 (Complement C3a)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160710
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-016-2733-8



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