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  1 / 25 MEDLINE  
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[PMID]:28612394
[Au] Autor:Ge H; Mu L; Jin L; Yang C; Chang YE; Long Y; DeLeon G; Deleyrolle L; Mitchell DA; Kubilis PS; Lu D; Qi J; Gu Y; Lin Z; Huang J
[Ad] Endereço:The Fourth Section of Department of Neurosurgery, the First Affiliated Hospital, Harbin Medical University, Harbin, China.
[Ti] Título:Tumor associated CD70 expression is involved in promoting tumor migration and macrophage infiltration in GBM.
[So] Source:Int J Cancer;141(7):1434-1444, 2017 Oct 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor migration/metastasis and immunosuppression are major obstacles in effective cancer therapy. Incidentally, these 2 hurdles usually coexist inside tumors, therefore making therapy significantly more complicated, as both oncogenic mechanisms must be addressed for successful therapeutic intervention. Our recent report highlights that the tumor expression of a TNF family member, CD70, is correlated with poor survival for primary gliomas. In this study, we investigated how CD70 expression by GBM affects the characteristics of tumor cells and the tumor microenvironment. We found that the ablation of CD70 in primary GBM decreased CD44 and SOX2 gene expression, and inhibited tumor migration, growth and the ability to attract monocyte-derived M2 macrophages in vitro. In the tumor microenvironment, CD70 was associated with immune cell infiltrates, such as T cells; myeloid-derived suppressor cells; and monocytes/macrophages based on the RNA-sequencing profile. The CD163+ macrophages were far more abundant than T cells were. This overwhelming level of macrophages was identified only in GBM and not in low-grade gliomas and normal brain specimens, implying their tumor association. CD70 was detected only on tumor cells, not on macrophages, and was highly correlated with CD163 gene expression in primary GBM. Additionally, the co-expression of the CD70 and CD163 genes was found to correlate with decreased survival for patients with primary GBM. Together, these data suggest that CD70 expression is involved in promoting tumor aggressiveness and immunosuppression via tumor-associated macrophage recruitment/activation. Our current efforts to target this molecule using chimeric antigen receptor T cells hold great potential for treating patients with GBM.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Ligante CD27/metabolismo
Glioblastoma/metabolismo
Glioblastoma/secundário
Tolerância Imunológica
[Mh] Termos MeSH secundário: Antígenos CD/análise
Antígenos CD/genética
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/análise
Antígenos de Diferenciação Mielomonocítica/genética
Antígenos de Diferenciação Mielomonocítica/metabolismo
Encéfalo/citologia
Neoplasias Encefálicas/imunologia
Ligante CD27/análise
Ligante CD27/genética
Linhagem Celular Tumoral
Ensaios de Migração de Macrófagos/métodos
Movimento Celular
Regulação Neoplásica da Expressão Gênica
Glioblastoma/imunologia
Glioblastoma/mortalidade
Seres Humanos
Receptores de Hialuronatos/genética
Receptores de Hialuronatos/metabolismo
Imunidade Celular
Macrófagos/química
Macrófagos/citologia
Macrófagos/imunologia
Metástase Neoplásica
Receptores de Superfície Celular/análise
Receptores de Superfície Celular/genética
Receptores de Superfície Celular/metabolismo
Fatores de Transcrição SOXB1/genética
Fatores de Transcrição SOXB1/metabolismo
Linfócitos T/citologia
Linfócitos T/imunologia
Microambiente Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD163 antigen); 0 (CD27 Ligand); 0 (CD44 protein, human); 0 (CD70 protein, human); 0 (Hyaluronan Receptors); 0 (Receptors, Cell Surface); 0 (SOXB1 Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30830


  2 / 25 MEDLINE  
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[PMID]:27615202
[Au] Autor:Loza K; Föhring I; Bünger J; Westphal GA; Köller M; Epple M; Sengstock C
[Ad] Endereço:a Inorganic Chemistry and Center for Nanointegration Duisburg-Essen (CeNIDE), University of Duisburg-Essen , Essen , Germany.
[Ti] Título:Barium sulfate micro- and nanoparticles as bioinert reference material in particle toxicology.
[So] Source:Nanotoxicology;10(10):1492-1502, 2016 Dec.
[Is] ISSN:1743-5404
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The inhalation of particles and their exposure to the bronchi and alveoli constitute a major public health risk. Chemical as well as particle-related properties are important factors for the biological response but are difficult to separate from each other. Barium sulfate is a completely inert chemical compound, therefore it is ideally suited to separate these two factors. The biological response of rat alveolar macrophages (NR8383) was analyzed after exposure to barium sulfate particles with three different diameters (40 nm, 270 nm, and 1.3 µm, respectively) for 24 h in vitro (particle concentrations from 12.5 to 200 µg mL ). The particles were colloidally stabilized as well as fluorescently-labeled by carboxymethylcellulose, conjugated with 6-aminofluorescein. All kinds of barium sulfate particles were efficiently taken up by NR8383 cells and found inside endo-lysosomes, but never in the cell nucleus. Neither an inflammatory nor a cytotoxic response was detected by the ability of dHL-60 and NR8383 cells to migrate towards a chemotactic gradient (conditioned media of NR8383 cells) and by the release of inflammatory mediators (CCL2, TNF-α, IL-6). The particles neither caused apoptosis (up to 200 µg mL ) nor necrosis (up to 100 µg mL ). As only adverse reaction, necrosis was found at a concentration of 200 µg mL of the largest barium sulfate particles (1.3 µm). Barium sulfate particles are ideally suited as bioinert control to study size-dependent effects such as uptake mechanisms of intracellular distributions of pure particles, especially in nanotoxicology.
[Mh] Termos MeSH primário: Sulfato de Bário/toxicidade
Quimiotaxia/efeitos dos fármacos
Macrófagos Alveolares/efeitos dos fármacos
Nanopartículas/toxicidade
[Mh] Termos MeSH secundário: Animais
Ensaios de Migração de Macrófagos
Células Cultivadas
Citometria de Fluxo
Interleucina-6/imunologia
Pulmão/efeitos dos fármacos
Macrófagos Alveolares/imunologia
Macrófagos Alveolares/metabolismo
Microscopia Confocal
Tamanho da Partícula
Ratos
Padrões de Referência
Propriedades de Superfície
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 25BB7EKE2E (Barium Sulfate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160913
[St] Status:MEDLINE


  3 / 25 MEDLINE  
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[PMID]:27565850
[Au] Autor:Schremmer I; Brik A; Weber DG; Rosenkranz N; Rostek A; Loza K; Brüning T; Johnen G; Epple M; Bünger J; Westphal GA
[Ad] Endereço:Institute for Prevention and Occupational Medicine of the German Social Accident Insurance - Institute of the Ruhr-University Bochum (IPA), Bürkle-de-la-Camp-Platz 1, 44789 Bochum, Germany. Electronic address: schremmer@ipa-dguv.de.
[Ti] Título:Kinetics of chemotaxis, cytokine, and chemokine release of NR8383 macrophages after exposure to inflammatory and inert granular insoluble particles.
[So] Source:Toxicol Lett;263:68-75, 2016 Nov 30.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Accumulation of macrophages and neutrophil granulocytes in the lung are key events in the inflammatory response to inhaled particles. The present study aims at the time course of chemotaxis in vitro in response to the challenge of various biopersistent particles and its functional relation to the transcription of inflammatory mediators. NR8383 rat alveolar macrophages were challenged with particles of coarse quartz, barium sulfate, and nanosized silica for one, four, and 16h and with coarse and nanosized titanium dioxide particles (rutile and anatase) for 16h only. The cell supernatants were used to investigate the chemotaxis of unexposed NR8383 macrophages. The transcription of inflammatory mediators in cells exposed to quartz, silica, and barium sulfate was analyzed by quantitative real-time PCR. Challenge with quartz, silica, and rutile particles induced significant chemotaxis of unexposed NR8383 macrophages. Chemotaxis caused by quartz and silica was accompanied by an elevated transcription of CCL3, CCL4, CXCL1, CXCL3, and TNFα. Quartz exposure showed an earlier onset of both effects compared to the nanosized silica. The strength of this response roughly paralleled the cytotoxic effects. Barium sulfate and anatase did not induce chemotaxis and barium sulfate as well caused no elevated transcription. In conclusion, NR8383 macrophages respond to the challenge with inflammatory particles with the release of chemotactic compounds that act on unexposed macrophages. The kinetics of the response differs between the various particles.
[Mh] Termos MeSH primário: Poluentes Atmosféricos/toxicidade
Quimiocinas/metabolismo
Quimiotaxia/efeitos dos fármacos
Citocinas/metabolismo
Macrófagos Alveolares/efeitos dos fármacos
Macrófagos Alveolares/metabolismo
Material Particulado/toxicidade
[Mh] Termos MeSH secundário: Animais
Sulfato de Bário/toxicidade
Linhagem Celular
Ensaios de Migração de Macrófagos
Perfilação da Expressão Gênica
Cinética
Nanopartículas/toxicidade
Quartzo/toxicidade
Ratos
Dióxido de Silício/toxicidade
Titânio/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Chemokines); 0 (Cytokines); 0 (Particulate Matter); 14808-60-7 (Quartz); 15FIX9V2JP (titanium dioxide); 25BB7EKE2E (Barium Sulfate); 7631-86-9 (Silicon Dioxide); D1JT611TNE (Titanium)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE


  4 / 25 MEDLINE  
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[PMID]:26011183
[Au] Autor:Teixeira D; Marques C; Pestana D; Faria A; Norberto S; Calhau C; Monteiro R
[Ad] Endereço:Faculty of Medicine, Department of Biochemistry, University of Porto, Centro De Investigação Médica, Porto, 4200-319, Portugal. dianamst@med.up.pt.
[Ti] Título:Effects of xenoestrogens in human M1 and M2 macrophage migration, cytokine release, and estrogen-related signaling pathways.
[So] Source:Environ Toxicol;31(11):1496-1509, 2016 Nov.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bisphenol A (BPA), bis(2-ethylhexyl)phthalate (DEHP) and di(n-butyl)phthalate (DBP) are environmental estrogens that have been associated with a wide range of adverse health outcomes for which inflammation has also been hypothesized as a potentially involved mechanism and where macrophages play a central role. This study was carried out to evaluate if xenoestrogen (XE) treatment of classically (M1) or alternatively (M2) activated macrophages could affect their behavior. For this purpose, human peripheral blood monocyte-derived macrophages either unstimulated or activated with lipopolysaccharide (100 ng/mL, M1) or with interleukin (IL) 4 (15 ng/mL, M2) were treated with 17ß-estradiol (E ), BPA, DEHP and DBP alone or in combination with selective ERα or ERß antagonists. Migratory capability, cytokine release, and estrogen-associated signaling pathways were evaluated to assess macrophage function. All tested XEs had a tendency to stimulate M2 migration, an effect that followed the same direction than E . Moreover, all XEs significantly induced IL10 in M1 and decreased IL6 and globally decreased IL10, IL6, TNFα, and IL1ß release by M2 macrophages. However, DEHP and DBP significantly increased IL1ß release in M1 and M2 macrophages, respectively. Some of the effects described above were shown to be mediated by either ERα or ERß and were simultaneous to modulation of NF-κB, AP1, JNK, or ERK signaling pathways. We provide new evidence of the effect of XE on macrophage behavior and their mechanisms with relevance to the understanding of the action of environmental chemicals on the immune system and inflammation-associated diseases. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1496-1509, 2016.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/toxicidade
Movimento Celular/efeitos dos fármacos
Citocinas/metabolismo
Dietilexilftalato/toxicidade
Estradiol/metabolismo
Macrófagos/efeitos dos fármacos
Fenóis/toxicidade
[Mh] Termos MeSH secundário: Ensaios de Migração de Macrófagos
Células Cultivadas
Quimiotaxia de Leucócito/efeitos dos fármacos
Feminino
Seres Humanos
Inflamação/metabolismo
Interleucina-1beta/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/fisiologia
Meia-Idade
NF-kappa B/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Cytokines); 0 (Interleukin-1beta); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Phenols); 0 (Tumor Necrosis Factor-alpha); 4TI98Z838E (Estradiol); C42K0PH13C (Diethylhexyl Phthalate); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150527
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22154


  5 / 25 MEDLINE  
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[PMID]:26238448
[Au] Autor:Shimojo N; Hashizume R; Kanayama K; Hara M; Suzuki Y; Nishioka T; Hiroe M; Yoshida T; Imanaka-Yoshida K
[Ad] Endereço:From the Department of Pathology and Matrix Biology (N.S., R.H., M.H., Y.S., T.N., M.H., T.Y., K.I.-Y.), and Department of Pathologic Oncology (K.K.), Mie University Graduate School of Medicine, Tsu, Mie, Japan; Mie University Research Center for Matrix Biology, Tsu, Mie, Japan (N.S., R.H., T.Y., K.
[Ti] Título:Tenascin-C may accelerate cardiac fibrosis by activating macrophages via the integrin αVß3/nuclear factor-κB/interleukin-6 axis.
[So] Source:Hypertension;66(4):757-66, 2015 Oct.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tenascin-C (TN-C) is an extracellular matrix protein not detected in normal adult heart, but expressed in several heart diseases closely associated with inflammation. Accumulating data suggest that TN-C may play a significant role in progression of ventricular remodeling. In this study, we aimed to elucidate the role of TN-C in hypertensive cardiac fibrosis and underlying molecular mechanisms. Angiotensin II was administered to wild-type and TN-C knockout mice for 4 weeks. In wild-type mice, the treatment induced increase of collagen fibers and accumulation of macrophages in perivascular areas associated with deposition of TN-C and upregulated the expression levels of interleukin-6 and monocyte chemoattractant protein-1 as compared with wild-type/control mice. These changes were significantly reduced in TN-C knockout/angiotensin II mice. In vitro, TN-C accelerated macrophage migration and induced accumulation of integrin αVß3 in focal adhesions, with phosphorylation of focal adhesion kinase (FAK) and Src. TN-C treatment also induced nuclear translocation of phospho-NF-κB and upregulated interleukin-6 expression of macrophages in an NF-κB-dependent manner; this being suppressed by inhibitors for integrin αVß3 and Src. Furthermore, interleukin-6 upregulated expression of collagen I by cardiac fibroblasts. TN-C may enhance inflammatory responses by accelerating macrophage migration and synthesis of proinflammatory/profibrotic cytokines via integrin αVß3/FAK-Src/NF-κB, resulting in increased fibrosis.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Cardiopatias/genética
Integrina alfaVbeta3/genética
Interleucina-6/genética
Ativação de Macrófagos/genética
RNA Mensageiro/genética
Tenascina/genética
[Mh] Termos MeSH secundário: Animais
Western Blotting
Ensaios de Migração de Macrófagos
Células Cultivadas
Modelos Animais de Doenças
Fibroblastos/metabolismo
Fibroblastos/patologia
Fibrose/genética
Fibrose/metabolismo
Fibrose/patologia
Imunofluorescência
Cardiopatias/metabolismo
Cardiopatias/patologia
Imuno-Histoquímica
Integrina alfaVbeta3/biossíntese
Interleucina-6/biossíntese
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Proteínas do Tecido Nervoso
Reação em Cadeia da Polimerase em Tempo Real
Tenascina/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Integrin alphaVbeta3); 0 (Interleukin-6); 0 (Nerve Tissue Proteins); 0 (RNA, Messenger); 0 (Tenascin); 0 (tenascin-N protein, mouse)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:160726
[Lr] Data última revisão:
160726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150805
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.115.06004


  6 / 25 MEDLINE  
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[PMID]:25730105
[Au] Autor:Karkeni E; Marcotorchino J; Tourniaire F; Astier J; Peiretti F; Darmon P; Landrier JF
[Ad] Endereço:Institut National de Recherche Agronomique, Unité Mixte de Recherche 1260; Inserm, Unité Mixte de Recherche 1062, Nutrition, Obésité et Risque Thrombotique; and Faculté de Médecine, Aix-Marseille Université, F-13385 Marseille Cedex 05, France.
[Ti] Título:Vitamin D limits chemokine expression in adipocytes and macrophage migration in vitro and in male mice.
[So] Source:Endocrinology;156(5):1782-93, 2015 May.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vitamin D (VD) displays immunoregulatory effects and reduces adipocyte inflammation, which may participate to a reduction of adipose tissue macrophage infiltration in the context of obesity-associated low-grade inflammation. These observations have been described mainly in vitro, through the evaluation of a limited number of inflammatory markers. Here, we studied the effects of 1,25 dihydroxy-VD on chemokine network expression in adipocytes (by transcriptomic approach), and we confirm the physiological relevance of these data in vivo, by demonstrating the effect of VD on cytokine and chemokine gene expression as well as on macrophage infiltration in adipose tissue. 1,25 dihydroxy-VD down-regulated (-1.3- to -10.8-fold) the mRNA expression of 29 chemokines and limited macrophage migration in TNFα-conditioned adipocyte medium (1.5-fold; P < .05). This effect was associated with a reduction in p65 and IκB (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha) phosphorylation (2-fold compared with TNFα; P < .05). The effects of VD were confirmed in mice injected ip with lipopolysaccharide (acute inflammation) and diet-induced obese mice (metabolic inflammation), where the levels of mRNA encoding proinflammatory cytokines and chemokines (∼2-fold) were reduced in adipocytes (acute and metabolic inflammation) and adipose tissue and that macrophage infiltration was also inhibited in the adipose tissue of obese mice (metabolic inflammation). Altogether, these results showed that VD displayed a global immunoregulatory impact on adipocytes, notably via the inhibition of chemokine expression and macrophage infiltration in inflamed adipose tissue.
[Mh] Termos MeSH primário: Adipócitos/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Quimiocinas/efeitos dos fármacos
Colecalciferol/farmacologia
Inflamação/genética
Macrófagos/efeitos dos fármacos
RNA Mensageiro/efeitos dos fármacos
Vitamina D/análogos & derivados
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/metabolismo
Animais
Linhagem Celular
Ensaios de Migração de Macrófagos
Quimiocinas/genética
Citocinas/efeitos dos fármacos
Citocinas/genética
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Técnicas In Vitro
Inflamação/metabolismo
Lipopolissacarídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Necrose Tumoral alfa/farmacologia
Vitamina D/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Lipopolysaccharides); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 1406-16-2 (Vitamin D); 1C6V77QF41 (Cholecalciferol); 66772-14-3 (1,25-dihydroxyvitamin D)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150418
[Lr] Data última revisão:
150418
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150303
[St] Status:MEDLINE
[do] DOI:10.1210/en.2014-1647


  7 / 25 MEDLINE  
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[PMID]:25349250
[Au] Autor:Ka SO; Song MY; Bae EJ; Park BH
[Ad] Endereço:Department of BiochemistryChonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 561-756, Republic of KoreaCollege of PharmacyWoosuk University, 443 Samnye-ro, Wanju, Jeonbuk 565-701, Republic of Korea.
[Ti] Título:Myeloid SIRT1 regulates macrophage infiltration and insulin sensitivity in mice fed a high-fat diet.
[So] Source:J Endocrinol;224(2):109-18, 2015 Feb.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inflammation is an important factor in the development of insulin resistance. SIRT1, a class 3 histone/protein deacetylase, has anti-inflammatory functions. Myeloid-specific deletion of Sirt1 promotes macrophage infiltration into insulin-sensitive organs and aggravates tissue inflammation. In this study, we investigated how SIRT1 in macrophages alters tissue inflammation in the pancreas as well as liver and adipose tissue, and further explored the role of SIRT1 in locomotion of macrophages. Myeloid-specific Sirt1-deleted mice (mS1KO) and WT littermates were fed a 60% calorie high-fat diet (HFD) for 16 weeks. Tissue inflammation and metabolic phenotypes were compared. Bone marrow macrophages (BMMs) from WT or mS1KO mice were used in in vitro chemotaxis assays and macrophage polarization studies. mS1KO mice fed a HFD exhibited glucose intolerance, reduced insulin secretion, and insulin sensitivity with a slight decrease in body weight. Consistent with these results, pancreatic islets of mS1KO mice fed a HFD displayed decreased mass with profound apoptotic cell damage and increased macrophage infiltration and inflammation. Liver and adipose tissues from mS1KO HFD mice also showed greater accumulation of macrophages and tissue inflammation. Results from in vitro experiments indicated that deletion of myeloid Sirt1 stimulated proinflammatory M1-like polarization of BMMs and augmented the adipocyte-mediated macrophage chemotaxis. The latter effect was accompanied by increased expression and acetylation of focal adhesion kinase, as well as nuclear factor kappa B. Our results indicate that myeloid SIRT1 plays a crucial role in macrophage polarization and chemotaxis, and thus regulates the development of HFD-induced pancreatic inflammation and insulin secretion, and metabolic derangements in liver and adipose tissue.
[Mh] Termos MeSH primário: Movimento Celular/genética
Dieta Hiperlipídica
Resistência à Insulina/genética
Macrófagos/imunologia
Sirtuína 1/fisiologia
[Mh] Termos MeSH secundário: Tecido Adiposo/imunologia
Animais
Atrofia/imunologia
Ensaios de Migração de Macrófagos
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Gorduras na Dieta/farmacologia
Células HEK293
Seres Humanos
Inflamação/imunologia
Ilhotas Pancreáticas/imunologia
Ilhotas Pancreáticas/patologia
Fígado/imunologia
Macrófagos/efeitos dos fármacos
Camundongos
Camundongos Knockout
Células Mieloides/efeitos dos fármacos
Células Mieloides/metabolismo
Sirtuína 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Fats); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:150113
[Lr] Data última revisão:
150113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141029
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-14-0527


  8 / 25 MEDLINE  
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[PMID]:24037939
[Au] Autor:Madsen SJ; Gach HM; Hong SJ; Uzal FA; Peng Q; Hirschberg H
[Ad] Endereço:Department of Health Physics and Diagnostic Sciences, University of Nevada, Las Vegas, Nevada, 89154.
[Ti] Título:Increased nanoparticle-loaded exogenous macrophage migration into the brain following PDT-induced blood-brain barrier disruption.
[So] Source:Lasers Surg Med;45(8):524-32, 2013 Oct.
[Is] ISSN:1096-9101
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: Photodynamic therapy (PDT)-induced disruption of the blood-brain barrier (BBB) has been investigated as a technique for the delivery of therapeutic agents to selective regions of the brain. The purpose of this study was to determine the effects of PDT on the migration of systemically administered exogenous macrophages (Ma) loaded with iron oxide nanoparticles in non-tumor bearing rats. MATERIALS AND METHODS: A control group consisting of three Sprague-Dawley rats was injected with iron oxide-loaded rat alveolar Ma via jugular vein catheter while two animals were subjected to intracranial injection of iron oxide-loaded Ma. PDT-treated animals were injected with photosensitizer (AlPcS2a ; 1 mg/kg i.p.) followed by light irradiation (wavelength = 670 nm; light dose = 2.5 J) 48 hours later. Light irradiation was performed through the skull. Prior to light irradiation, iron oxide-loaded Ma were administered to each animal. Animals in all groups were imaged in a 7 Tesla (T) magnetic resonance (MR) imager to determine the extent of PDT-induced edema and to evaluate for the presence of iron oxide nanoparticles. Animals were sacrificed 7 days post-Ma administration and their brains analyzed for the presence of iron oxide using Perls staining. RESULTS: Significant uptake of iron oxide nanoparticles by rat alveolar Ma was observed thus providing the rationale for their use as delivery vectors. Histopathological analyses failed to find evidence of iron oxide in normal rat brain. Accumulations of iron oxide-loaded Ma were observed in both MR images and histological sections of non-tumor bearing rat brain following PDT-induced disruption of the BBB. CONCLUSIONS: MR imaging was shown to be useful for localizing iron-oxide loaded Ma in rat brains. Exogenous Ma are incapable of traversing the normal BBB and therefore, the use of Ma as delivery vehicles into the brain requires selective disruption of the BBB.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/efeitos dos fármacos
Indóis/farmacologia
Macrófagos Alveolares/metabolismo
Compostos Organometálicos/farmacologia
Fármacos Fotossensibilizantes/farmacologia
[Mh] Termos MeSH secundário: Animais
Ensaios de Migração de Macrófagos
Meios de Contraste
Dextranos
Indóis/administração & dosagem
Imagem por Ressonância Magnética
Nanopartículas de Magnetita
Masculino
Compostos Organometálicos/administração & dosagem
Fotoquimioterapia
Fármacos Fotossensibilizantes/administração & dosagem
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Contrast Media); 0 (Dextrans); 0 (Indoles); 0 (Magnetite Nanoparticles); 0 (Organometallic Compounds); 0 (Photosensitizing Agents); 68637-19-4 (aluminum phthalocyanine disulfonate); G6N3J05W84 (ferumoxides)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130917
[St] Status:MEDLINE
[do] DOI:10.1002/lsm.22172


  9 / 25 MEDLINE  
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[PMID]:23747421
[Au] Autor:Zhang L; Xia X; Zhang M; Wang Y; Xing G; Yin X; Song L; He F; Zhang L
[Ad] Endereço:Department of Biomedical Engineering, Chinese PLA 307 Hospital, Beijing 100071, China.
[Ti] Título:Integrated analysis of genomics and proteomics reveals that CKIP-1 is a novel macrophage migration regulator.
[So] Source:Biochem Biophys Res Commun;436(3):382-7, 2013 Jul 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Casein kinase-2 interacting protein-1 (CKIP-1) has been identified to play an important role in cell morphology, differentiation and apoptosis. However, the role of CKIP-1 in other cellular processes is still unknown. Here we investigated transcriptome profiles of WT and CKIP-1-deficient mouse embryonic fibroblasts (MEFs), and found that innate immunity and cell migration related pathways were significantly correlated with CKIP-1 expression. As macrophage is a key cell type in innate immunity, we then used murine macrophage RAW264.7 cells to discover CKIP-1 interacting proteins by immunoprecipitation/mass spectrometry (IP/MS). Analysis of these proteins revealed migration related pathways were enriched. Further experiments indicated that knockdown of CKIP-1 in RAW264.7 cells resulted in impaired cell migration. Our study suggests that CKIP-1 is a novel regulator of macrophage migration.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Movimento Celular
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte/genética
Ensaios de Migração de Macrófagos
Fatores Quimiotáticos/farmacologia
Fibroblastos/metabolismo
Técnicas de Inativação de Genes
Genômica
Macrófagos/efeitos dos fármacos
Camundongos
N-Formilmetionina Leucil-Fenilalanina/farmacologia
Mapeamento de Interação de Proteínas
Proteômica
Transdução de Sinais
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CKIP-1 protein, mouse); 0 (Carrier Proteins); 0 (Chemotactic Factors); 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:130708
[Lr] Data última revisão:
130708
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130611
[St] Status:MEDLINE


  10 / 25 MEDLINE  
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[PMID]:23559030
[Au] Autor:Larmann J; Frenzel T; Schmitz M; Hahnenkamp A; Demmer P; Immenschuh S; Tietge UJ; Bremer C; Theilmeier G
[Ad] Endereço:Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, Hannover, Germany.
[Ti] Título:In vivo fluorescence-mediated tomography imaging demonstrates atorvastatin-mediated reduction of lesion macrophages in ApoE-/- mice.
[So] Source:Anesthesiology;119(1):129-41, 2013 Jul.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Macrophage recruitment into atherosclerotic plaques drives lesion progression, destabilization, and rupture. Chronic statin treatment reduces macrophage plaque content. Information on dynamics of macrophage recruitment would help assessing plaque vulnerability and guiding therapy. Techniques to image macrophage homing to vulnerable plaques in vivo are scarcely available. The authors tested if noninvasive fluorescence-mediated tomography (FMT) can assess plaque-stabilizing effects of short-term high-dosage atorvastatin. METHODS: Macrophages from green-fluorescent-protein-transgenic mice were labeled with a near-infrared fluorescent dye and were injected IV in apolipoprotein E-deficient mice (n=9) on Western diet 7 days after guidewire-injury of the carotid artery. FMT-scans, 2 and 7 days thereafter, quantified macrophage recruitment into carotid artery plaques. Atorvastatin was tested for macrophage adhesion, proliferation, and viability (n=5 to 6) in vitro. Fourteen mice received atorvastatin or vehicle for 4 days after 16 weeks on Western diet. FMT assessed macrophage recruitment into aortic and innominate artery lesions. Means (±SD)% are reported. RESULTS: Double-labeled macrophages were recruited into carotid artery lesions. FMT resolved fluorescence projecting on the injured carotid artery and detected a signal increase to 300% (±191) after guidewire injury. Atorvastatin reduced macrophage adhesion to activated endothelial cells by 36% (±19). In a clinically relevant proof-of-concept intervention, FMT-imaging detected that 4 days atorvastatin treatment reduced macrophage recruitment by 57% (±8) indicating plaque stabilization. Immunohistochemistry confirmed reduced macrophage infiltration. CONCLUSIONS: FMT optical imaging proved its high potential for clinical applicability for tracking recruitment of near-infrared fluorescent-labeled macrophages to vulnerable plaques in vivo. FMT-based quantification of macrophage recruitment demonstrated rapid plaque stabilization by 4-day atorvastatin treatment in apolipoprotein E-deficient mice.
[Mh] Termos MeSH primário: Apolipoproteínas E/genética
Ácidos Heptanoicos/farmacologia
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Macrófagos/metabolismo
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Animais
Artérias/citologia
Artérias/efeitos dos fármacos
Atorvastatina Cálcica
Ensaios de Migração de Macrófagos
Células Cultivadas
Dieta
Fluorescência
Proteínas de Fluorescência Verde
Imuno-Histoquímica
Lipoproteínas LDL/farmacologia
Macrófagos/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Placa Aterosclerótica/patologia
Tomografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Heptanoic Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Lipoproteins, LDL); 0 (Pyrroles); 147336-22-9 (Green Fluorescent Proteins); 48A5M73Z4Q (Atorvastatin Calcium)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:130406
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0b013e318291c18b



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