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[PMID]:29408309
[Au] Autor:Mohamed DI; Nabih ES; El-Waseef DAA; El-Kharashi OA; Abd El Samad AA
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
[Ti] Título:The protective effect of pentoxifylline versus silymarin on the pancreas through increasing adenosine by CD39 in a rat model of liver cirrhosis: Pharmacological, biochemical and histological study.
[So] Source:Gene;651:9-22, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Impaired glucose homoeostasis due to insulin resistance and decrease sensitivity of pancreatic ß-cells is a feature of liver disease and results into hepatogenous diabetes. Decrease expression of CD39 was linked to inflammation and occurrence of diabetes. Therefore, we performed this study to explore the protective effect of pentoxifylline (PTX) and silymarin administration on the ß-cells of the pancreas in a rat model of thioacetamide induced liver cirrhosis. Biochemical, histological and immunohistochemistry studies of the liver and pancreas were performed and provided an evidence on the protective effect of PTX to pancreatic ß-cells compared to silymarin. Also, silymarin induced a significant improvement of liver cirrhosis compared to PTX. In conclusion, the potential protective effect of PTX against ß-cells deterioration could be attributed to increasing pancreatic CD39 expression and the subsequent increase of adenosine.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Antígenos CD/metabolismo
Apirase/metabolismo
Cirrose Hepática Experimental/tratamento farmacológico
Pâncreas/efeitos dos fármacos
Pentoxifilina/uso terapêutico
Substâncias Protetoras/uso terapêutico
Silimarina/uso terapêutico
[Mh] Termos MeSH secundário: Amilases/sangue
Animais
Modelos Animais de Doenças
Células Secretoras de Insulina/efeitos dos fármacos
Fígado/patologia
Cirrose Hepática Experimental/metabolismo
Cirrose Hepática Experimental/patologia
Testes de Função Hepática
Masculino
Pâncreas/patologia
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Protective Agents); 0 (Silymarin); 0 (Transforming Growth Factor beta1); EC 3.2.1.- (Amylases); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine); SD6QCT3TSU (Pentoxifylline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29377939
[Au] Autor:Budzyn M; Iskra M; Turkiewicz W; Krasinski Z; Gryszczynska B; Kasprzak MP
[Ad] Endereço:Department of General Chemistry, Chair of Chemistry and Clinical Biochemistry, Poznan University of Medical Sciences, Poznan, Poland.
[Ti] Título:Plasma concentration of selected biochemical markers of endothelial dysfunction in women with various severity of chronic venous insufficiency (CVI)-A pilot study.
[So] Source:PLoS One;13(1):e0191902, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although the endothelial dysfunction is considered to be implicated in the pathogenesis of chronic venous insufficiency (CVI) the endothelial status in patients with venous disorders is still not fully evaluated. Therefore the aim of the study was to measure the concentration of selected markers of endothelial dysfunction: von Willebrand factor (vWf), soluble P-selectin (sP-selectin), soluble thrombomodulin (sTM) and soluble VE-cadherin (sVE-cadherin) in CVI women who constitute the most numerous group of patients suffering from venous disease. MATERIALS AND METHODS: Forty four women with CVI were involved in the study and divided into subgroups based on CEAP classification. Concentration of vWf, sP-selectin, sTM and sVE-cadherin were measured and compared with those obtained in 25 healthy age and sex-matched women. RESULTS: It was found that the concentration of sTM increased and sVEcadherin decreased along with disease severity in CVI women. A significant rise of sTM was observed especially in CVI women, with the highest inflammation status reflected by hsCRP or elastase concentration, and in CVI women with a high oxidative stress manifested by an increased plasma MDA. A significant fall of circulating sVE-cadherin was reported in CVI women with moderate to highest intensity of inflammation and oxidative stress. There was no change in vWF and sP-selectin concentration at any stage of CVI severity. CONCLUSIONS: The results of the present study demonstrate the presence of endothelial dysfunction in women suffering from CVI which seems to progress with the disease severity and may be associated with inflammation and enhanced oxidative stress.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Endotélio Vascular/fisiopatologia
Insuficiência Venosa/sangue
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/sangue
Caderinas/sangue
Doença Crônica
Feminino
Seres Humanos
Meia-Idade
Selectina-P/sangue
Projetos Piloto
Índice de Gravidade de Doença
Trombomodulina/sangue
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers); 0 (Cadherins); 0 (P-Selectin); 0 (Thrombomodulin); 0 (cadherin 5); 0 (von Willebrand Factor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191902


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[PMID]:29339155
[Au] Autor:Kuwabara J; Umakoshi A; Abe N; Sumida Y; Ohsumi S; Usa E; Taguchi K; Choudhury ME; Yano H; Matsumoto S; Kunieda T; Takahashi H; Yorozuya T; Watanabe Y; Tanaka J
[Ad] Endereço:Department of Gastrointestinal Surgery and Surgical Oncology, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
[Ti] Título:Truncated CD200 stimulates tumor immunity leading to fewer lung metastases in a novel Wistar rat metastasis model.
[So] Source:Biochem Biophys Res Commun;496(2):542-548, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD200 mediates immunosuppression in immune cells that express its receptor, CD200R. There are two CD200 variants; truncated CD200 that lacks the part of N-terminal sequence necessary for CD200R binding (CD200S) and full-length CD200 (CD200L). We established a novel lung metastasis model by subcutaneously transplanting C6 glioma cells into the backs of neonatal Wistar rats. All transplanted rats developed large back tumors, nearly 90% of which bore lung metastases. To compare the effects of CD200S and CD200L on tumor immunity, CD200L (C6-L)- or CD200S (C6-S)-expressing C6 cells were similarly transplanted. The results showed that 100% of rats with C6-L tumors developed lung metastases, while metastases were found in only 44% of rats with C6-S tumors (n = 25). Tumors disappeared in approximately 20% of the C6-S-bearing rats, and these animals evaded death 180 d after transplantation, while all C6-L tumor-bearing rats died after 45 d. Next generation sequencing revealed that C6-S tumors expressed chemokines and granzyme B at much higher levels than C6-L tumors. Flow cytometry revealed that C6-S tumors contained more dead cells and more CD45 cells, including natural killer cells and CD8 lymphocytes. In particular, multiple subsets of dendritic cells expressing CD11c, MHC class II, CD8, and/or CD103 were more abundant in C6-S than in C6-L tumors. These results suggested that CD200S induced the accumulation of multiple dendritic cell subsets that activated cytotoxic T lymphocytes, leading to the elimination of metastasizing tumor cells.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
Glioma/imunologia
Glioma/patologia
Neoplasias Pulmonares/imunologia
Neoplasias Pulmonares/secundário
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Células Dendríticas/imunologia
Células Dendríticas/patologia
Regulação Neoplásica da Expressão Gênica
Glioma/genética
Tolerância Imunológica
Imunidade Celular
Pulmão/imunologia
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Mutação
Ratos Wistar
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (antigens, CD200)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29191879
[Au] Autor:Engblom C; Pfirschke C; Zilionis R; Da Silva Martins J; Bos SA; Courties G; Rickelt S; Severe N; Baryawno N; Faget J; Savova V; Zemmour D; Kline J; Siwicki M; Garris C; Pucci F; Liao HW; Lin YJ; Newton A; Yaghi OK; Iwamoto Y; Tricot B; Wojtkiewicz GR; Nahrendorf M; Cortez-Retamozo V; Meylan E; Hynes RO; Demay M; Klein A; Bredella MA; Scadden DT; Weissleder R; Pittet MJ
[Ad] Endereço:Center for Systems Biology, Massachusetts General Hospital Research Institute and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Título:Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF neutrophils.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow-derived myeloid cells can accumulate within tumors and foster cancer outgrowth. Local immune-neoplastic interactions have been intensively investigated, but the contribution of the systemic host environment to tumor growth remains poorly understood. Here, we show in mice and cancer patients ( = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis. Animal studies reveal that the cancer-induced bone phenotype involves bone-resident osteocalcin-expressing (Ocn ) osteoblastic cells. These cells promote cancer by remotely supplying a distinct subset of tumor-infiltrating SiglecF neutrophils, which exhibit cancer-promoting properties. Experimentally reducing Ocn cell numbers suppresses the neutrophil response and lung tumor outgrowth. These observations posit osteoblasts as remote regulators of lung cancer and identify SiglecF neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Osso e Ossos/patologia
Lectinas/metabolismo
Neoplasias Pulmonares/patologia
Infiltração de Neutrófilos
Neutrófilos/metabolismo
Neutrófilos/patologia
Osteoblastos/patologia
[Mh] Termos MeSH secundário: Animais
Densidade Óssea
Células da Medula Óssea/patologia
Osso e Ossos/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células Mieloides/patologia
Neoplasias Experimentais/patologia
Osteocalcina/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Lectins); 0 (Receptor for Advanced Glycation End Products); 0 (SIGLEC5 protein, human); 0 (sRAGE protein, human); 104982-03-8 (Osteocalcin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:28922790
[Au] Autor:Marisa L; Svrcek M; Collura A; Becht E; Cervera P; Wanherdrick K; Buhard O; Goloudina A; Jonchère V; Selves J; Milano G; Guenot D; Cohen R; Colas C; Laurent-Puig P; Olschwang S; Lefèvre JH; Parc Y; Boige V; Lepage C; André T; Fléjou JF; Dérangère V; Ghiringhelli F; de Reynies A; Duval A
[Ad] Endereço:Programme "Cartes d'Identité des Tumeurs," Ligue Nationale Contre le Cancer, Paris, France; INSERM, UMRS 938 - Centre de Recherche Saint-Antoine, Equipe "Instabilité des Microsatellites et Cancers," Equipe labellisée par la Ligue Nationale contre le Cancer, Paris, France; Sorbonne Université, UPMC U
[Ti] Título:The Balance Between Cytotoxic T-cell Lymphocytes and Immune Checkpoint Expression in the Prognosis of Colon Tumors.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Immune checkpoint (ICK) expression might represent a surrogate measure of tumor-infiltrating T cell (CTL) exhaustion and therefore be a more accurate prognostic biomarker for colorectal cancer (CRC) patients than CTL enumeration as measured by the Immunoscore. Methods: The expression of ICKs, Th1, CTLs, cytotoxicity-related genes, and metagenes, including Immunoscore-like metagenes, were evaluated in three independent cohorts of CRC samples (260 microsatellite instable [MSI], 971 non-MSI). Their associations with patient survival were analyzed by Cox models, taking into account the microsatellite instability (MSI) status and affiliation with various Consensus Molecular Subgroups (CMS). PD-L1 and CD8 expression were examined on a subset of tumors with immunohistochemistry. All statistical tests were two-sided. Results: The expression of Immunoscore-like metagenes was statistically significantly associated with improved outcome in non-MSI tumors displaying low levels of both CTLs and immune checkpoints (ICKs; CMS2 and CMS3; hazard ratio [HR] = 0.63, 95% confidence interval [CI] = 0.43 to 0.92, P = .02; and HR = 0.55, 95% CI = 0.34 to 0.90, P = .02, respectively), but clearly had no prognostic relevance in CRCs displaying higher levels of CTLs and ICKs (CMS1 and CMS4; HR = 0.46, 95% CI = 0.10 to 2.10, P = .32; and HR = 1.13, 95% CI = 0.79 to 1.63, P = .50, respectively), including MSI tumors. ICK metagene expression was statistically significantly associated with worse prognosis independent of tumor staging in MSI tumors (HR = 3.46, 95% CI = 1.41 to 8.49, P = .007). ICK expression had a negative impact on the proliferation of infiltrating CD8 T cells in MSI neoplasms (median = 0.56 in ICK low vs median = 0.34 in ICK high, P = .004). Conclusions: ICK expression cancels the prognostic relevance of CTLs in highly immunogenic colon tumors and predicts a poor outcome in MSI CRC patients.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Biomarcadores Tumorais/imunologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/imunologia
Linfócitos do Interstício Tumoral
Linfócitos T Citotóxicos
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígeno B7-H1/análise
Antígeno B7-H1/genética
Antígenos CD8/análise
Antígeno CTLA-4/genética
Colo/química
Neoplasias Colorretais/química
Neoplasias Colorretais/patologia
Feminino
Expressão Gênica
Receptor Celular 2 do Vírus da Hepatite A/genética
Seres Humanos
Proteína Coestimuladora de Linfócitos T Induzíveis/genética
Masculino
Instabilidade de Microssatélites
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Proteína 2 Ligante de Morte Celular Programada 1/genética
Receptor de Morte Celular Programada 1/genética
Estudos Retrospectivos
Taxa de Sobrevida
Células Th1
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antigens, CD); 0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD223 antigen); 0 (CD274 protein, human); 0 (CD8 Antigens); 0 (CTLA-4 Antigen); 0 (HAVCR2 protein, human); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (ICOS protein, human); 0 (Inducible T-Cell Co-Stimulator Protein); 0 (PDCD1 protein, human); 0 (PDCD1LG2 protein, human); 0 (Programmed Cell Death 1 Ligand 2 Protein); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx136


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[PMID]:28454543
[Au] Autor:Subramanian S; Pallati PK; Sharma P; Agrawal DK; Nandipati KC
[Ad] Endereço:Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE, USA.
[Ti] Título:TREM-1 associated macrophage polarization plays a significant role in inducing insulin resistance in obese population.
[So] Source:J Transl Med;15(1):85, 2017 Apr 28.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: TREM-1 acts as an amplifier of inflammation expressed on macrophages. The objective of this study was to evaluate the relationship between TREM-1 and macrophage polarization, and association of TREM-1 and M1 macrophage polarization with insulin resistance (IR) in obese population compared to non-obese population. METHODS: We enrolled 38 patients after obtaining IRB approval for this study. We evaluated the mRNA and protein expression levels of general macrophage marker (CD68), M1 marker (CD86, CCR7, iNOS, IFNγ, TNF-α and IL-6,), M2 marker (CD206, CD163, IL-10, IL-4) and chemokine axis (MCP-1, CCR2 and CCR5) along with TREM-1 and TREM-2 in omentum fat, subcutaneous fat, and liver biopsy tissues of non-obese (N = 5), obese non-diabetics, (N = 16) and obese diabetics (N = 17). RESULTS: The results of our study showed over-expression of TREM-1, M1 markers and down-regulation of TREM-2 and M2 markers in the omentum, subcutaneous and liver biopsies of obese patients (diabetics and non-diabetics) compared to non-obese patients. Overall, the obese diabetic group showed a significant (p < 0.05) higher number of patients with over expression of M1 markers (TREM-1, CD68, CD86, CCR-7, iNOS, IFN-γ, TNF-α, IL-6, MCP-1, CCR-2 and CCR-5) and down-regulation of M2 markers (CD206, CD163 and IL-4) in liver biopsy compared to obese non-diabetics. CONCLUSIONS: TREM-1 expression is significantly increased along with the M1 markers in liver biopsy of obese diabetic (17/17) and obese non-diabetic patients (9/16). Our data suggests that TREM-1 overexpression and M1 macrophage polarization are associated with obesity-induced IR.
[Mh] Termos MeSH primário: Polaridade Celular
Resistência à Insulina
Macrófagos/patologia
Obesidade/patologia
Receptor Gatilho 1 Expresso em Células Mieloides/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Biomarcadores/metabolismo
Biópsia
Comorbidade
Citocinas/metabolismo
Demografia
Diabetes Mellitus/genética
Diabetes Mellitus/patologia
Feminino
Fluorescência
Seres Humanos
Fígado/patologia
Masculino
Meia-Idade
Óxido Nítrico Sintase Tipo II/metabolismo
Obesidade/genética
Omento/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Quimiocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers); 0 (Cytokines); 0 (RNA, Messenger); 0 (Receptors, Chemokine); 0 (TREM1 protein, human); 0 (Triggering Receptor Expressed on Myeloid Cells-1); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1187-7


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[PMID]:29367523
[Au] Autor:Umeda N; Matsumoto I; Sumida T
[Ad] Endereço:Department of Rheumatology, Tsuchiura Kyodo General Hospital.
[Ti] Título:[The pathogenic role of ACPA in rheumatoid arthritis].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(6):391-395, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  In rheumatoid arthritis (RA), ACPA (anti-citrullinated protein/peptide antibody) is elevated with high specificity, and clinically, anti-CCP (cyclic citrullinated peptide) antibody is widely used for diagnosis of RA. It is thought ACPAs are produced with genetic background such as HLA-DR, environmental factors such as periodontal disease and smoking, however, the pathogenic role of ACPA in RA has not been elucidated. These were showed immune complexes including ACPA or ACPA itself promoted inflammatory cytokine production such as TNF. PADs (peptidylarginine deiminases) were expressed and citrullinated proteins existed in RA synovium. ACPAs were deposited on the site of citrulline in CD68 positive cells of RA synovium. The damage of bone and cartilage is observed in RA. It was also suggested that deposition of ACPAs caused osteoclastogenesis and bone loss. We introduce several findings about the pathogenic role of ACPA in RA.
[Mh] Termos MeSH primário: Anticorpos Anti-Proteína Citrulinada/efeitos adversos
Anticorpos Anti-Proteína Citrulinada/imunologia
Artrite Reumatoide/imunologia
[Mh] Termos MeSH secundário: Antígenos CD
Antígenos de Diferenciação Mielomonocítica
Artrite Reumatoide/diagnóstico
Artrite Reumatoide/metabolismo
Artrite Reumatoide/patologia
Reabsorção Óssea/imunologia
Osso e Ossos/patologia
Cartilagem/patologia
Citrulina/imunologia
Citrulina/metabolismo
Antígenos HLA-DR
Seres Humanos
Mediadores da Inflamação/metabolismo
Osteogênese/imunologia
Doenças Periodontais
Desiminases de Arginina em Proteínas/metabolismo
Fumar
Membrana Sinovial/citologia
Membrana Sinovial/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Citrullinated Protein Antibodies); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); 0 (HLA-DR Antigens); 0 (Inflammation Mediators); 0 (Tumor Necrosis Factor-alpha); 29VT07BGDA (Citrulline); EC 3.5.3.15 (Protein-Arginine Deiminases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.391


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[PMID]:29284783
[Au] Autor:Gordiienko I; Shlapatska L; Kholodniuk VM; Kovalevska L; Ivanivskaya TS; Sidorenko SP
[Ad] Endereço:Department of Molecular and Cellular Pathobiology, R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, NAS of Ukraine, Kyiv 03022, Ukraine.
[Ti] Título:CD150 and CD180 are involved in regulation of transcription factors expression in chronic lymphocytic leukemia cells.
[So] Source:Exp Oncol;39(4):291-298, 2017 Dec.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sequential stages of B-cell development is stringently coordinated by transcription factors (TFs) network that include B-lineage commitment TFs (Ikaros, Runx1/Cbfb, E2A, and FOXO1), B-lineage maintenance TFs (EBF1 and PAX5) and stage specific set of TFs (IRF4, IRF8, BCL6, BLIMP1). Deregulation of TFs expression and activity is often occurs in malignant B cells. The aim of this study was to evaluate TFs expression in chronic lymphocytic leukemia cells taking into consideration CD150 cell surface expression. From other side we attempted to regulate TFs expression via CD150 and CD180 cell surface receptors. MATERIALS AND METHODS: Studies were performed on normal peripheral blood B-cell subpopulations and chronic lymphocytic leukemia (CLL) cells isolated from peripheral blood of 67 primary untreated patients with CLL. Evaluation of TFs expression was performed on mRNA level using qRT-PCR and on protein level by western blot analysis. RESULTS: Median of PAX5 and EBF1 mRNA expression was higher in cell surface CD150 positive (csCD150 ) compared to csCD150 CLL cases or normal CD19 and CD19 CD5 B-cell subsets. Differences in mRNA expression of IRF8, IRF4 and BLIMP1 between studied groups of CLL and normal B cells were not revealed. All CLL cases were characterized by downregulated expression of PU.1 and BCL6 mRNAs in comparison to normal B cells. At the same time elevated SPIB mRNA expression level was restricted to CLL cells. Protein expression of IRF4, IRF8 and BCL6 was uniformly distributed between csCD150 and csCD150 CLL cases. PU.1 protein and CD20 that is direct PU.1 target gene positively correlated with CD150 cell surface expression on CLL cells. Ligation of CD150 and CD180 alone or in combination upregulated IRF8 and PU.1 while downregulated the IRF4 mRNA expression. Signaling via CD150 or CD180 alone elevated the level of BCL6 mRNA. Strong downregulation of IRF4 mRNA was observed after CD150, CD180 or CD150 andCD180 coligation on CLL cells. We found that in CLL cells CD150 is a negative regulator of SPIB while CD180 is involved in upregulation of EBF1 expression level. Moreover, CD180 ligation on CLL cells caused increase of CD150 mRNA level that is a one of the EBF1 target genes. CONCLUSIONS: Analysis of TFs expression profile revealed upregulated SPIB mRNA level and downregulated PU.1 in CLL cells. CD150 and CD180 receptors may modulate transcriptional program in CLL cells by regulating the TFs expression levels.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Regulação Neoplásica da Expressão Gênica/fisiologia
Leucemia Linfocítica Crônica de Células B/metabolismo
Membro 1 da Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
Fatores de Transcrição/biossíntese
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD180 protein, human); 0 (SLAMF1 protein, human); 0 (Transcription Factors); 169535-43-7 (Signaling Lymphocytic Activation Molecule Family Member 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE


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[PMID]:29385359
[Au] Autor:Sarantopoulos S
[Ad] Endereço:From the Department of Medicine, Division of Hematological Malignancies and Cellular Therapy, Duke Cancer Institute, Duke University Medical Center, Durham, NC.
[Ti] Título:Allogeneic Stem-Cell Transplantation - A T-Cell Balancing ACT.
[So] Source:N Engl J Med;378(5):480-482, 2018 Feb 01.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Transplante de Células-Tronco Hematopoéticas
Interleucina-33/metabolismo
Subpopulações de Linfócitos T/imunologia
Imunologia de Transplantes
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Antígenos CD
Modelos Animais de Doenças
Interleucina-9/biossíntese
Camundongos
Transplante Homólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Interleukin-33); 0 (Interleukin-9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMcibr1713238


  10 / 58759 MEDLINE  
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[PMID]:29374703
[Au] Autor:Kang S; Oh SC; Min BW; Lee DH
[Ad] Endereço:Department of Surgery, Korea University Guro Hospital, Seoul, Republic of Korea.
[Ti] Título:Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells.
[So] Source:Anticancer Res;38(2):787-794, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). MATERIALS AND METHODS: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (-) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. RESULTS: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and ß-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. CONCLUSION: The metastatic potential of CSCs arises from highly expressed TGM2.
[Mh] Termos MeSH primário: Neoplasias Colorretais/enzimologia
Proteínas de Ligação ao GTP/biossíntese
Células-Tronco Neoplásicas/enzimologia
Transglutaminases/biossíntese
[Mh] Termos MeSH secundário: Antígeno AC133/biossíntese
Antígenos CD/metabolismo
Biomarcadores Tumorais
Caderinas/metabolismo
Linhagem Celular Tumoral
Movimento Celular/fisiologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Regulação para Baixo
Transição Epitelial-Mesenquimal
Proteínas de Ligação ao GTP/genética
Proteínas de Ligação ao GTP/metabolismo
Técnicas de Silenciamento de Genes
Seres Humanos
Imuno-Histoquímica
Invasividade Neoplásica
Metástase Neoplásica
Células-Tronco Neoplásicas/patologia
Transglutaminases/genética
Transglutaminases/metabolismo
Células Tumorais Cultivadas
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Antigens, CD); 0 (Biomarkers, Tumor); 0 (CDH1 protein, human); 0 (CDH2 protein, human); 0 (Cadherins); 0 (PROM1 protein, human); 0 (Vimentin); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE



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