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[PMID]:27770558
[Au] Autor:Labonte AC; Sung SJ; Jennelle LT; Dandekar AP; Hahn YS
[Ad] Endereço:Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA.
[Ti] Título:Expression of scavenger receptor-AI promotes alternative activation of murine macrophages to limit hepatic inflammation and fibrosis.
[So] Source:Hepatology;65(1):32-43, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The liver maintains an immunologically tolerant environment as a result of continuous exposure to food and bacterial constituents from the digestive tract. Hepatotropic pathogens can take advantage of this niche and establish lifelong chronic infections causing hepatic fibrosis and hepatocellular carcinoma. Macrophages (MÏ•) play a critical role in regulation of immune responses to hepatic infection and regeneration of tissue. However, the factors crucial for MÏ• in limiting hepatic inflammation or resolving liver damage have not been fully understood. In this report, we demonstrate that expression of C-type lectin receptor scavenger receptor-AI (SR-AI) is crucial for promoting M2-like MÏ• activation and polarization during hepatic inflammation. Liver MÏ• uniquely up-regulated SR-AI during hepatotropic viral infection and displayed increased expression of alternative MÏ• activation markers, such as YM-1, arginase-1, and interleukin-10 by activation of mer receptor tyrosine kinase associated with inhibition of mammalian target of rapamycin. Expression of these molecules was reduced on MÏ• obtained from livers of infected mice deficient for the gene encoding SR-AI (msr1). Furthermore, in vitro studies using an SR-AI-deficient MÏ• cell line revealed impeded M2 polarization and decreased phagocytic capacity. Direct stimulation with virus was sufficient to activate M2 gene expression in the wild-type (WT) cell line, but not in the knockdown cell line. Importantly, tissue damage and fibrosis were exacerbated in SR-AI mice following hepatic infection and adoptive transfer of WT bone-marrow-derived MÏ• conferred protection against fibrosis in these mice. CONCLUSION: SR-AI expression on liver MÏ• promotes recovery from infection-induced tissue damage by mediating a switch to a proresolving MÏ• polarization state. (Hepatology 2017;65:32-43).
[Mh] Termos MeSH primário: Hepatite/etiologia
Cirrose Hepática/etiologia
Ativação de Macrófagos
Receptores Depuradores Classe A/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Scavenger Receptors, Class A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28873


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[PMID]:29019900
[Au] Autor:Sun G; Zhang C; Feng M; Liu W; Xie H; Qin Q; Zhao E; Wan L
[Ad] Endereço:aSchool of Public Health, Xinjiang Medical University bDepartment of Chronic and Non-communicable Diseases Control, City Center for Disease Control and Prevention cThe Fifth Affiliated Hospital of Xinjiang Medical University dDepartment of Inspection, Affiliated Tumor Hospital of Xinjiang Medical University eUrumqi Health and Family Commission, Urumqi, China.
[Ti] Título:Methylation analysis of p16, SLIT2, SCARA5, and Runx3 genes in hepatocellular carcinoma.
[So] Source:Medicine (Baltimore);96(41):e8279, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study is to investigate the methylation status of multiple tumor suppressor 1 (p16), secreted glycoprotein 2 (SLIT2), scavenger receptor class A, member 5 putative (SCARA5), and human runt-related transcription factor 3 (Runx3) genes in the peripheral blood of hepatocellular carcinoma (HCC).This is a case-control study. The peripheral blood samples were collected from 25 HCC patients, 25 patients with high risk of HCC (defined as "internal control group"), and 25 healthy individuals (defined as "external control group"), respectively. Then the methylation status of p16, SLIT2, SCARA5, and Runx3 genes in the blood samples were analyzed by pyrosequencing. The relationship between the methylation and the clinical features of HCC patients were evaluated.The methylation levels in the 7 CpG loci of p16 gene in HCC patients were low and without statistically significant difference (P > .05) compared to the control groups. Although the methylation levels of CpG3 and CpG4 in SLIT2 gene loci were higher than those of the control groups, there was no statistically significant difference (P > .05). However, the methylation rate of CpG2 locus in SCARA5 gene in HCC patients was significantly higher (P < .05). And the methylation rates of CpG1, CpG2, CpG3, CpG4, CpG5, and CpG8 in Runx3 gene in HCC patients were significantly different to that of control groups (P < .05). We also have analyzed the correlations between the CpG islands methylation of Runx3 or SCARA5 genes and the age, gender, hepatitis B, liver cirrhosis, alpha fetal protein, or hepatitis B surface antigen (HBsAg) of the HCC patients, which all showed no significant correlations (P > .05).The methylation status of SCARA5 and Runx3 genes are abnormal in HCC patients, which may further be used as molecular markers for early auxiliary diagnosis of liver cancer.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular
Subunidade alfa 3 de Fator de Ligação ao Core
Inibidor p16 de Quinase Dependente de Ciclina
Metilação de DNA/genética
Peptídeos e Proteínas de Sinalização Intercelular
Neoplasias Hepáticas
Proteínas do Tecido Nervoso
Receptores Depuradores Classe A
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/sangue
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Estudos de Casos e Controles
Subunidade alfa 3 de Fator de Ligação ao Core/sangue
Subunidade alfa 3 de Fator de Ligação ao Core/genética
Inibidor p16 de Quinase Dependente de Ciclina/sangue
Inibidor p16 de Quinase Dependente de Ciclina/genética
Epigênese Genética
Inativação Gênica
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/sangue
Peptídeos e Proteínas de Sinalização Intercelular/genética
Neoplasias Hepáticas/sangue
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Proteínas do Tecido Nervoso/sangue
Proteínas do Tecido Nervoso/genética
Receptores Depuradores Classe A/sangue
Receptores Depuradores Classe A/genética
Estatística como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 3 Subunit); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (Intercellular Signaling Peptides and Proteins); 0 (Nerve Tissue Proteins); 0 (Runx3 protein, human); 0 (SCARA5 protein, human); 0 (Scavenger Receptors, Class A); 0 (Slit homolog 2 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008279


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[PMID]:28705936
[Au] Autor:An D; Hao F; Zhang F; Kong W; Chun J; Xu X; Cui MZ
[Ad] Endereço:From the Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996.
[Ti] Título:CD14 is a key mediator of both lysophosphatidic acid and lipopolysaccharide induction of foam cell formation.
[So] Source:J Biol Chem;292(35):14391-14400, 2017 Sep 01.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macrophage uptake of oxidized low-density lipoprotein (oxLDL) plays an important role in foam cell formation and the pathogenesis of atherosclerosis. We report here that lysophosphatidic acid (LPA) enhances lipopolysaccharide (LPS)-induced oxLDL uptake in macrophages. Our data revealed that both LPA and LPS highly induce the CD14 expression at messenger RNA and protein levels in macrophages. The role of CD14, one component of the LPS receptor cluster, in LPA-induced biological functions has been unknown. We took several steps to examine the role of CD14 in LPA signaling pathways. Knockdown of CD14 expression nearly completely blocked LPA/LPS-induced oxLDL uptake in macrophages, demonstrating for the first time that CD14 is a key mediator responsible for both LPA- and LPS-induced oxLDL uptake/foam cell formation. To determine the molecular mechanism mediating CD14 function, we demonstrated that both LPA and LPS significantly induce the expression of scavenger receptor class A type I (SR-AI), which has been implicated in lipid uptake process, and depletion of CD14 levels blocked LPA/LPS-induced SR-AI expression. We further showed that the SR-AI-specific antibody, which quenches SR-AI function, blocked LPA- and LPS-induced foam cell formation. Thus, SR-AI is the downstream mediator of CD14 in regulating LPA-, LPS-, and LPA/LPS-induced foam cell formation. Taken together, our results provide the first experimental evidence that CD14 is a novel connecting molecule linking both LPA and LPS pathways and is a key mediator responsible for LPA/LPS-induced foam cell formation. The LPA/LPS-CD14-SR-AI nexus might be the new convergent pathway, contributing to the worsening of atherosclerosis.
[Mh] Termos MeSH primário: Células Espumosas/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Receptores de Lipopolissacarídeos/metabolismo
Lisofosfolipídeos/metabolismo
Macrófagos/metabolismo
Receptores de Ácidos Lisofosfatídicos/agonistas
Receptores Depuradores Classe A/metabolismo
[Mh] Termos MeSH secundário: Absorção Fisiológica/efeitos dos fármacos
Animais
Biomarcadores/metabolismo
Células da Medula Óssea/citologia
Células Cultivadas
Células Espumosas/efeitos dos fármacos
Células Espumosas/imunologia
Células Espumosas/patologia
Seres Humanos
Isoxazóis/farmacologia
Receptores de Lipopolissacarídeos/química
Receptores de Lipopolissacarídeos/genética
Lipopolissacarídeos/toxicidade
Lipoproteínas LDL/metabolismo
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia de Fluorescência
Propionatos/farmacologia
Interferência de RNA
Receptores de Ácidos Lisofosfatídicos/antagonistas & inibidores
Receptores de Ácidos Lisofosfatídicos/genética
Receptores de Ácidos Lisofosfatídicos/metabolismo
Receptores Depuradores Classe A/agonistas
Receptores Depuradores Classe A/antagonistas & inibidores
Receptores Depuradores Classe A/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acid); 0 (Biomarkers); 0 (Isoxazoles); 0 (Lipopolysaccharide Receptors); 0 (Lipopolysaccharides); 0 (Lipoproteins, LDL); 0 (Lysophospholipids); 0 (Msr1 protein, mouse); 0 (Propionates); 0 (Receptors, Lysophosphatidic Acid); 0 (Scavenger Receptors, Class A); 0 (oxidized low density lipoprotein); PG6M3969SG (lysophosphatidic acid)
[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:170715
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.781807


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[PMID]:28646038
[Au] Autor:Wong CK; Smith CA; Sakamoto K; Kaminski N; Koff JL; Goldstein DR
[Ad] Endereço:Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520.
[Ti] Título:Aging Impairs Alveolar Macrophage Phagocytosis and Increases Influenza-Induced Mortality in Mice.
[So] Source:J Immunol;199(3):1060-1068, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Influenza viral infections often lead to increased mortality in older people. However, the mechanisms by which aging impacts immunity to influenza lung infection remain unclear. We employed a murine model of influenza infection to identify these mechanisms. With aging, we found reduced numbers of alveolar macrophages, cells essential for lung homeostasis. We also determined that these macrophages are critical for influenza-induced mortality with aging. Furthermore, aging vastly alters the transcriptional profile and specifically downregulates cell cycling pathways in alveolar macrophages. Aging impairs the ability of alveolar macrophages to limit lung damage during influenza infection. Moreover, aging decreases alveolar macrophage phagocytosis of apoptotic neutrophils, downregulates the scavenging receptor CD204, and induces retention of neutrophils during influenza infection. Thus, aging induces defective phagocytosis by alveolar macrophages and increases lung damage. These findings indicate that therapies that enhance the function of alveolar macrophages may improve outcomes in older people infected with respiratory viruses.
[Mh] Termos MeSH primário: Envelhecimento
Influenza Humana/mortalidade
Macrófagos Alveolares/imunologia
Infecções por Orthomyxoviridae/imunologia
Infecções por Orthomyxoviridae/mortalidade
Fagocitose
[Mh] Termos MeSH secundário: Animais
Ciclo Celular
Modelos Animais de Doenças
Seres Humanos
Vírus da Influenza A Subtipo H1N1/imunologia
Influenza Humana/imunologia
Influenza Humana/virologia
Pulmão/imunologia
Pulmão/patologia
Pulmão/virologia
Macrófagos Alveolares/metabolismo
Camundongos
Neutrófilos/imunologia
Neutrófilos/patologia
Neutrófilos/virologia
Infecções por Orthomyxoviridae/virologia
Receptores Depuradores Classe A/genética
Receptores Depuradores Classe A/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Msr1 protein, mouse); 0 (Scavenger Receptors, Class A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700397


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[PMID]:28639912
[Au] Autor:Zhang B; Cao M; He Y; Liu Y; Zhang G; Yang C; Du Y; Xu J; Hu J; Gao F
[Ad] Endereço:1 Department of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, P.R. China.
[Ti] Título:Increased circulating M2-like monocytes in patients with breast cancer.
[So] Source:Tumour Biol;39(6):1010428317711571, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:M2-like tumor-associated macrophages promote breast tumor growth and survival and may migrate into the peripheral blood. However, the frequency of circulating M2-like monocytes in the peripheral blood of breast cancer patients has not been clarified. The objective of this study was to determine the percentages of circulating M2-like monocytes in patients with breast cancer. Immunofluorescence staining for CD68 and CD163 was performed to detect M2-like macrophages in pathological tissues. Flow cytometry was used to assess the frequencies of circulating CD14 CD163 /CD14 CD204 /CD14 CD163 CD204 M2-like monocytes in 99 breast cancer patients, 56 patients with benign breast disease, and 60 healthy controls. Receiver operating characteristic curve analysis was used to compare the diagnostic values of circulating M2-like monocytes, carcinoembryonic antigen, and cancer antigen 15-3. The associations among circulating M2-like monocytes and clinical breast cancer parameters were analyzed. The number of CD68 CD163 M2-like macrophages was significantly higher in breast cancer tissues than in benign tissues. In the peripheral blood, CD14 CD163 /CD14 CD204 /CD14 CD163 CD204 M2-like monocytes were elevated in breast cancer patients compared with normal controls and patients with benign breast disease. The area under the receiver operating curve for circulating CD14 CD163 CD204 M2-like monocytes was 0.888 (95% confidence interval: 0.839-0.936), a value higher than those for carcinoembryonic antigen and cancer antigen 15-3. High frequencies of circulating CD14 CD204 and CD14 CD163 CD204 M2-like monocytes were associated with tumor-node-metastasis stage, lymph node metastasis, histological differentiation, and estrogen receptor expression. Circulating M2-like monocytes may serve as a diagnostic biomarker in breast cancer and have a potential role in reflecting breast cancer progression.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Neoplasias da Mama/sangue
Receptores de Lipopolissacarídeos/sangue
Macrófagos/metabolismo
Glicoproteínas de Membrana/sangue
Receptores Depuradores/sangue
Receptores Depuradores Classe A/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Neoplasias da Mama/patologia
Progressão da Doença
Feminino
Citometria de Fluxo
Seres Humanos
Metástase Linfática
Macrófagos/patologia
Meia-Idade
Monócitos/metabolismo
Monócitos/patologia
Receptores de Superfície Celular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Lipopolysaccharide Receptors); 0 (M160 protein, human); 0 (MSR1 protein, human); 0 (Membrane Glycoproteins); 0 (Receptors, Cell Surface); 0 (Receptors, Scavenger); 0 (Scavenger Receptors, Class A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317711571


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[PMID]:28632969
[Au] Autor:Xu Z; Han K; Chen J; Wang C; Dong Y; Yu M; Bai R; Huang C; Hou L
[Ad] Endereço:Department of Neurosurgery in Chang Zheng Hospital, Neurosurgery Research Institution of Shanghai, Second Military Medical University, Shanghai, China.
[Ti] Título:Vascular endothelial growth factor is neuroprotective against ischemic brain injury by inhibiting scavenger receptor A expression on microglia.
[So] Source:J Neurochem;142(5):700-709, 2017 Sep.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Vascular endothelial growth factor (VEGF) is a secreted mitogen associated with angiogenesis. VEGF has long been thought to be a potent neurotrophic factor for the survival of spinal cord neurons. However, the role of VEGF in the regulation of ischemic brain injury remains unclear. In this study, rats were subjected to MCAO (middle cerebral artery occlusion) followed by intraperitoneal injection of VEGF165 (10 mg/kg) immediately after surgery and once daily until the day 10. The expression of target genes was assayed using qPCR, western blot and immunofluorescence to investigate the role of VEGF165 in regulating ischemic brain injury. We found that VEGF165 significantly inhibited MCAO-induced up-regulation of Scavenger receptor class A (SR-A) on microglia in a VEGFR1-dependent manner. VEGF165 inhibited lipopolysaccharide (LPS)-induced expression of proinflammatory cytokines IL-1ß, tumor necrosis factor alpha (TNF-α) and iNOS in microglia. More importantly, the role of VEGF165 in inhibiting neuroinflammation is partially abolished by SR-A over-expression. SR-A further reduced the protective effect of VEGF165 in ischemic brain injury. These data suggest that VEGF165 suppresses neuroinflammation and ischemic brain injury by inhibiting SR-A expression, thus offering a new target for prevention of ischemic brain injury.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Isquemia Encefálica/prevenção & controle
Microglia/metabolismo
Fármacos Neuroprotetores/uso terapêutico
Receptores Depuradores Classe A/biossíntese
Fator A de Crescimento do Endotélio Vascular/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/genética
Células Cultivadas
Expressão Gênica
Masculino
Microglia/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Receptores Depuradores Classe A/antagonistas & inibidores
Receptores Depuradores Classe A/genética
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Scavenger Receptors, Class A); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, rat)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14108


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[PMID]:28574667
[Au] Autor:Miyasato Y; Shiota T; Ohnishi K; Pan C; Yano H; Horlad H; Yamamoto Y; Yamamoto-Ibusuki M; Iwase H; Takeya M; Komohara Y
[Ad] Endereço:Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
[Ti] Título:High density of CD204-positive macrophages predicts worse clinical prognosis in patients with breast cancer.
[So] Source:Cancer Sci;108(8):1693-1700, 2017 Aug.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent studies have indicated the clinical significance of tumor-associated macrophages (TAM) in several malignant tumors including breast cancer. Although recent studies have focused on CD68-positive or CD163-positive TAM in breast cancer, no study has investigated the significance of CD204-positive TAM in breast cancer. We found that CD204 expression on macrophages was evaluated following stimulation with the conditioned medium (CM) of breast cancer cell lines. Paraffin sections of 149 breast cancer samples which were diagnosed as invasive ductal carcinoma were immunohistochemically analyzed for CD68, CD163 and CD204 expression. The results of analyses indicated that a high number of CD204-positive TAM was associated with worse clinical prognoses, including relapse-free survival, distant relapse-free survival and breast cancer-specific survival; however, neither the numbers of CD68-positive or CD163-positive TAM were associated with clinical courses. Of the clinicopathological factors investigated, estrogen receptor, Ki-67 index, hormone subtype, and histological grade were significantly related to the increased number of CD163-positive and CD204-positive TAM. These data indicate the clinical significance of CD204-positive TAM in breast cancer progression and CD204 is a marker for predicting clinical prognosis in breast cancer.
[Mh] Termos MeSH primário: Técnicas de Cocultura/métodos
Macrófagos/citologia
Macrófagos/metabolismo
Receptores Depuradores Classe A/metabolismo
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Meios de Cultivo Condicionados/farmacologia
Feminino
Seres Humanos
Células MCF-7
Macrófagos/patologia
Meia-Idade
Prognóstico
Análise de Sobrevida
Neoplasias de Mama Triplo Negativas/patologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (MSR1 protein, human); 0 (Scavenger Receptors, Class A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13287


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[PMID]:28552585
[Au] Autor:Morioka S; Nigorikawa K; Hazeki K; Ohmura M; Sakamoto H; Matsumura T; Takasuga S; Hazeki O
[Ad] Endereço:Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.
[Ti] Título:Phosphoinositide phosphatase Sac3 regulates the cell surface expression of scavenger receptor A and formation of lipid droplets in macrophages.
[So] Source:Exp Cell Res;357(2):252-259, 2017 Aug 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The findings of this study suggest that the phosphoinositide phosphatase Sac3 maintains the protein level of scavenger receptor A (SR-A) and regulates foam cell formation. RAW264.7 macrophages were transfected with short hairpin RNAs that target Sac3. The knockdown decreased the level of the cell surface SR-A and suppressed the acetylated low density lipoprotein-induced foam cell formation. The associated regulator of PIKfyve (ArPIKfyve) is a scaffold protein that protects Sac3 from proteasome-dependent degradation. The knockdown of ArPIKfyve decreased Sac3, cell surface SR-A, and foam cell formation. The knockdown of PIKfyve had no effect on SR-A protein levels. These results suggest that the ArPIKfyve-Sac3 complex regulates SR-A protein levels independently of its effect on PIKfyve activity.
[Mh] Termos MeSH primário: Flavoproteínas/metabolismo
Gotículas Lipídicas/metabolismo
Macrófagos/metabolismo
Fosfatases de Fosfoinositídeos/metabolismo
Monoéster Fosfórico Hidrolases/metabolismo
Receptores Depuradores/metabolismo
[Mh] Termos MeSH secundário: Animais
Membrana Celular/metabolismo
Flavoproteínas/genética
Técnicas de Silenciamento de Genes/métodos
Seres Humanos
Camundongos
Fosfatases de Fosfoinositídeos/genética
Monoéster Fosfórico Hidrolases/genética
Células RAW 264.7
Receptores Depuradores Classe A/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flavoproteins); 0 (Receptors, Scavenger); 0 (Scavenger Receptors, Class A); EC 3.1.3.- (FIG4 protein, human); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (Fig4 protein, mouse); EC 3.1.3.36 (Phosphoinositide Phosphatases)
[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:170530
[St] Status:MEDLINE


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[PMID]:28483986
[Au] Autor:PrabhuDas MR; Baldwin CL; Bollyky PL; Bowdish DME; Drickamer K; Febbraio M; Herz J; Kobzik L; Krieger M; Loike J; McVicker B; Means TK; Moestrup SK; Post SR; Sawamura T; Silverstein S; Speth RC; Telfer JC; Thiele GM; Wang XY; Wright SD; El Khoury J
[Ad] Endereço:Division of Allergy, Immunology and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852; mprabhudas@niaid.nih.gov jelkhoury@mgh.harvard.edu.
[Ti] Título:A Consensus Definitive Classification of Scavenger Receptors and Their Roles in Health and Disease.
[So] Source:J Immunol;198(10):3775-3789, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Scavenger receptors constitute a large family of proteins that are structurally diverse and participate in a wide range of biological functions. These receptors are expressed predominantly by myeloid cells and recognize a diverse variety of ligands including endogenous and modified host-derived molecules and microbial pathogens. There are currently eight classes of scavenger receptors, many of which have multiple names, leading to inconsistencies and confusion in the literature. To address this problem, a workshop was organized by the United States National Institute of Allergy and Infectious Diseases, National Institutes of Health, to help develop a clear definition of scavenger receptors and a standardized nomenclature based on that definition. Fifteen experts in the scavenger receptor field attended the workshop and, after extensive discussion, reached a consensus regarding the definition of scavenger receptors and a proposed scavenger receptor nomenclature. Scavenger receptors were defined as cell surface receptors that typically bind multiple ligands and promote the removal of nonself or altered-self targets. They often function by mechanisms that include endocytosis, phagocytosis, adhesion, and signaling that ultimately lead to the elimination of degraded or harmful substances. Based on this definition, nomenclature and classification of these receptors into 10 classes were proposed. This classification was discussed at three national meetings and input from participants at these meetings was requested. The following manuscript is a consensus statement that combines the recommendations of the initial workshop and incorporates the input received from the participants at the three national meetings.
[Mh] Termos MeSH primário: Receptores Depuradores/classificação
Receptores Depuradores/fisiologia
[Mh] Termos MeSH secundário: Animais
Endocitose
Seres Humanos
Ligantes
Camundongos
National Institute of Allergy and Infectious Diseases (U.S.)/normas
Fagocitose
Receptores Imunológicos/fisiologia
Receptores Depuradores Classe A/fisiologia
Transdução de Sinais
Terminologia como Assunto
Estados Unidos
[Pt] Tipo de publicação:CONSENSUS DEVELOPMENT CONFERENCE, NIH; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (Receptors, Immunologic); 0 (Receptors, Scavenger); 0 (Scavenger Receptors, Class A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700373


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[PMID]:28472786
[Au] Autor:Ling Q; Yu X; Wang T; Wang SG; Ye ZQ; Liu JH
[Ti] Título:Roles of the Exogenous H2S-Mediated SR-A Signaling Pathway in Renal Ischemia/ Reperfusion Injury in Regulating Endoplasmic Reticulum Stress-Induced Autophagy in a Rat Model.
[So] Source:Cell Physiol Biochem;41(6):2461-2474, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study aims to explore the effects of the exogenous hydrogen sulfide (H2S)-mediated scavenger receptor A (SR-A) signaling pathway on renal ischemia/reperfusion injury (IRI) by regulating endoplasmic reticulum (ER) stress-induced autophagy in rats. METHODS: A total of 48 normal Sprague-Dawley (SD) rats and SR-A knockout rats were selected and divided into six groups (n = 8): wild-type (WT) + sham, WT + ischemia-reperfusion (I/R), WT + I/R + NaHS, SR-A-/- + sham, SR-A-/- + I/R and SR-A-/- + I/R + NaHS. The concentrations of urinary protein, blood urea nitrogen (BUN), serum creatinine (SCR), malondialdehyde (MDA) and H2S in renal tissue were detected. qRT-PCR and Western blotting were used to detect the mRNA and protein levels of IL-6, TGF-ß, SR-A, LC3I, LC3II, P62, PERK, ATF6 and IRE1 pathway-related genes. A TUNEL assay was used to detect cell apoptosis. Electron microscopy was applied to observe the structure of renal autophagosomes. RESULTS: Compared with the WT + sham group, in the rates of the WT + I/R group, the urine volume, urinary protein, BUN, SCR and MDA concentrations, the mRNA and protein expression of IL-6, TGF-ß, LC3II/I, and ER stress pathway-related genes, the cell apoptosis index, and the number of autophagosomes were significantly increased 24 h after I/R, while P62 and SR-A protein expression and SOD and H2S concentrations were significantly decreased (all P < 0.05). The levels of renal injury, autophagy and ER stress pathway-related genes were decreased in the WT + I/R + NaHS group but were increased in the SR-A-/- + I/R group relative to the WT + I/R group. No significant differences were observed in the urine volume; the concentrations of urinary protein, BUN, SCR and MDA; the SOD activity; the mRNA and protein expression of IL-6, TGF-ß, SR-A, GRP78, SR-A, GPR94, ATF4, IRE1, XBP1, ATF6, and eIF2α; the cell apoptosis index; or the number of autophagosomes in rats of the SR-A-/- + I/R and SR-A-/- + I/R + NaHS groups (all P > 0.05). CONCLUSION: These results demonstrate that the exogenous H2S-mediated SR-A signaling pathway reduces renal IRI injury by up-regulating ER stress-induced autophagy in rats.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Sulfeto de Hidrogênio/toxicidade
Receptores Depuradores Classe A/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Creatina/sangue
Modelos Animais de Doenças
Proteínas de Choque Térmico/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Rim/metabolismo
Rim/patologia
Rim/ultraestrutura
Masculino
Malondialdeído/análise
Malondialdeído/metabolismo
Microscopia Eletrônica
Proteínas Associadas aos Microtúbulos/metabolismo
Ratos
Ratos Sprague-Dawley
Traumatismo por Reperfusão/induzido quimicamente
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Receptores Depuradores Classe A/deficiência
Receptores Depuradores Classe A/genética
Superóxido Dismutase/análise
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heat-Shock Proteins); 0 (Interleukin-6); 0 (LC3 protein, rat); 0 (Microtubule-Associated Proteins); 0 (Scavenger Receptors, Class A); 0 (Transforming Growth Factor beta); 0 (molecular chaperone GRP78); 4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); MU72812GK0 (Creatine); YY9FVM7NSN (Hydrogen Sulfide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1159/000475915



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