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[PMID]:29381400
[Au] Autor:Song ZY; Wang F; Cui SX; Qu XJ
[Ad] Endereço:a Department of Pharmacology, School of Basic Medical Sciences , Capital Medical University , Beijing , China.
[Ti] Título:Knockdown of CXCR4 Inhibits CXCL12-Induced Angiogenesis in HUVECs through Downregulation of the MAPK/ERK and PI3K/AKT and the Wnt/ß-Catenin Pathways.
[So] Source:Cancer Invest;36(1):10-18, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CXCL12 is an extracellular chemokine binding to cell surface receptor CXCR4. We found that activation of CXCL12/CXCR4 axis stimulated angiogenesis in endothelial cells. Knockdown of CXCR4 in endothelial cells prevented the branch points of angiogenesis. Endothelial cells exposed to CXCL12 presented high level of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase MMP-2, but not in CXCR4 knockdown cells. Further studies revealed that activation of CXCL12/CXCR4 axis in vascular endothelial cells stimulates the angiogenesis through upregulation of the MAPK/ERK and PI3K/AKT and Wnt/ß-catenin pathways. Conclusion, downregulation of CXCR4 could inhibit angiogenesis in cancer tissues.
[Mh] Termos MeSH primário: Quimiocina CXCL12/genética
Regulação para Baixo/genética
Regulação Neoplásica da Expressão Gênica/genética
Neovascularização Patológica/genética
Receptores CXCR4/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Células Endoteliais/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Metaloproteinase 2 da Matriz/genética
Proteínas Quinases Ativadas por Mitógeno/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Receptor do Fator de Crescimento Epidérmico/genética
Regulação para Cima/genética
Fator A de Crescimento do Endotélio Vascular/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Receptors, CXCR4); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1422512


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[PMID]:28453954
[Au] Autor:Pakulska MM; Tator CH; Shoichet MS
[Ad] Endereço:Department of Chemical Engineering and Applied Chemistry, University of Toronto, Toronto, ON, M5S 3E5, Canada; Institute for Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, M5S 3G9, Canada.
[Ti] Título:Local delivery of chondroitinase ABC with or without stromal cell-derived factor 1α promotes functional repair in the injured rat spinal cord.
[So] Source:Biomaterials;134:13-21, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Traumatic spinal cord injury (SCI) is a devastating event for which functional recovery remains elusive. Due to the complex nature of SCI pathology, a combination treatment strategy will likely be required for success. We hypothesized that tissue and functional repair would be achieved in a rat model of impact-compression SCI by combining degradation of the glial scar, using chondroitinase ABC (ChABC), with recruitment of endogenous neural precursor cells (NPCs), using stromal cell-derived factor 1α (SDF). To test this hypothesis, we designed a crosslinked methylcellulose hydrogel (XMC) for minimally invasive, localized, and sustained intrathecal drug delivery. ChABC was released from XMC using protein-peptide affinity interactions while SDF was delivered by electrostatic affinity interactions from polymeric nanoparticles embedded in XMC. Rats with SCI were treated acutely with a combination of SDF and ChABC, SDF alone, ChABC alone, or vehicle alone, and compared to injury only. Treatment with ChABC, both alone and in combination with SDF, resulted in faster and more sustained behavioural improvement over time than other groups. The significantly reduced chondroitin sulfate proteoglycan levels and greater distribution of NPCs throughout the spinal cord tissue with ChABC delivery, both alone and in combination with SDF, may explain the improved locomotor function. Treatment with SDF alone had no apparent effect on NPC number or distribution nor synergistic effect with ChABC delivery. Thus, in this model of SCI, tissue and functional repair is attributed to ChABC.
[Mh] Termos MeSH primário: Quimiocina CXCL12/química
Condroitina ABC Liase/metabolismo
Traumatismos da Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL12/metabolismo
Quimiocina CXCL12/uso terapêutico
Condroitina ABC Liase/química
Proteoglicanas de Sulfatos de Condroitina/química
Ensaio de Imunoadsorção Enzimática
Feminino
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Imuno-Histoquímica
Metilcelulose/química
Células-Tronco Neurais/citologia
Células-Tronco Neurais/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Traumatismos da Medula Espinal/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Chondroitin Sulfate Proteoglycans); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 9004-67-5 (Methylcellulose); EC 4.2.2.20 (Chondroitin ABC Lyase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29254288
[Au] Autor:Dyszkiewicz-Konwinska M; Bryja A; Jopek K; Budna J; Khozmi R; Jeseta M; Bukowska D; Antosik P; Bruska M; Nowicki M; Zabel M; Kempisty B
[Ad] Endereço:Department of Biomaterials and Experimental Dentistry, Poznan University of Medical Sciences, Poznan, Poland.
[Ti] Título:Expression of genes responsible for cell morphogenesis involved in differentiation in porcine buccal pouch mucosal cells during long-term primary culture and real-time proliferation in vitro.
[So] Source:J Biol Regul Homeost Agents;31(4):855-864, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Recently, using experimental animal model, we demonstrated that porcine buccal pouch mucosal cells reflect increased proliferation capability during primary cultivation in vitro. Although the histological structure and morphogenesis in oral cavity is well recognized, the molecular mechanisms which regulate this process still need further investigation. This study was aimed to analyze the molecular marker expression profile involved in morphogenesis and differentiation capacity of porcine buccal pouch mucosal cells during their long-term primary cultivation in vitro. The experiment was performed on buccal pouch mucosal cells isolated from 80 pubertal crossbred Landrace gilts. After collection, the cells were treated enzymatically and transferred into a primary in vitro culture (IVC) system and cultured for 30 days. The cells were collected for RNA isolation after 7, 15 and 30 days of IVC and were checked for their real-time proliferative status using the RTCA system. We found an increased expression of FN1 and SOX9 genes when calculated against ACTB after 7, and 30 days of IVC, (P less than 0.01, P less than 0.001, respectively). The CXCL12 mRNA was down-regulated after 7, 15 and 30 days of IVC, but not statistically significant. Similar expression profile was observed when calculated against HPRT, however, DAB2 was found to be higher expressed at day 15 of IVC, (P less than 0.05). The cell index measured during real-time cell proliferation was substantially increased between 96 h and 147h of IVC and reached the log phase. Since FN1 and SOX9 revealed significant increase of expression after long-term culture in vitro, it is suggested that expression of these differentiation and stemness genes is accompanied by cell proliferation. Moreover, FN1 and SOX9 might be recognized as new markers of buccal pouch mucosal cell proliferation and differentiation in pigs in in vitro primary culture model.
[Mh] Termos MeSH primário: Células Epiteliais/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Lipocalina-2/genética
Morfogênese/genética
Mucosa Bucal/metabolismo
Fatores de Transcrição SOX9/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular
Quimiocina CXCL12/genética
Quimiocina CXCL12/metabolismo
Células Epiteliais/citologia
Feminino
Perfilação da Expressão Gênica
Hipoxantina Fosforribosiltransferase/genética
Hipoxantina Fosforribosiltransferase/metabolismo
Lipocalina-2/metabolismo
Mucosa Bucal/citologia
Mucosa Bucal/crescimento & desenvolvimento
Cultura Primária de Células
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fatores de Transcrição SOX9/metabolismo
Transdução de Sinais
Suínos
Proteínas Supressoras de Tumor/genética
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Lipocalin-2); 0 (RNA, Messenger); 0 (SOX9 Transcription Factor); 0 (Tumor Suppressor Proteins); EC 2.4.2.8 (Hypoxanthine Phosphoribosyltransferase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:28749367
[Au] Autor:Gondalia R; Avery CL; Napier MD; Méndez-Giráldez R; Stewart JD; Sitlani CM; Li Y; Wilhelmsen KC; Duan Q; Roach J; North KE; Reiner AP; Zhang ZM; Tinker LF; Yanosky JD; Liao D; Whitsel EA
[Ad] Endereço:Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
[Ti] Título:Genome-wide Association Study of Susceptibility to Particulate Matter-Associated QT Prolongation.
[So] Source:Environ Health Perspect;125(6):067002, 2017 06 08.
[Is] ISSN:1552-9924
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ambient particulate matter (PM) air pollution exposure has been associated with increases in QT interval duration (QT). However, innate susceptibility to PM-associated QT prolongation has not been characterized. OBJECTIVE: To characterize genetic susceptibility to PM-associated QT prolongation in a multi-racial/ethnic, genome-wide association study (GWAS). METHODS: Using repeated electrocardiograms (1986­2004), longitudinal data on PM<10 µm in diameter (PM ), and generalized estimating equations methods adapted for low-prevalence exposure, we estimated approximately 2.5×10 SNP×PM interactions among nine Women's Health Initiative clinical trials and Atherosclerosis Risk in Communities Study subpopulations (n=22,158), then combined subpopulation-specific results in a fixed-effects, inverse variance-weighted meta-analysis. RESULTS: A common variant (rs1619661; coded allele: ) significantly modified the QT-PM association (p=2.11×10 ). At PM concentrations >90th percentile, QT increased 7 ms across the CC and TT genotypes: 397 (95% confidence interval: 396, 399) to 404 (403, 404) ms. However, QT changed minimally across rs1619661 genotypes at lower PM concentrations. The rs1619661 variant is on chromosome 10, 132 kilobase (kb) downstream from CXCL12, which encodes a chemokine, stromal cell-derived factor 1, that is expressed in cardiomyocytes and decreases calcium influx across the L-type Ca channel. CONCLUSIONS: The findings suggest that biologically plausible genetic factors may alter susceptibility to PM -associated QT prolongation in populations protected by the U.S. Environmental Protection Agency's National Ambient Air Quality Standards. Independent replication and functional characterization are necessary to validate our findings. https://doi.org/10.1289/EHP347
[Mh] Termos MeSH primário: Poluição do Ar/estatística & dados numéricos
Arritmias Cardíacas/epidemiologia
Exposição Ambiental/estatística & dados numéricos
[Mh] Termos MeSH secundário: Poluentes Atmosféricos/análise
Quimiocina CXCL12
Suscetibilidade a Doenças
Estudo de Associação Genômica Ampla
Seres Humanos
Material Particulado/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Air Pollutants); 0 (CXCL12 protein, human); 0 (Chemokine CXCL12); 0 (Particulate Matter)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1289/EHP347


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[PMID]:27775742
[Au] Autor:Kingsmore KM; Logsdon DK; Floyd DH; Peirce SM; Purow BW; Munson JM
[Ad] Endereço:Department of Biomedical Engineering, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
[Ti] Título:Interstitial flow differentially increases patient-derived glioblastoma stem cell invasion via CXCR4, CXCL12, and CD44-mediated mechanisms.
[So] Source:Integr Biol (Camb);8(12):1246-1260, 2016 12 05.
[Is] ISSN:1757-9708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) prognosis remains dismal due in part to the invasiveness of GBM cells. Interstitial fluid flow (IFF) has been shown to increase invasion of glioma cells in vitro through the CXCR4 receptor interacting with autologous, pericellular gradients of CXCL12 (autologous chemotaxis) or through the CD44 receptor interactions with the extracellular matrix (hyaluronan-mediated mechanotransduction). These mechanisms have not been examined together and thus we hypothesized that both mechanisms contribute to invasion in populations of cancer cells. Therefore, we examined IFF-stimulated CXCR4-, CXCL12-, and CD44-dependent invasion in patient-derived glioblastoma stem cells (GSCs). Using our 3D in vitro assay and correlative in vivo studies we demonstrated GSC lines show increased invasion with flow. This flow-stimulated invasion was reduced by blockade of CXCR4, CXCL12, and/or CD44, revealing that GSC invasion may be mediated simultaneously by both mechanisms. Characterization of CXCR4 , CXCL12 , and CD44 populations in four GSC lines revealed different percentages of protein positive subpopulations for each line. We developed an agent-based model to identify the contributions of each subpopulation to flow-stimulated invasion and validated the model through comparisons with experimental blocking studies. Clinically relevant radiation therapy increased flow-stimulated invasion in one GSC line. Our agent-based model predicted that IFF-stimulated invasion is driven primarily by CXCR4 CXCL12 populations, and, indeed our irradiated cells had an increase in this subpopulation. Together, these data indicate that different mechanisms govern the flow response across GSCs, but that within a single patient, there are subpopulations of GSCs that respond to flow via either CD44- or CXCR4-CXCL12 mechanisms.
[Mh] Termos MeSH primário: Quimiocina CXCL12/imunologia
Glioblastoma/imunologia
Glioblastoma/patologia
Receptores de Hialuronatos/imunologia
Mecanotransdução Celular/imunologia
Células-Tronco Neoplásicas/imunologia
Receptores CXCR4/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Líquido Extracelular/imunologia
Seres Humanos
Invasividade Neoplásica
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD44 protein, human); 0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Hyaluronan Receptors); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29253907
[Au] Autor:Dingenouts CKE; Bakker W; Lodder K; Wiesmeijer KC; Moerkamp AT; Maring JA; Arthur HM; Smits AM; Goumans MJ
[Ad] Endereço:Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, the Netherlands.
[Ti] Título:Inhibiting DPP4 in a mouse model of HHT1 results in a shift towards regenerative macrophages and reduces fibrosis after myocardial infarction.
[So] Source:PLoS One;12(12):e0189805, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: Hereditary Hemorrhagic Telangiectasia type-1 (HHT1) is a genetic vascular disorder caused by haploinsufficiency of the TGFß co-receptor endoglin. Dysfunctional homing of HHT1 mononuclear cells (MNCs) towards the infarcted myocardium hampers cardiac recovery. HHT1-MNCs have elevated expression of dipeptidyl peptidase-4 (DPP4/CD26), which inhibits recruitment of CXCR4-expressing MNCs by inactivation of stromal cell-derived factor 1 (SDF1). We hypothesize that inhibiting DPP4 will restore homing of HHT1-MNCs to the infarcted heart and improve cardiac recovery. METHODS AND RESULTS: After inducing myocardial infarction (MI), wild type (WT) and endoglin heterozygous (Eng+/-) mice were treated for 5 days with the DPP4 inhibitor Diprotin A (DipA). DipA increased the number of CXCR4+ MNCs residing in the infarcted Eng+/- hearts (Eng+/- 73.17±12.67 vs. Eng+/- treated 157.00±11.61, P = 0.0003) and significantly reduced infarct size (Eng+/- 46.60±9.33% vs. Eng+/- treated 27.02±3.04%, P = 0.03). Echocardiography demonstrated that DipA treatment slightly deteriorated heart function in Eng+/- mice. An increased number of capillaries (Eng+/- 61.63±1.43 vs. Eng+/- treated 74.30±1.74, P = 0.001) were detected in the infarct border zone whereas the number of arteries was reduced (Eng+/- 11.88±0.63 vs. Eng+/- treated 6.38±0.97, P = 0.003). Interestingly, while less M2 regenerative macrophages were present in Eng+/- hearts prior to DipA treatment, (WT 29.88±1.52% vs. Eng+/- 12.34±1.64%, P<0.0001), DPP4 inhibition restored the number of M2 macrophages to wild type levels. CONCLUSIONS: In this study, we demonstrate that systemic DPP4 inhibition restores the impaired MNC homing in Eng+/- animals post-MI, and enhances cardiac repair, which might be explained by restoring the balance between the inflammatory and regenerative macrophages present in the heart.
[Mh] Termos MeSH primário: Dipeptidil Peptidase 4/química
Inibidores da Dipeptidil Peptidase IV/química
Macrófagos/metabolismo
Infarto do Miocárdio/metabolismo
Telangiectasia Hemorrágica Hereditária/genética
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL12/metabolismo
Modelos Animais de Doenças
Endoglina/metabolismo
Fibrose/metabolismo
Haploinsuficiência
Ventrículos do Coração/patologia
Heterozigoto
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Infarto do Miocárdio/complicações
Miocárdio/metabolismo
Miocárdio/patologia
Regeneração
Telangiectasia Hemorrágica Hereditária/patologia
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Endoglin); 0 (Transforming Growth Factor beta); EC 3.4.14.5 (Dipeptidyl Peptidase 4); EC 3.4.14.5 (Dpp4 protein, mouse)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189805


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[PMID]:27775528
[Au] Autor:Hou J; Luo T; Ng KL; Leung AY; Liang R; Sun D
[Ti] Título:Characterization of Drug Effect on Leukemia Cells Through Single Cell Assay With Optical Tweezers and Dielectrophoresis.
[So] Source:IEEE Trans Nanobioscience;15(8):820-827, 2016 12.
[Is] ISSN:1558-2639
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:One of the greatest challenges in acute myeloid leukemia (AML) treatment is preventing relapse. Leukemia cells can hide in bone marrow niche or vascular niche. Hence, many chemical drugs cannot kill these cells. To characterize migration and adhesion properties of leukemia cells in specific niches, CXCR4/SDF- 1α signal pathway has been widely used for investigation. AMD3100 is treated as one of the most common chemical drugs that can inhibit this signal. In the current study, we particularly investigate the effect of AMD3100 on the adhesion property of leukemia cells on stromal cells by using engineering tools, namely, optical tweezers (OT) and dielectrophoresis (DEP), to probe single cell property. AMD3100 not only inhibits the CXCR4/SDF- 1α signal pathway but also reduces gene expression of CXCR4 and VLA-4 on leukemia cells. The drug also softens leukemia cells. This work provides a new way to investigate cell behavior under drug treatment. The use of combined engineering tools will benefit drug discovery and assessment for leukemia treatment.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Eletroforese/métodos
Compostos Heterocíclicos/farmacologia
Leucemia Mieloide Aguda/metabolismo
Pinças Ópticas
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Quimiocina CXCL12/análise
Quimiocina CXCL12/genética
Quimiocina CXCL12/metabolismo
Técnicas de Cocultura
Seres Humanos
Receptores CXCR4/análise
Receptores CXCR4/genética
Receptores CXCR4/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Estromais/citologia
Células Estromais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Heterocyclic Compounds); 0 (Receptors, CXCR4); 155148-31-5 (JM 3100)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1109/TNB.2016.2616160


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[PMID]:29176797
[Au] Autor:Pinheiro D; Leirós L; Dáu JBT; Stumbo AC; Thole AA; Cortez EAC; Mandarim-de-Lacerda CA; Carvalho L; Carvalho SN
[Ad] Endereço:Laboratory of Stem Cell Research, Department of Histology and Embryology, Institute of Biology Roberto Alcântara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Título:Cytokines, hepatic cell profiling and cell interactions during bone marrow cell therapy for liver fibrosis in cholestatic mice.
[So] Source:PLoS One;12(11):e0187970, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow cells (BMC) migrate to the injured liver after transplantation, contributing to regeneration through multiple pathways, but mechanisms involved are unclear. This work aimed to study BMC migration, characterize cytokine profile, cell populations and proliferation in mice with liver fibrosis transplanted with GFP+ BMC. Confocal microscopy analysis showed GFP+ BMC near regions expressing HGF and SDF-1 in the fibrotic liver. Impaired liver cell proliferation in fibrotic groups was restored after BMC transplantation. Regarding total cell populations, there was a significant reduction in CD68+ cells and increased Ly6G+ cells in transplanted fibrotic group. BMC contributed to the total populations of CD144, CD11b and Ly6G cells in the fibrotic liver, related to an increment of anti-fibrotic cytokines (IL-10, IL-13, IFN-γ and HGF) and reduction of pro-inflammatory cytokines (IL-17A and IL-6). Therefore, HGF and SDF-1 may represent important chemoattractants for transplanted BMC in the injured liver, where these cells can give rise to populations of extrahepatic macrophages, neutrophils and endothelial progenitor cells that can interact synergistically with other liver cells towards the modulation of an anti-fibrotic cytokine profile promoting the onset of liver regeneration.
[Mh] Termos MeSH primário: Células da Medula Óssea/citologia
Transplante de Medula Óssea
Comunicação Celular
Colestase/terapia
Citocinas/metabolismo
Hepatócitos/metabolismo
Cirrose Hepática/terapia
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Proliferação Celular
Quimiocina CXCL12/metabolismo
Colestase/complicações
Colestase/genética
Colestase/patologia
Colágeno/metabolismo
Citocinas/genética
Imunofluorescência
Regulação da Expressão Gênica
Proteínas de Fluorescência Verde/metabolismo
Fator de Crescimento de Hepatócito/metabolismo
Fígado/metabolismo
Fígado/patologia
Cirrose Hepática/complicações
Cirrose Hepática/genética
Cirrose Hepática/patologia
Masculino
Camundongos Endogâmicos C57BL
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL12); 0 (Cytokines); 147336-22-9 (Green Fluorescent Proteins); 67256-21-7 (Hepatocyte Growth Factor); 9007-34-5 (Collagen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187970


  9 / 5525 MEDLINE  
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[PMID]:29024813
[Au] Autor:Wang J; Man GCW; Chan TH; Kwong J; Wang CC
[Ad] Endereço:Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Hong Kong.
[Ti] Título:A prodrug of green tea polyphenol (-)-epigallocatechin-3-gallate (Pro-EGCG) serves as a novel angiogenesis inhibitor in endometrial cancer.
[So] Source:Cancer Lett;412:10-20, 2018 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Anti-angiogenesis effect of a prodrug of green tea polyphenol (-)-epigallocatechin-3-gallate (Pro-EGCG) in malignant tumors is not well studied. Here, we investigated how the treatment with Pro-EGCG inhibited tumor angiogenesis in endometrial cancer. Tumor xenografts of human endometrial cancer were established and subjected to microarray analysis after Pro-EGCG treatment. First, we showed Pro-EGCG inhibited tumor angiogenesis in xenograft models through down-regulation of vascular endothelial growth factor A (VEGFA) and hypoxia inducible factor 1 alpha (HIF1α) in tumor cells and chemokine (C-X-C motif) ligand 12 (CXCL12) in host stroma by immunohistochemical staining. Next, we investigated how HIF1α/VEGFA was down-regulated and how the reduction of CXCL12 inhibited tumor angiogenesis. We found that VEGFA secretion from endometrial cancer cells was decreased by Pro-EGCG treatment through inhibiting PI3K/AKT/mTOR/HIF1α pathway. Furthermore, the down-regulation of CXCL12 in stromal cells by Pro-EGCG treatment restricted migration and differentiation of macrophages thereby inhibited infiltration of VEGFA-expressing tumor-associated macrophages (TAMs). Taken together, we demonstrated that treatment with Pro-EGCG not only decreases cancer cell-secreted VEGFA but also inhibits TAM-secreted VEGFA in endometrial cancer. These findings demonstrate that Pro-EGCG is a novel angiogenesis inhibitor for endometrial cancer.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Catequina/análogos & derivados
Neoplasias do Endométrio/tratamento farmacológico
Pró-Fármacos/farmacologia
Chá/química
[Mh] Termos MeSH secundário: Animais
Catequina/farmacologia
Movimento Celular
Quimiocina CXCL12/fisiologia
Feminino
Seres Humanos
Macrófagos/fisiologia
Camundongos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fator A de Crescimento do Endotélio Vascular/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Chemokine CXCL12); 0 (Prodrugs); 0 (Tea); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE


  10 / 5525 MEDLINE  
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[PMID]:29017963
[Au] Autor:Meng W; Xue S; Chen Y
[Ad] Endereço:Division of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Institute of Genetics, Zhejiang University, Hangzhou, Zhejiang, China.
[Ti] Título:The role of CXCL12 in tumor microenvironment.
[So] Source:Gene;641:105-110, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The chemokine ligand C-X-C motif chemokine ligand 12 (CXCL12) is a kind of small molecules of cytokines that widely expressed in diversified tissues. Recent evidence suggests that CXCL12 plays an important role in the communication of tumor cells with their surrounding microenvironment. The interaction of CXCL12 and its receptors subsequently excite the downstream signaling pathways to affect tumor angiogenesis, tumor cell proliferation and chemoresistance, and thus represents a potential target for cancer therapy. Outpouring molecules targeting CXCL12/CXCR4 axis in tumor microenvironment combined with traditional chemotherapy have drawn more and more attentions, which will be a promising method in anti-cancer therapies. Our review focuses on these roles of CXCL12 and summarizes strategies for treating cancer by disrupting this interaction with special emphasis on the CXCR4/CXCL12 axis.
[Mh] Termos MeSH primário: Comunicação Celular/fisiologia
Quimiocina CXCL12/metabolismo
Neoplasias/patologia
Neovascularização Patológica/patologia
Receptores CXCR4/metabolismo
Microambiente Tumoral/fisiologia
[Mh] Termos MeSH secundário: Antineoplásicos/uso terapêutico
Adesão Celular/fisiologia
Seres Humanos
Metástase Neoplásica/patologia
Neoplasias/tratamento farmacológico
Neoplasias/genética
Microambiente Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CXCL12 protein, human); 0 (CXCR4 protein, human); 0 (Chemokine CXCL12); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE



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