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[PMID]:27777141
[Au] Autor:Politikos I; T Kim H; Karantanos T; Brown J; McDonough S; Li L; Cutler C; Antin JH; Ballen KK; Ritz J; Boussiotis VA
[Ad] Endereço:Hematology-Oncology and Cancer Biology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
[Ti] Título:Angiogenic Factors Correlate with T Cell Immune Reconstitution and Clinical Outcomes after Double-Unit Umbilical Cord Blood Transplantation in Adults.
[So] Source:Biol Blood Marrow Transplant;23(1):103-112, 2017 Jan.
[Is] ISSN:1523-6536
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Umbilical cord blood (UCB) is a valuable graft source for allogeneic hematopoietic stem cell transplantation (HSCT) in patients who lack adult donors. UCB transplantation (UCBT) in adults results in delayed immune reconstitution, leading to high infection-related morbidity and mortality. Angiogenic factors and markers of endothelial dysfunction have biologic and prognostic significance in conventional HSCT, but their role in UCBT has not been investigated. Furthermore, the interplay between angiogenesis and immune reconstitution has not been studied. Here we examined whether angiogenic cytokines, angiopoietin-1 (ANG-1) and vascular endothelial growth factor (VEGF), or markers of endothelial injury, thrombomodulin (TM) and angiopoietin-2 (ANG-2), associate with thymic regeneration as determined by T cell receptor excision circle (TREC) values and recovery of T cell subsets, as well as clinical outcomes in adult recipients of UCBT. We found that plasma levels of ANG-1 significantly correlated with the reconstitution of naive CD4 CD45RA and CD8 CD45RA T cell subsets, whereas plasma levels of VEGF displayed a positive correlation with CD4 CD45RO T cells and regulatory T cells and a weak correlation with TRECs. Assessment of TM and ANG-2 revealed a strong inverse correlation of both factors with naive T cells and TRECs. The angiogenic capacity of each patient's plasma, as determined by an in vitro angiogenesis assay, positively correlated with VEGF levels and with reconstitution of CD4 T cell subsets. Higher VEGF levels were associated with worse progression-free survival and higher risk of relapse, whereas higher levels of TM were associated with chronic graft-versus-host disease and nonrelapse mortality. Thus, angiogenic factors may serve as valuable markers associated with T cell reconstitution and clinical outcomes after UCBT.
[Mh] Termos MeSH primário: Indutores da Angiogênese/sangue
Transplante de Células-Tronco de Sangue do Cordão Umbilical/normas
Neoplasias Hematológicas/terapia
Reconstituição Imune/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Angiopoietina-1/sangue
Angiopoietina-2/sangue
Biomarcadores/sangue
Transplante de Células-Tronco de Sangue do Cordão Umbilical/métodos
Intervalo Livre de Doença
Feminino
Doença Enxerto-Hospedeiro
Seres Humanos
Masculino
Meia-Idade
Receptores de Antígenos de Linfócitos T
Recidiva
Subpopulações de Linfócitos T/imunologia
Linfócitos T/imunologia
Trombomodulina/sangue
Resultado do Tratamento
Fator A de Crescimento do Endotélio Vascular/sangue
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Angiopoietin-1); 0 (Angiopoietin-2); 0 (Biomarkers); 0 (Receptors, Antigen, T-Cell); 0 (Thrombomodulin); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:28460335
[Au] Autor:Feng Y; Li Q; Wu D; Niu Y; Yang C; Dong L; Wang C
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau SAR, China.
[Ti] Título:A macrophage-activating, injectable hydrogel to sequester endogenous growth factors for in situ angiogenesis.
[So] Source:Biomaterials;134:128-142, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Biomaterials scaffolds designed for many regenerative applications are expected to support neo-vascularisation, which is now being hampered by two limitations - the instability of exogenous growth factors (GFs) that are delivered to promote angiogenesis; and the loss of extracellular matrix components that bind and stabilise GFs. Here, we report the design and evaluation of an injectable hydrogel system aimed at restoring a GF-binding microenvironment to enhance the pro-angiogenic functions of endogenous GFs. This gel comprises two polysaccharides with their unique bioactivities: Konjac glucomannan (KGM) as the building block of the gel scaffold, for its demonstrated capacity to activate macrophages/monocytes to secrete pro-angiogenic/-mitogenic GFs; and heparin (Hep), a representative glycosaminoglycan molecule that binds numerous pro-angiogenic GFs, as functional moieties to sequester the macrophage-produced GFs. Modified with tyramine (TA) groups, the two polysaccharides can be co-polymerised and rapidly form into hydrogel upon enzyme catalysis. The designed KGM-TA/Hep-TA hydrogel successfully preserves the macrophage-activating function and GF-binding affinity of the two components, respectively, and, once subcutaneously implanted, effectively sequestered the locally-produced GFs in situ and promote the formation and maturation of blood vessels in mice. In summary, the designed hydrogel system demonstrates a feasible approach to stimulate the production and harness the function of endogenous GFs for inducing blood vessel formation in vivo, without the addition of any exogenous proteins. This design may provide an innovative, open platform to promote vascularisation for various regenerative purposes.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Materiais Biocompatíveis/farmacologia
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Hidrogel de Polietilenoglicol-Dimetacrilato/farmacologia
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Indutores da Angiogênese/química
Indutores da Angiogênese/farmacologia
Animais
Glicosaminoglicanos/metabolismo
Seres Humanos
Integrina beta1/metabolismo
Lectinas Tipo C/metabolismo
Masculino
Mananas/metabolismo
Lectinas de Ligação a Manose/metabolismo
Camundongos
Neovascularização Fisiológica/efeitos dos fármacos
Polissacarídeos/metabolismo
Células RAW 264.7
Receptores de Superfície Celular/metabolismo
Células THP-1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Biocompatible Materials); 0 (Glycosaminoglycans); 0 (Integrin beta1); 0 (Intercellular Signaling Peptides and Proteins); 0 (Lectins, C-Type); 0 (Mannans); 0 (Mannose-Binding Lectins); 0 (Polysaccharides); 0 (Receptors, Cell Surface); 0 (mannose receptor); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 36W3E5TAMG ((1-6)-alpha-glucomannan)
[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:170502
[St] Status:MEDLINE


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[PMID]:28455450
[Au] Autor:Ghosh A; Freestone NS; Anim-Nyame N; Arrigoni FIF
[Ad] Endereço:School of Life Sciences, Pharmacy and Chemistry, Kingston University London, Kingston upon Thames, UK.
[Ti] Título:Microvascular function in pre-eclampsia is influenced by insulin resistance and an imbalance of angiogenic mediators.
[So] Source:Physiol Rep;5(8), 2017 Apr.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In preeclampsia, maternal microvascular function is disrupted and angiogenesis is dysfunctional. Insulin resistance that occurs in some pregnancies also pathologically affects microvascular function. We wished to examine the relationship of angiogenic mediators and insulin resistance on microvascular health in pregnancy. We performed a nested, case-control study of 16 women who developed preeclampsia with 17 normal pregnant controls. We hypothesized that the impaired microvascular blood flow in preeclamptic women associated with an increased ratio of the antiangiogenic factors; (s-endoglin [sEng] and soluble fms-like tyrosine kinase-1 [sFlt-1]) and proangiogenic molecule (placental growth factor [PlGF]) could be influenced by insulin resistance. Serum samples taken after 28 weeks of gestation were measured for the angiogenic factors, insulin, and glucose alongside the inflammatory marker; tumor necrosis factor-α and endothelial activation, namely; soluble vascular cell adhesion molecule 1, intercellular adhesion molecule-1, and e-selectin. Maternal microvascular blood flow, measured by strain gauge plethysmography, correlated with ratios of pro- and antiangiogenic mediators independently of preeclampsia. Decreased microvascular function measured in preeclampsia strongly correlated with both the antiangiogenic factor (sFlt-1 + sEng): PlGF ratio and high levels of insulin resistance, and combining insulin resistance with antiangiogenic factor ratios further strengthened this relationship. In pregnancy, microvascular blood flow is strongly associated with perturbations in pro- and antiangiogenic mediators. In preeclampsia, the relationship of maternal microvascular dysfunction with antiangiogenic mediators is strengthened when combined with insulin resistance.
[Mh] Termos MeSH primário: Indutores da Angiogênese/sangue
Resistência à Insulina/fisiologia
Microcirculação/fisiologia
Pré-Eclâmpsia/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Inibidores da Angiogênese/fisiologia
Glicemia/metabolismo
Estudos de Casos e Controles
Endoglina/sangue
Feminino
Seres Humanos
Mediadores da Inflamação/metabolismo
Insulina/sangue
Proteínas de Membrana/sangue
Proteínas de Membrana/fisiologia
Microvasos/fisiopatologia
Pré-Eclâmpsia/sangue
Gravidez
Estudos Prospectivos
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Angiogenesis Inhibitors); 0 (Blood Glucose); 0 (ENG protein, human); 0 (Endoglin); 0 (Inflammation Mediators); 0 (Insulin); 0 (Membrane Proteins); 0 (PIGF protein, human); EC 2.7.10.1 (FLT1 protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29215518
[Au] Autor:Lecarpentier E; Gris JC; Cochery-Nouvellon E; Mercier E; Touboul C; Thadhani R; Karumanchi SA; Haddad B
[Ad] Endereço:University Paris Est Créteil and CHI Créteil, Créteil, France; the Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; the Department of Hematology, University Hospital Caremeau, Nîmes UPRES EA2992, and faculty of pharmaceutical and biological sciences, University of Montpellier, Montpellier, France; and the Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
[Ti] Título:Angiogenic Factor Profiles in Pregnant Women With a History of Early-Onset Severe Preeclampsia Receiving Low-Molecular-Weight Heparin Prophylaxis.
[So] Source:Obstet Gynecol;131(1):63-69, 2018 Jan.
[Is] ISSN:1873-233X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate whether daily low-molecular-weight (LMW) heparin prophylaxis during pregnancy alters profile of circulating angiogenic factors that have been linked with the pathogenesis of preeclampsia and fetal growth restriction. METHODS: This is a planned ancillary study of the Heparin-Preeclampsia trial, a randomized trial in pregnant women with a history of severe early-onset preeclampsia (less than 34 weeks of gestation). In the parent study, all women were treated with aspirin and then randomized to receive LMW heparin or aspirin alone. In this study, we measured serum levels of circulating angiogenic factors (soluble fms-like tyrosine kinase-1, placental growth factor, and soluble endoglin by immunoassay) at the following gestational windows: 10-13 6/7 weeks, 14-17 6/7 weeks, 18-21 6/7 weeks, 22-25 6/7 weeks, 26-29 6/7 weeks, 30-33 6/7 weeks, and 34-37 6/7 weeks. RESULTS: Samples were available from 185 patients: LMW heparin+aspirin (n=92) and aspirin alone (n=93). The two groups had comparable baseline characteristics and had similar adverse composite outcomes (35/92 [38.0%] compared with 36/93 [38.7%]; P=.92). There were no significant differences in serum levels of soluble fms-like tyrosine kinase-1, placental growth factor, and soluble endoglin in the participants who received LMW heparin and aspirin compared with those who received aspirin alone regardless of gestational age period. Finally, women who developed an adverse composite outcome at less than 34 weeks of gestation demonstrated significant alterations in serum angiogenic profile as early as 10-13 6/7 weeks that was most dramatic 6-8 weeks preceding delivery. CONCLUSION: Prophylactic LMW heparin therapy when beginning from before 14 weeks of gestation with aspirin during pregnancy is not associated with an improved angiogenic profile. This may provide a molecular explanation for the lack of clinical benefit noted in recent trials. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, NCT00986765.
[Mh] Termos MeSH primário: Indutores da Angiogênese/sangue
Aspirina/administração & dosagem
Heparina de Baixo Peso Molecular/administração & dosagem
Pré-Eclâmpsia/sangue
Pré-Eclâmpsia/prevenção & controle
Resultado da Gravidez
[Mh] Termos MeSH secundário: Adulto
Diagnóstico Precoce
Feminino
França
Idade Gestacional
Seres Humanos
Idade Materna
Gravidez
Cuidado Pré-Natal/métodos
Medição de Risco
Índice de Gravidade de Doença
Centros de Atenção Terciária
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Heparin, Low-Molecular-Weight); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171208
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1097/AOG.0000000000002380


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[PMID]:29196053
[Au] Autor:Dewangan J; Kaushik S; Rath SK; Balapure AK
[Ad] Endereço:Genotoxicity Lab, Division of Toxicology & Experimental Medicine, CSIR-Central Drug Research Institute, Lucknow, Uttar Pradesh 226031, India.
[Ti] Título:Centchroman regulates breast cancer angiogenesis via inhibition of HIF-1α/VEGFR2 signalling axis.
[So] Source:Life Sci;193:9-19, 2018 Jan 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Angiogenesis is a recognized hallmark of cancer which promotes cancer cell progression and metastasis. Inhibition of angiogenesis to attenuate cancer growth is becoming desirable strategy for breast cancer management. The present study is aimed to investigate the antiangiogenic efficacy of a novel selective estrogen receptor modulator Centchroman (CC) on human breast cancer cells. MAIN METHODS: Effect of CC on cell viability was evaluated using Sulforhodamine B assay. Endothelial cell proliferation, wound healing, Boyden chamber cell invasion, tube formation and chorioallantoic membrane (CAM) assays were performed to assess the effect of CC on migration, invasion and angiogenesis. Apoptosis, reactive oxygen species generation, caspase-3/7 and intracellular calcium ion level were measured through flow cytometry. Expression levels of HIF-1α, VEGF, VEGFR2, AKT and ERK were assessed by western blot analysis. KEY FINDINGS: CC selectively induces apoptosis in human breast cancer cells without affecting non-tumorigenic breast epithelial cells MCF-10A. Moreover, it inhibits migratory, invasive and mammosphere forming potential of breast cancer. Furthermore, CC also inhibited VEGF-induced migration, invasion and tube formation of HUVECs in vitro. CC effectively inhibited neovasculature formation in chicken CAM. Western blot analysis demonstrated that CC inhibited expression of HIF-1α and its downstream target VEGF. Interestingly, CC also suppressed VEGFR2 phosphorylation and consequently attenuated AKT and ERK phosphorylation. SIGNIFICANCE: Our findings suggest that CC downregulates VEGF-induced angiogenesis by modulating HIF-1α/VEGFR2 pathway and recommend it (CC) as a potential therapeutic drug for breast cancer treatment.
[Mh] Termos MeSH primário: Centocromano/metabolismo
Centocromano/uso terapêutico
[Mh] Termos MeSH secundário: Indutores da Angiogênese
Inibidores da Angiogênese/farmacologia
Apoptose
Mama/metabolismo
Neoplasias da Mama/metabolismo
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Feminino
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Sistema de Sinalização das MAP Quinases
Neovascularização Patológica/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Angiogenesis Inhibitors); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Vascular Endothelial Growth Factor A); 31477-60-8 (Centchroman); EC 2.7.10.1 (KDR protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


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[PMID]:29244857
[Au] Autor:Zbucka-Kretowska M; Charkiewicz K; Goscik J; Wolczynski S; Laudanski P
[Ad] Endereço:Department of Reproduction and Gynecological Endocrinology, Medical University of Bialystok, Bialystok, Poland.
[Ti] Título:Maternal plasma angiogenic and inflammatory factor profiling in foetal Down syndrome.
[So] Source:PLoS One;12(12):e0189762, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE AND DESIGN: Angiogenic factors are proteins that are related to certain foetal chromosomal abnormalities. The aim of this study was to determine the concentration of 60 angiogenic factors in the plasma of women with offspring possessing trisomy 21/Down syndrome (DS). METHOD: After analysing karyotyping results, we selected 20 patients with foetuses possessing DS, and for the control group, we selected 28 healthy patients with uncomplicated pregnancies who delivered healthy newborns at term (i.e., 15-18 weeks of gestation). To assess the concentration of proteins in the blood plasma, we used a protein macroarray which enabled simultaneous determination of 60 angiogenic factors per sample. RESULTS: We observed a statistically significant increase in the concentration of these five angiogenic and inflammatory factors: TGFb1 (p = 0.039), angiostatin (p = 0.0142), I-309 (p = 0.0476), TGFb3 (p = 0.0395), and VEGF-D (p = 0.0173)-compared to concentrations in patients with healthy foetuses. CONCLUSION: Our findings suggest that angiogenic factors may play role in DS pathogenesis.
[Mh] Termos MeSH primário: Indutores da Angiogênese/sangue
Proteínas Sanguíneas/genética
Síndrome de Down/sangue
Herança Materna/genética
[Mh] Termos MeSH secundário: Angiostatinas/sangue
Quimiocina CCL1/sangue
Aberrações Cromossômicas
Síndrome de Down/genética
Síndrome de Down/patologia
Feminino
Seres Humanos
Recém-Nascido
Cariotipagem
Gravidez
Fator de Crescimento Transformador beta1/sangue
Fator de Crescimento Transformador beta3/sangue
Fator D de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Blood Proteins); 0 (CCL1 protein, human); 0 (Chemokine CCL1); 0 (TGFB1 protein, human); 0 (TGFB3 protein, human); 0 (Transforming Growth Factor beta1); 0 (Transforming Growth Factor beta3); 0 (Vascular Endothelial Growth Factor D); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189762


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[PMID]:29240802
[Au] Autor:Hase K; Kanda A; Hirose I; Noda K; Ishida S
[Ad] Endereço:Laboratory of Ocular Cell Biology and Visual Science, Department of Ophthalmology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
[Ti] Título:Systemic factors related to soluble (pro)renin receptor in plasma of patients with proliferative diabetic retinopathy.
[So] Source:PLoS One;12(12):e0189696, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:(Pro)renin receptor [(P)RR], a new component of the tissue renin-angiotensin system (RAS), plays a crucial role in inflammation and angiogenesis in the eye, thus contributing to the development of proliferative diabetic retinopathy (PDR). In this study, we investigated systemic factors related to plasma levels of soluble form of (P)RR [s(P)RR] in patients with PDR. Twenty type II diabetic patients with PDR and 20 age-matched, non-diabetic patients with idiopathic macular diseases were enrolled, and plasma levels of various molecules were measured by enzyme-linked immunosorbent assays. Human retinal microvascular endothelial cells were stimulated with several diabetes-related conditions to evaluate changes in gene expression using real-time quantitative PCR. Of various systemic parameters examined, the PDR patients had significantly higher blood sugar and serum creatinine levels than non-diabetic controls. Protein levels of s(P)RR, prorenin, tumor necrosis factor (TNF)-α, complement factor D (CFD), and leucine-rich α-2-glycoprotein 1 (LRG1) significantly increased in the plasma of PDR subjects as compared to non-diabetes, with positive correlations detected between s(P)RR and these inflammatory molecules but not prorenin. Estimated glomerular filtration rate and serum creatinine were also correlated with plasma s(P)RR, but not prorenin, levels. Among the inflammatory molecules correlated with s(P)RR in the plasma, TNF-α, but not CFD or LRG1, application to retinal endothelial cells upregulated the mRNA expression of (P)RR but not prorenin, while stimulation with high glucose enhanced both (P)RR and prorenin expression. These findings suggested close relationships between plasma s(P)RR and diabetes-induced factors including chronic inflammation, renal dysfunction, and hyperglycemia in patients with PDR.
[Mh] Termos MeSH primário: Retinopatia Diabética/sangue
Receptores de Superfície Celular/sangue
[Mh] Termos MeSH secundário: Indutores da Angiogênese/sangue
Células Cultivadas
Diabetes Mellitus Tipo 2/complicações
Retinopatia Diabética/complicações
Endotélio Vascular/citologia
Endotélio Vascular/metabolismo
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Mediadores da Inflamação/sangue
Rim/fisiopatologia
Masculino
Meia-Idade
Vasos Retinianos/citologia
Vasos Retinianos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Inflammation Mediators); 0 (Receptors, Cell Surface); 0 (prorenin receptor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189696


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[PMID]:29242904
[Au] Autor:Takahashi K; Shimazawa M; Izawa H; Inoue Y; Kuse Y; Hara H
[Ad] Endereço:Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.
[Ti] Título:Platelet-Derived Growth Factor-BB Lessens Light-Induced Rod Photoreceptor Damage in Mice.
[So] Source:Invest Ophthalmol Vis Sci;58(14):6299-6307, 2017 Dec 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Platelet-derived growth factor (PDGF)-BB is known to have neuroprotective effects against various neurodegenerative disorders. The purpose of this study was to determine whether PDGF-BB can be neuroprotective against light-induced photoreceptor damage in mice. Methods: Mice were exposed to 8000-lux luminance for 3 hours to induce phototoxicity. Two hours before light exposure, the experimental mice were injected with PDGF-BB intravitreally, and the control mice were injected with phosphate-buffered saline. The light-exposed PDGF-BB-injected mice and saline-injected mice were evaluated electroretinographically and histologically. The site and expression levels of PDGFR-ß and PDGF-BB were determined by immunostaining and Western blotting, respectively. The effect of PDGF-BB on light-induced cone and rod photoreceptor damage was also evaluated in vitro in 661W cells, a murine cone photoreceptor cell line, and in primary retinal cell cultures. Results: An intravitreal injection of PDGF-BB significantly reduced the decrease in the amplitudes of the electroretinograms (ERGs) and the thinning of the outer nuclear layer (ONL) induced by the light exposure. It also reduced the number of TUNEL-positive cells in the ONL. PDGFR-ß was expressed in the rod outer segments (OSs) but not the cone OSs. The levels of PDGF-BB and PDGFR-ß were decreased after light irradiation. In addition, PDGF-BB had protective effects against light-induced damage to cells of rod photoreceptors but had no effect on the 661W cells in vitro. Conclusions: These findings indicate that PDGF-BB reduces the degree of light-induced retinal damage by activating PDGFR-ß in rod photoreceptors. These findings suggest that PDGF-BB could play a role in the prevention of degeneration in eyes susceptible to phototoxicity.
[Mh] Termos MeSH primário: Luz/efeitos adversos
Células Fotorreceptoras de Vertebrados/efeitos dos fármacos
Prenhez
Proteínas Proto-Oncogênicas c-sis/administração & dosagem
Lesões Experimentais por Radiação/prevenção & controle
Doenças Retinianas/prevenção & controle
[Mh] Termos MeSH secundário: Indutores da Angiogênese/administração & dosagem
Animais
Animais Recém-Nascidos
Western Blotting
Morte Celular/efeitos dos fármacos
Morte Celular/efeitos da radiação
Linhagem Celular
Eletrorretinografia
Feminino
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Injeções Intravítreas
Masculino
Camundongos
Células Fotorreceptoras de Vertebrados/patologia
Células Fotorreceptoras de Vertebrados/efeitos da radiação
Fator de Crescimento Derivado de Plaquetas/administração & dosagem
Gravidez
Lesões Experimentais por Radiação/etiologia
Lesões Experimentais por Radiação/fisiopatologia
Proteínas Recombinantes
Doenças Retinianas/etiologia
Doenças Retinianas/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Platelet-Derived Growth Factor); 0 (Proto-Oncogene Proteins c-sis); 0 (Recombinant Proteins); 0 (platelet-derived growth factor A); 1B56C968OA (becaplermin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22556


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[PMID]:27777063
[Au] Autor:Ke J; Wei R; Yu F; Zhang J; Hong T
[Ad] Endereço:Department of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China.
[Ti] Título:Liraglutide restores angiogenesis in palmitate-impaired human endothelial cells through PI3K/Akt-Foxo1-GTPCH1 pathway.
[So] Source:Peptides;86:95-101, 2016 Dec.
[Is] ISSN:1873-5169
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucagon-like peptide-1 (GLP-1) and its analogues have a beneficial role in cardiovascular system. Here, we aimed to investigate whether liraglutide, a GLP-1 analogue, modulated angiogenesis impaired by palmitic acid (PA) in cultured human umbilical vein endothelial cells (HUVECs). Cells were incubated with liraglutide (3-100 nmol/L) in the presence of PA (0.5mmol/L), and endothelial tube formation was observed and quantified. The protein levels of signaling molecules were analyzed and the specific inhibitors were used to identify the signaling pathways through which liraglutide affected angiogenesis. Results showed that liraglutide ameliorated endothelial tube formation impaired by PA in HUVECs in a dose-dependent manner. Meanwhile, liraglutide increased the phosphorylation of Akt and forkhead box O1 (Foxo1), and upregulated the levels of guanosine 5'-triphosphate cyclohydrolase 1 (GTPCH1) and endothelial nitric oxide synthase (eNOS) in PA-impaired HUVECs. Notably, addition of the PI3K inhibitor LY294002, Foxo1 nuclear export inhibitor trifluoperazine dihydrochloride (TFP), GTPCH1 inhibitor 2,4-diamino-6-hydroxypyrimidine (DAHP) or NOS inhibitor N-nitro-l-arginine-methyl ester (L-NAME) eliminated the angiogenic effect of liraglutide. Moreover, either LY294002 or TFP abolished the liraglutide-induced upregulation of GTPCH1 and eNOS protein levels. In conclusion, liraglutide restores angiogenesis in PA-impaired HUVECs. The effect is mediated via upregulation of GTPCH1 and eNOS levels in a PI3K/Akt-Foxo1-dependent mechanism.
[Mh] Termos MeSH primário: Indutores da Angiogênese/farmacologia
Células Endoteliais da Veia Umbilical Humana/fisiologia
Liraglutida/farmacologia
[Mh] Termos MeSH secundário: Células Cultivadas
Avaliação Pré-Clínica de Medicamentos
Proteína Forkhead Box O1/metabolismo
GTP Cicloidrolase/metabolismo
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Seres Humanos
Óxido Nítrico Sintase Tipo III/metabolismo
Ácido Palmítico/farmacologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (FOXO1 protein, human); 0 (Forkhead Box Protein O1); 2V16EO95H1 (Palmitic Acid); 839I73S42A (Liraglutide); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.5.4.16 (GTP Cyclohydrolase)
[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:161030
[St] Status:MEDLINE


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[PMID]:28994269
[Au] Autor:Lee KH; Kim SH; Lee JM; Kang EC; Koh HJ
[Ad] Endereço:Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:Peripapillary Choroidal Thickness Change of Polypoidal Choroidal Vasculopathy after Anti-vascular Endothelial Growth Factor.
[So] Source:Korean J Ophthalmol;31(5):431-438, 2017 Oct.
[Is] ISSN:2092-9382
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To investigate the peripapillary choroidal thickness (PCT) of polypoidal choroidal vasculopathy (PCV) and exudative age-related macular degeneration (AMD) and to evaluate their responses to anti-vascular endothelial growth factor (VEGF). METHODS: Thirty eyes with PCV and 25 eyes with exudative AMD who were treatment naïve were included in this study. PCT and subfoveal choroidal thickness were evaluated both before and after intravitreal anti-VEGF. RESULTS: The initial mean PCT of PCV (153.78 ± 56.23 µm) was thicker than that of exudative AMD (88.77 ± 23.11 µm, p < 0.001). Temporal, superior, nasal, and inferior PCTs of PCV were all thicker than those observedin exudative AMD (all p < 0.05). After anti-VEGF, the mean PCT of PCV was significantly reduced (134.17 ± 41.66 µm, p < 0.001), but the same was not true not in exudative AMD (86.87 ± 22.54 µm, p = 0.392). PCTshowed a similar tendency in all quadrants. CONCLUSIONS: PCV exhibits a thick choroid in the peripapillary region. PCT decreases after anti-VEGF in PCV but not in exudative AMD. In exudative AMD, subfoveal choroidal thickness decreased, but that in the peripapillary region did not.
[Mh] Termos MeSH primário: Indutores da Angiogênese/administração & dosagem
Doenças da Coroide/diagnóstico
Corioide/irrigação sanguínea
Disco Óptico/patologia
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
[Mh] Termos MeSH secundário: Idoso
Bevacizumab/administração & dosagem
Corioide/patologia
Doenças da Coroide/tratamento farmacológico
Feminino
Angiofluoresceinografia
Seguimentos
Fundo de Olho
Seres Humanos
Injeções Intravítreas
Macula Lutea/patologia
Masculino
Meia-Idade
Ranibizumab/administração & dosagem
Estudos Retrospectivos
Tomografia de Coerência Óptica
Resultado do Tratamento
Acuidade Visual
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Vascular Endothelial Growth Factor A); 2S9ZZM9Q9V (Bevacizumab); ZL1R02VT79 (Ranibizumab)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.3341/kjo.2016.0101



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