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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]:28679845
[Au] Autor:Farnoodian M; Wang S; Dietz J; Nickells RW; Sorenson CM; Sheibani N
[Ad] Endereço:Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, U.S.A.
[Ti] Título:Negative regulators of angiogenesis: important targets for treatment of exudative AMD.
[So] Source:Clin Sci (Lond);131(15):1763-1780, 2017 Aug 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Angiogenesis contributes to the pathogenesis of many diseases including exudative age-related macular degeneration (AMD). It is normally kept in check by a tightly balanced production of pro- and anti-angiogenic factors. The up-regulation of the pro-angiogenic factor, vascular endothelial growth factor (VEGF), is intimately linked to the pathogenesis of exudative AMD, and its antagonism has been effectively targeted for treatment. However, very little is known about potential changes in expression of anti-angiogenic factors and the role they play in choroidal vascular homeostasis and neovascularization associated with AMD. Here, we will discuss the important role of thrombospondins and pigment epithelium-derived factor, two major endogenous inhibitors of angiogenesis, in retinal and choroidal vascular homeostasis and their potential alterations during AMD and choroidal neovascularization (CNV). We will review the cell autonomous function of these proteins in retinal and choroidal vascular cells. We will also discuss the potential targeting of these molecules and use of their mimetic peptides for therapeutic development for exudative AMD.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/fisiologia
Neovascularização de Coroide/fisiopatologia
Proteínas do Olho/fisiologia
Degeneração Macular/fisiopatologia
Fatores de Crescimento Neural/fisiologia
Serpinas/fisiologia
Trombospondinas/fisiologia
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/uso terapêutico
Angiostatinas/uso terapêutico
Neovascularização de Coroide/tratamento farmacológico
Endostatinas/uso terapêutico
Seres Humanos
Degeneração Macular/tratamento farmacológico
Terapia de Alvo Molecular/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Endostatins); 0 (Eye Proteins); 0 (Nerve Growth Factors); 0 (Serpins); 0 (Thrombospondins); 0 (pigment epithelium-derived factor); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170066


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[PMID]:28013203
[Au] Autor:Arriens C; Wren JD; Munroe ME; Mohan C
[Ad] Endereço:Department of Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation.
[Ti] Título:Systemic lupus erythematosus biomarkers: the challenging quest.
[So] Source:Rheumatology (Oxford);56(suppl_1):i32-i45, 2017 Apr 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:SLE, a multisystem heterogeneous disease, is characterized by production of antibodies to cellular components, with activation of both the innate and the adaptive immune system. Decades of investigation of blood biomarkers has resulted in incremental improvements in the understanding of SLE. Owing to the heterogeneity of immune dysregulation, no single biomarker has emerged as a surrogate for disease activity or prediction of disease. Beyond identification of surrogate biomarkers, a multitude of clinical trials have sought to inhibit elevated SLE biomarkers for therapeutic benefit. Armed with new -omics technologies, the necessary yet daunting quest to identify better surrogate biomarkers and successful therapeutics for SLE continues with tenacity.
[Mh] Termos MeSH primário: Anticorpos Antinucleares/imunologia
Proteínas do Sistema Complemento/imunologia
Citocinas/imunologia
Lúpus Eritematoso Sistêmico/imunologia
[Mh] Termos MeSH secundário: Angiostatinas/urina
Autoanticorpos/imunologia
Biomarcadores/metabolismo
Quimiocina CCL2/urina
Citocina TWEAK
DNA/imunologia
Ferritinas/metabolismo
Seres Humanos
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Lipocalina-2/urina
Lúpus Eritematoso Sistêmico/metabolismo
Fatores de Necrose Tumoral/urina
Molécula 1 de Adesão de Célula Vascular/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Autoantibodies); 0 (Biomarkers); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Cytokine TWEAK); 0 (Cytokines); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (Lipocalin-2); 0 (TNFSF12 protein, human); 0 (Tumor Necrosis Factors); 0 (Vascular Cell Adhesion Molecule-1); 86090-08-6 (Angiostatins); 9007-36-7 (Complement System Proteins); 9007-49-2 (DNA); 9007-73-2 (Ferritins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161226
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kew407


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[PMID]:27710144
[Au] Autor:Campochiaro PA; Lauer AK; Sohn EH; Mir TA; Naylor S; Anderton MC; Kelleher M; Harrop R; Ellis S; Mitrophanous KA
[Ad] Endereço:1 The Wilmer Eye Institute, Johns Hopkins University School of Medicine , Baltimore, Maryland.
[Ti] Título:Lentiviral Vector Gene Transfer of Endostatin/Angiostatin for Macular Degeneration (GEM) Study.
[So] Source:Hum Gene Ther;28(1):99-111, 2017 Jan.
[Is] ISSN:1557-7422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neovascular age-related macular degeneration (NVAMD) is a prevalent cause of vision loss. Intraocular injections of VEGF-neutralizing proteins provide benefit, but many patients require frequent injections for a prolonged period. Benefits are often lost over time due to lapses in treatment. New treatments that sustain anti-angiogenic activity are needed. This study tested the safety and expression profile of a lentiviral Equine Infectious Anemia Virus (EIAV) vector expressing endostatin and angiostatin (RetinoStat ). Patients with advanced NVAMD were enrolled at three centers in the United States, and the study eye received a subretinal injection of 2.4 × 10 (n = 3), 2.4 × 10 (n = 3), or 8.0 × 10 transduction units (TU; n = 15). Each of the doses was well-tolerated with no dose-limiting toxicities. There was little or no ocular inflammation. There was one procedure-related serious adverse event (AE), a macular hole, which was managed without difficulty and resolved. There was a vector dose-related increase in aqueous humor levels of endostatin and angiostatin with high reproducibility among subjects within cohorts. Mean levels of endostatin and angiostatin peaked between 12 and 24 weeks after injection of 2.4 × 10 TU or 8.0 × 10 TU at 57-81 ng/mL for endostatin and 15-27 ng/mL for angiostatin, and remained stable through the last measurement at week 48. Long-term follow-up demonstrated expression was maintained at last measurement (2.5 years in eight subjects and >4 years in two subjects). Despite an apparent reduction in fluorescein angiographic leakage that broadly correlated with the expression levels in the majority of patients, only one subject showed convincing evidence of anti-permeability activity in these late-stage patients. There was no significant change in mean lesion size in subjects injected with 8.0 × 10 TU. These data demonstrate that EIAV vectors provide a safe platform with robust and sustained transgene expression for ocular gene therapy.
[Mh] Termos MeSH primário: Endostatinas/genética
Terapia Genética
Vetores Genéticos/administração & dosagem
Lentivirus/genética
Degeneração Macular/terapia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Angiostatinas/genética
Estudos de Coortes
Feminino
Seres Humanos
Injeções Intraoculares
Degeneração Macular/genética
Masculino
Dose Máxima Tolerável
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Endostatins); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170823
[Lr] Data última revisão:
170823
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161007
[St] Status:MEDLINE
[do] DOI:10.1089/hum.2016.117


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[PMID]:27583825
[Au] Autor:Böhm MR; Hodes F; Brockhaus K; Hummel S; Schlatt S; Melkonyan H; Thanos S
[Ad] Endereço:Department of Ophthalmology Clinic for Diseases of the Anterior Segments of the Eyes, Essen University Hospital, Essen, Germany
[Ti] Título:Is Angiostatin Involved in Physiological Foveal Avascularity?
[So] Source:Invest Ophthalmol Vis Sci;57(11):4536-52, 2016 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The primate central retina is characterized by an avascular fovea and well-defined perifoveal capillary plexus. Neither blood vessels nor their accompanying astrocytes enter the fovea during any stage of retinal development; a balance of angiogenic and angiostatic factors probably maintains foveal avascularity throughout life. The aim of this study was to identify potentially angiorepulsive factors involved in the development of the avascular primate retinal fovea. Methods: Retinas of newborn, juvenile, and adult Callithrix jacchus and Macaca fascicularis monkeys and control human retinas were studied to determine the localization of angiostatin relative to III ß-tubulin, glial fibrillary acidic protein, vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM), and the angiostatin receptor αvß3-integrin in the foveal, macular, and peripheral retina. Expression studies were performed using immunohistochemistry (IHC) on retinal whole-mount and paraffin sections, and Western blotting on frozen material. The complex network of the main retinal cell types was identified by IHC of retinal whole mounts. Results: In general, lifetime expression of angiostatin was found in all retinas. Colabeling with different markers revealed retinal ganglion cells as the main source of angiostatin expression in the primate retina, whereas PECAM-immunopositive blood capillaries expressed the angiostatin receptor αvß3-integrin, and capillary-associated astrocytes expressed VEGF. Conclusions: This study provides the first evidence of angiostatin expression in the primate retina; the expression of angiostatin in the avascular foveal region and the peripheral retina suggests that angiostatin may play a role in the regulation of retinal vascularization, providing a possible explanation for the development and persistence of an avascular fovea.
[Mh] Termos MeSH primário: Angiostatinas/biossíntese
Fóvea Central/irrigação sanguínea
Vasos Retinianos/metabolismo
[Mh] Termos MeSH secundário: Idoso
Animais
Animais Recém-Nascidos
Western Blotting
Callithrix
Capilares/citologia
Capilares/metabolismo
Feminino
Fóvea Central/citologia
Fóvea Central/metabolismo
Proteína Glial Fibrilar Ácida/biossíntese
Seres Humanos
Imuno-Histoquímica
Macaca fascicularis
Masculino
Meia-Idade
Células Ganglionares da Retina/citologia
Células Ganglionares da Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170526
[Lr] Data última revisão:
170526
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-19286


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[PMID]:27299570
[Au] Autor:Szymczyszyn A; Doroszko A; Szahidewicz-Krupska E; Rola P; Gutherc R; Jasiczek J; Mazur G; Derkacz A
[Ad] Endereço:Department of Internal and Occupational Diseases, Hypertension and Clinical Oncology, Wroclaw Medical University, Borowska 213 Street, 50-552, Wroclaw, Poland.
[Ti] Título:Effect of the transdermal low-level laser therapy on endothelial function.
[So] Source:Lasers Med Sci;31(7):1301-7, 2016 Sep.
[Is] ISSN:1435-604X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effect of low-level laser therapy (LLLT) on the cardiovascular system is not fully established. Since the endothelium is an important endocrine element, establishing the mechanisms of LLLT action is an important issue.The aim of the study was to evaluate the effect of transdermal LLLT on endothelial function.In this study, healthy volunteers (n = 40, age = 20-40 years) were enrolled. N = 30 (14 female, 16 male, mean age 30 ± 5 years) constituted the laser-irradiated group (LG). The remaining 10 subjects (6 women, 4 men, mean age 28 ± 5 years) constituted the control group (CG). Participants were subjected to LLLT once a day for three consecutive days. Blood for biochemical assessments was drawn before the first irradiation and 24 h after the last session. In the LG, transdermal illumination of radial artery was conducted (a semiconductor laser λ = 808 nm, irradiation 50 mW, energy density 1.6 W/cm(2) and a dose 20 J/day, a total dose of 60 J). Biochemical parameters (reflecting angiogenesis: vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), angiostatin; antioxidative status: glutathione (GSH) and the nitric oxide metabolic pathway: symmetric dimethylarginine (SDMA), asymmetric dimethylarginine (ADMA) and L-arginine) were assessed. In the LG, a significant increase in GSH levels and considerable decrease in angiostatin concentration following the LLLT were observed. No significant differences in levels of the VEGF, FGF, SDMA, ADMA were observed.LLLT modifies vascular endothelial function by increasing its antioxidant and angiogenic potential. We found no significant differences in levels of the nitric oxide pathway metabolites within 24 h following the LLLT irradiation.
[Mh] Termos MeSH primário: Lasers Semicondutores/uso terapêutico
Terapia com Luz de Baixa Intensidade/métodos
Fator A de Crescimento do Endotélio Vascular/efeitos da radiação
[Mh] Termos MeSH secundário: Adulto
Angiostatinas/efeitos da radiação
Arginina/análogos & derivados
Arginina/efeitos da radiação
Feminino
Fatores de Crescimento de Fibroblastos/efeitos da radiação
Glutationa/efeitos da radiação
Seres Humanos
Masculino
Óxido Nítrico/efeitos da radiação
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vascular Endothelial Growth Factor A); 31C4KY9ESH (Nitric Oxide); 49787G1ULV (symmetric dimethylarginine); 62031-54-3 (Fibroblast Growth Factors); 63CV1GEK3Y (N,N-dimethylarginine); 86090-08-6 (Angiostatins); 94ZLA3W45F (Arginine); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160615
[St] Status:MEDLINE
[do] DOI:10.1007/s10103-016-1971-2


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[PMID]:27255598
[Au] Autor:Guzyk MM; Tykhomyrov AA; Nedzvetsky VS; Prischepa IV; Grinenko TV; Yanitska LV; Kuchmerovska TM
[Ad] Endereço:Department of Vitamin and Coenzyme Biochemistry, Palladin Institute of Biochemistry of National Academy of Sciences of Ukraine, Kyiv, Ukraine.
[Ti] Título:Poly(ADP-Ribose) Polymerase-1 (PARP-1) Inhibitors Reduce Reactive Gliosis and Improve Angiostatin Levels in Retina of Diabetic Rats.
[So] Source:Neurochem Res;41(10):2526-2537, 2016 Oct.
[Is] ISSN:1573-6903
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetic retinopathy (DR) is a multifactorial disease characterized by reactive gliosis and disbalance of angiogenesis regulators, contributing to endothelial dysfunction and microvascular complications. This study was organized to elucidate whether poly(ADP-ribose) polymerase-1 (PARP-1) inhibition could attenuate diabetes-induced damage to macroglia and correct angiogenic disbalance in diabetic rat retina. After 8 weeks of streptozotocin (STZ)-induced diabetes, Wistar male rats were treated with PARP-1 inhibitors, nicotinamide (NAm) or 3-aminobenzamide (3-AB) (100 and 30 mg/kg/daily i.p., respectively), for 14 days. After the 10-weeks experiment period, retinas were undergone an immunohistochemical staining for glial fibrillary acidic protein (GFAP), while western blots were performed to evaluate effects of PAPR-1 inhibitors on the levels of PARP-1, poly(ADP-ribosyl)ated proteins (PARs), GFAP, and angiostatin isoforms. Diabetes induced significant up-regulation and activation of retinal PARP-1, reactive gliosis development, and GFAP overexpression compared to non-diabetic control. Moreover, extensive fragmentation of both PARP-1 and GFAP (hallmarks of apoptosis and macroglia reactivation, respectively) in diabetic retina was also observed. Levels of angiostatin isoforms were dramatically decreased in diabetic retina, sustaining aberrant pro-angiogenic condition. Both NAm and 3-AB markedly attenuated damage to macroglia, evidenced by down-regulation of PARP-1, PARs and total GFAP compared to diabetic non-treated group. PARP-1-inhibitory therapy prevented formation of PARP-1 and GFAP cleavage-derived products. In retinas of anti-PARP-treated diabetic animals, partial restoration of angiostatin's levels was shown. Therefore, PARP-1 inhibitors counteract diabetes-induced injuries and manifest retinoprotective effects, including attenuation of reactive gliosis and improvement of angiogenic status, thus, such agents could be considered as promising candidates for DR management.
[Mh] Termos MeSH primário: Angiostatinas/metabolismo
Diabetes Mellitus Experimental/metabolismo
Gliose/metabolismo
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia
Retina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo/efeitos dos fármacos
Masculino
Ratos Wistar
Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Poly(ADP-ribose) Polymerase Inhibitors); 86090-08-6 (Angiostatins); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160604
[St] Status:MEDLINE


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[PMID]:27121159
[Au] Autor:Ranjbar K; Rahmani-Nia F; Shahabpour E
[Ad] Endereço:Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Guilan, Rasht, Iran.
[Ti] Título:Aerobic training and l-arginine supplementation promotes rat heart and hindleg muscles arteriogenesis after myocardial infarction.
[So] Source:J Physiol Biochem;72(3):393-404, 2016 Sep.
[Is] ISSN:1877-8755
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Arteriogenesis is a main defense mechanism to prevent heart and local tissues dysfunction in occlusive artery disease. TGF-ß and angiostatin have a pivotal role in arteriogenesis. We tested the hypothesis that aerobic training and l-arginine supplementation promotes cardiac and skeletal muscles arteriogenesis after myocardial infarction (MI) parallel to upregulation of TGF-ß and downregulation of angiostatin. For this purpose, 4 weeks after LAD occlusion, 50 male Wistar rats were randomly distributed into five groups: (1) sham surgery without MI (sham, n = 10), (2) control-MI (Con-MI, n = 10), (3) l-arginine-MI (La-MI, n = 10), (4) exercise training-MI (Ex-MI, n = 10), and (5) exercise and l-arginine-MI (Ex + La-MI). Exercise training groups running on a treadmill for 10 weeks with moderate intensity. Rats in the l-arginine-treated groups drank water containing 4 % l-arginine. Arteriolar density with different diameters (11-25, 26-50, 51-75, and 76-150 µm), TGF-ß, and angiostatin gene expression were measured in cardiac (area at risk) and skeletal (soleus and gastrocnemius) muscles. Smaller arterioles decreased in cardiac after MI. Aerobic training and l-arginine increased the number of cardiac arterioles with 11-25 and 26-50 µm diameters parallel to TGF-ß overexpression. In gastrocnemius muscle, the number of arterioles/mm(2) was only increased in the 11 to 25 µm in response to training with and without l-arginine parallel to angiostatin downregulation. Soleus arteriolar density with different size was not different between experimental groups. Results showed that 10 weeks aerobic exercise training and l-arginine supplementation promotes arteriogenesis of heart and gastrocnemius muscles parallel to overexpression of TGF-ß and downregulation of angiostatin in MI rats.
[Mh] Termos MeSH primário: Arginina/uso terapêutico
Vasos Coronários/fisiopatologia
Suplementos Nutricionais
Músculo Esquelético/irrigação sanguínea
Infarto do Miocárdio/reabilitação
Neovascularização Fisiológica
Condicionamento Físico Animal
[Mh] Termos MeSH secundário: Indutores da Angiogênese/uso terapêutico
Angiostatinas/antagonistas & inibidores
Angiostatinas/genética
Angiostatinas/metabolismo
Animais
Arteríolas/fisiopatologia
Arteriolosclerose/dietoterapia
Arteriolosclerose/fisiopatologia
Arteriolosclerose/terapia
Terapia Combinada
Regulação da Expressão Gênica
Coração/fisiopatologia
Membro Posterior
Masculino
Atividade Motora
Músculo Esquelético/metabolismo
Músculo Esquelético/fisiopatologia
Infarto do Miocárdio/etiologia
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/fisiopatologia
Miocárdio/metabolismo
Distribuição Aleatória
Ratos Wistar
Fator de Crescimento Transformador beta/agonistas
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Transforming Growth Factor beta); 86090-08-6 (Angiostatins); 94ZLA3W45F (Arginine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160429
[St] Status:MEDLINE
[do] DOI:10.1007/s13105-016-0480-x


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[PMID]:26885625
[Au] Autor:Almeida I; Oliveira Gomes A; Lima M; Silva I; Vasconcelos C
[Ad] Endereço:Clinical Immunology Unit, Dept. of Medicine, Hosp. de Santo António (HSA), Centro Hospitalar do Porto (CHP); and Multidisciplinary Unit for Biomedical Investigation (UMIB), Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Univ. do Porto, Portugal.
[Ti] Título:Different contributions of angiostatin and endostatin in angiogenesis impairment in systemic sclerosis: a cohort study.
[So] Source:Clin Exp Rheumatol;34 Suppl 100(5):37-42, 2016 Sep-Oct.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To determine the concentrations of circulating endostatin and angiostatin in patients with systemic sclerosis (SSc) and to assess its relationship to disease subsets, evolution phase, organ involvement and nailfold capillaroscopic changes. METHODS: Endostatin and angiostatin serum levels were measured by ELISA in a cohort of 57 patients with SSc, and correlated with disease subsets, evolution phase, organ involvement and nailfold capillaroscopic changes. RESULTS: Endostatin and angiostatin serum levels were significantly higher in patients with SSc than in healthy controls. Also, angiostatin was elevated in diffuse cutaneous SSc (dcSSc) and limited cutaneous SSc (lcSSc), but not in pre-SSc, while endostatin was increased in all SSc subsets. Moreover, endostatin was augmented in lcSSc, with or without CREST syndrome, whereas angiostatin was increased exclusively in patients with CREST. Analysis according to disease evolution phase found that endostatin was elevated in all phases while angiostatin was only significantly higher in intermediate and late phases of disease. Analysis regarding organ involvement revealed that angiostatin was significantly higher in patients with osteoarticular involvement and with more serious lung affection; no significant differences were found for endostatin. Finally, endostatin was significantly increased in all nailfold capillaroscopy stages, while angiostatin was only elevated in active and late phases. CONCLUSIONS: In accordance with previous studies, we found that endostatin and angiostatin concentrations are elevated in SSc patients. Additionally, we recognised the important role that endostatin might play as an early disease marker and realized that angiostatin is a marker of late disease and relates to lung disease severity.
[Mh] Termos MeSH primário: Angiostatinas/sangue
Endostatinas/sangue
Neovascularização Patológica
Esclerodermia Difusa/sangue
Esclerodermia Limitada/sangue
Pele/irrigação sanguínea
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Síndrome CREST/sangue
Síndrome CREST/patologia
Estudos de Casos e Controles
Estudos de Coortes
Progressão da Doença
Diagnóstico Precoce
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Angioscopia Microscópica
Meia-Idade
Valor Preditivo dos Testes
Esclerodermia Difusa/patologia
Esclerodermia Limitada/patologia
Índice de Gravidade de Doença
Transdução de Sinais
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Endostatins); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160218
[St] Status:MEDLINE


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[PMID]:26717601
[Au] Autor:Tykhomyrov AA; Vovchuk IL; Grinenko TV
[Ti] Título:PLASMINOGEN AND ANGIOSTATIN LEVELS IN FEMALE BENIGN BREAST LESIONS.
[So] Source:Ukr Biochem J;87(5):103-12, 2015 Sep-Oct.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:It is known that benign breast tissue exhibit relatively low angiogenic capacity. Activation of angiogenesis in mammary pre-malignant lesions could be associated with disease progression and high risk of transformation into the breast cancer. However, insight into the underlying molecular mechanisms involved in angiogenesis regulation in non-cancerous breast pathologies is still poorly defined. The purpose of the present study was to determine levels of plasminogen and its proteolytic fragments (angiostatins) in mammary dysplasia (mastopathy and breast cyst) and benign neoplasms (fibroadenomas). Plasminogen and angiostatins were analyzed using immunoblotting and quantified by densitometric scanning. The significant increase in plasminogen levels was found in fibrocystic, cysts, and non-proliferatious fibroadenoma masses (4.7-, 3.7-, and 3.5-fold, respectively) compared to healthy breast tissues (control). In the same benign lesions, 6.7-, 4-, and 3.7-fold increase in plasminogen 50 kDa fragment (angiostatin) levels as compared with control were also observed. Activation of matrix metalloproteinase-9, which was detected using gelatine zymography, could be responsible for plasminogen cleavage and abundance of angiostatin infibrocystic and cyst masses. In contrast, dramatic decrease of both plasminogen and angiostatin levels (3.8- and 5.3-folds, respectively) was shown in tissues of proliferatious form of fibroadenoma in comparison with that of the dormant type of this neoplasm. Based on the obtained results, we concluded that angiostatin, a potent vessel growth inhibitor and anti-inflammatory molecule, can play a crucial role in pathophysiology of non-cancerous breast diseases. Further studies are needed to evaluate potential diagnostic and clinical implications of these proteins for prediction and therapy of benign breast pathologies.
[Mh] Termos MeSH primário: Angiostatinas/metabolismo
Cisto Mamário/metabolismo
Neoplasias da Mama/metabolismo
Fibroadenoma/metabolismo
Doença da Mama Fibrocística/metabolismo
Plasminogênio/metabolismo
[Mh] Termos MeSH secundário: Cisto Mamário/irrigação sanguínea
Cisto Mamário/patologia
Neoplasias da Mama/irrigação sanguínea
Neoplasias da Mama/patologia
Feminino
Fibroadenoma/irrigação sanguínea
Fibroadenoma/patologia
Doença da Mama Fibrocística/irrigação sanguínea
Doença da Mama Fibrocística/patologia
Seres Humanos
Immunoblotting
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
86090-08-6 (Angiostatins); 9001-91-6 (Plasminogen)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:151231
[Lr] Data última revisão:
151231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160101
[St] Status:MEDLINE



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