Base de dados : MEDLINE
Pesquisa : G09.330.630 [Categoria DeCS]
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[PMID]:28453729
[Au] Autor:Chen Z; Xie J; Hao H; Lin H; Wang L; Zhang Y; Chen L; Cao S; Huang X; Liao W; Bin J; Liao Y
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, 1838, Guangzhou Avenue North, Guangzhou 510515, China.
[Ti] Título:Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3ß/cyclin D1 signalling pathway.
[So] Source:Cardiovasc Res;113(6):620-632, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: To resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms. Methods and results: Neonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3ß and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3ß inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. Conclusion: Ablation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3ß/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/deficiência
Ciclina D1/metabolismo
Infarto do Miocárdio/enzimologia
Miocárdio/enzimologia
Fosfatidilinositol 3-Quinase/metabolismo
Regeneração
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Moléculas de Adesão Celular/genética
Células Cultivadas
Modelos Animais de Doenças
Fibrose
Camundongos Knockout
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/fisiopatologia
Miocárdio/patologia
Neovascularização Fisiológica
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regeneração/efeitos dos fármacos
Proteínas Repressoras/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccnd1 protein, mouse); 0 (Cell Adhesion Molecules); 0 (GSKIP protein, mouse); 0 (Postn protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Repressor Proteins); 136601-57-5 (Cyclin D1); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx001


  2 / 21705 MEDLINE  
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[PMID]:29237531
[Au] Autor:Yue Y; Qu Y; Mu DZ
[Ad] Endereço:Department of Pediatrics, West China Second Hospital, Sichuan University/Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu 610041, China. mudz@scu.edu.cn.
[Ti] Título:[Research advances in mesenchymal stem cell-derived exosomes in treatment of brain injury].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(12):1285-1290, 2017 Dec.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Mesenchymal stem cell (MSC) transplantation is considered one of the most promising therapeutic strategies for the repair of brain injuries and plays an important role in various links of nerve repair. Recent studies have shown that MSC-derived exosomes may dominate the repair of brain injuries and help to promote angiogenesis, regulate immunity, inhibit apoptosis, and repair the nerves, and therefore, they have a great potential in the treatment of brain injuries in neonates. With reference to these studies, this article reviews the mechanism of action of exosomes in the repair of brain injuries and related prospects and challenges, in order to provide new directions for the treatment of brain injuries in neonates with stem cells.
[Mh] Termos MeSH primário: Lesões Encefálicas/terapia
Exossomos/fisiologia
Transplante de Células-Tronco Mesenquimais
[Mh] Termos MeSH secundário: Apoptose
Seres Humanos
Inflamação/prevenção & controle
Neovascularização Fisiológica
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE


  3 / 21705 MEDLINE  
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[PMID]:28468789
[Au] Autor:Bobi J; Solanes N; Fernández-Jiménez R; Galán-Arriola C; Dantas AP; Fernández-Friera L; Gálvez-Montón C; Rigol-Monzó E; Agüero J; Ramírez J; Roqué M; Bayés-Genís A; Sánchez-González J; García-Álvarez A; Sabaté M; Roura S; Ibáñez B; Rigol M
[Ad] Endereço:August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Institut de Malalties Cardiovasculars, Hospital Clínic de Barcelona, Universitat de Barcelona, Spain.
[Ti] Título:Intracoronary Administration of Allogeneic Adipose Tissue-Derived Mesenchymal Stem Cells Improves Myocardial Perfusion But Not Left Ventricle Function, in a Translational Model of Acute Myocardial Infarction.
[So] Source:J Am Heart Assoc;6(5), 2017 May 03.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Autologous adipose tissue-derived mesenchymal stem cells (ATMSCs) therapy is a promising strategy to improve post-myocardial infarction outcomes. In a porcine model of acute myocardial infarction, we studied the long-term effects and the mechanisms involved in allogeneic ATMSCs administration on myocardial performance. METHODS AND RESULTS: Thirty-eight pigs underwent 50 minutes of coronary occlusion; the study was completed in 33 pigs. After reperfusion, allogeneic ATMSCs or culture medium (vehicle) were intracoronarily administered. Follow-ups were performed at short (2 days after acute myocardial infarction vehicle-treated, n=10; ATMSCs-treated, n=9) or long term (60 days after acute myocardial infarction vehicle-treated, n=7; ATMSCs-treated, n=7). At short term, infarcted myocardium analysis showed reduced apoptosis in the ATMSCs-treated animals (48.6±6% versus 55.9±5.7% in vehicle; =0.017); enhancement of the reparative process with up-regulated vascular endothelial growth factor, granulocyte macrophage colony-stimulating factor, and stromal-derived factor-1α gene expression; and increased M2 macrophages (67.2±10% versus 54.7±10.2% in vehicle; =0.016). In long-term groups, increase in myocardial perfusion at the anterior infarct border was observed both on day-7 and day-60 cardiac magnetic resonance studies in ATMSCs-treated animals, compared to vehicle (87.9±28.7 versus 57.4±17.7 mL/min per gram at 7 days; =0.034 and 99±22.6 versus 43.3±14.7 22.6 mL/min per gram at 60 days; =0.0001, respectively). At day 60, higher vascular density was detected at the border zone in the ATMSCs-treated animals (118±18 versus 92.4±24.3 vessels/mm in vehicle; =0.045). Cardiac magnetic resonance-measured left ventricular ejection fraction of left ventricular volumes was not different between groups at any time point. CONCLUSIONS: In this porcine acute myocardial infarction model, allogeneic ATMSCs-based therapy was associated with increased cardioprotective and reparative mechanisms and with better cardiac magnetic resonance-measured perfusion. No effect on left ventricular volumes or ejection fraction was observed.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Circulação Coronária
Transplante de Células-Tronco Mesenquimais/métodos
Células Mesenquimais Estromais
Infarto do Miocárdio/cirurgia
Disfunção Ventricular Esquerda/cirurgia
Função Ventricular Esquerda
[Mh] Termos MeSH secundário: Proteínas Angiogênicas/metabolismo
Animais
Células Cultivadas
Angiografia por Tomografia Computadorizada
Angiografia Coronária/métodos
Citocinas/metabolismo
Modelos Animais de Doenças
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Imagem por Ressonância Magnética
Masculino
Transplante de Células-Tronco Mesenquimais/efeitos adversos
Células Mesenquimais Estromais/metabolismo
Tomografia Computadorizada Multidetectores
Infarto do Miocárdio/diagnóstico por imagem
Infarto do Miocárdio/metabolismo
Infarto do Miocárdio/fisiopatologia
Miocárdio/metabolismo
Miocárdio/patologia
Neovascularização Fisiológica
Imagem de Perfusão/métodos
Recuperação de Função Fisiológica
Regeneração
Sus scrofa
Fatores de Tempo
Transfecção
Transplante Homólogo
Disfunção Ventricular Esquerda/diagnóstico por imagem
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenic Proteins); 0 (Cytokines); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28454696
[Au] Autor:Ozmen A; Unek G; Korgun ET
[Ad] Endereço:Department of Histology and Embryology, Medical Faculty, Akdeniz University, 07070 Antalya, Turkey.
[Ti] Título:Effect of glucocorticoids on mechanisms of placental angiogenesis.
[So] Source:Placenta;52:41-48, 2017 Apr.
[Is] ISSN:1532-3102
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The benefits of antenatal glucocorticoid (GC) treatment to promote human fetal lung maturation are well established. However, reports have emerged indicating that maternal exposure to high concentrations of circulating GCs alters placental and fetal development. Because many adult-onset metabolic and cardiovascular disorders have their origins in utero, the importance of prenatal conditions should be considered in detail. Therefore, this review aims to present an overview of the GC effect on placental and fetal development, specifically with regard to mechanisms of placental angiogenesis. We assumed that GC overexposure affects fetal development by altering placental angiogenesis. Disturbances in the development of the villous tree and pathological changes in the villous vascular system with insufficient uteroplacental blood flow have been linked to the pathogenesis of intrauterine growth retardation. Moreover, low birth weight is a serious risk factor known to correlate with an increased risk of adult-onset diseases. Although there have been many circumstances in which maternal GCs are elevated, we focused on exogenous synthetic GCs that are applied for therapeutic reasons. However, some questions about the use of steroids remain unanswered, which will require further studies that lead us to review alterations in placental angiogenesis under the perspective of GC overexposure.
[Mh] Termos MeSH primário: Desenvolvimento Fetal/efeitos dos fármacos
Glucocorticoides/farmacologia
Neovascularização Patológica
Neovascularização Fisiológica/efeitos dos fármacos
Placenta/irrigação sanguínea
Placenta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucocorticoids)
[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:170430
[St] Status:MEDLINE


  5 / 21705 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


  6 / 21705 MEDLINE  
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[PMID]:28464921
[Au] Autor:Montali M; Panvini FM; Barachini S; Ronca F; Carnicelli V; Mazzoni S; Petrini I; Pacini S
[Ad] Endereço:Department of Clinical and Experimental Medicine, Hematology Division, University of Pisa, Via Roma 56, 56126, Pisa, Italy.
[Ti] Título:Human adult mesangiogenic progenitor cells reveal an early angiogenic potential, which is lost after mesengenic differentiation.
[So] Source:Stem Cell Res Ther;8(1):106, 2017 May 02.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mesangiogenic progenitor cells (MPCs) have shown the ability to differentiate in-vitro toward mesenchymal stromal cells (MSCs) as well as angiogenic potential. MPCs have so far been described in detail as progenitors of the mesodermal lineage and appear to be of great significance in tissue regeneration and in hemopoietic niche regulation. On the contrary, information regarding the MPC angiogenic process is still incomplete and requires further clarification. In particular, genuine MPC angiogenic potential should be confirmed in-vivo. METHODS: In the present article, markers and functions associated with angiogenic cells have been dissected. MPCs freshly isolated from human bone marrow have been induced to differentiate into exponentially growing MSCs (P2-MSCs). Cells have been characterized and angiogenesis-related gene expression was evaluated before and after mesengenic differentiation. Moreover, angiogenic potential has been tested by in-vitro and in-vivo functional assays. RESULTS: MPCs showed a distinctive gene expression profile, acetylated-low density lipoprotein uptake, and transendothelial migration capacity. However, mature endothelial markers and functions of endothelial cells, including the ability to form new capillaries, were absent, thus suggesting MPCs to be very immature endothelial progenitors. MPCs showed marked 3D spheroid sprouting activating the related molecular machinery, a clear in-vitro indication of early angiogenesis. Indeed, MPCs applied to chicken chorioallantoic membrane induced and participated in neovessel formation. All of these features were lost in mesengenic terminally differentiated P2-MSCs, showing definite separation of the two differentiation lineages. CONCLUSION: Our results confirm the bona-fide angiogenic potential of MPCs and suggest that the high variability reported for MSC cultures, responsible for the controversies regarding MSC angiogenic potential, could be correlated to variable percentages of co-isolated MPCs in the different culture conditions so far used.
[Mh] Termos MeSH primário: Células-Tronco Adultas/citologia
Diferenciação Celular
Células Mesenquimais Estromais/citologia
Neovascularização Fisiológica
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adipócitos/metabolismo
Células-Tronco Adultas/metabolismo
Células Cultivadas
Feminino
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Masculino
Células Mesenquimais Estromais/metabolismo
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s13287-017-0562-x


  7 / 21705 MEDLINE  
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[PMID]:28467355
[Au] Autor:Zhuang SF; Liu DX; Wang HJ; Zhang SH; Wei JY; Fang WG; Zhang K; Cao L; Zhao WD; Chen YH
[Ad] Endereço:Department of Developmental Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, 77 Puhe Road, Shenbei New District, Shenyang 110122, China. zsfcmu@163.com.
[Ti] Título:Atg7 Regulates Brain Angiogenesis via NF-κB-Dependent IL-6 Production.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The formation of brain vasculature is an essential step during central nervous system development. The molecular mechanism underlying brain angiogenesis remains incompletely understood. The role of Atg7, an autophagy-related protein, in brain angiogenesis was investigated in this study. We found that the microvessel density in mice brains with endothelial-specific knockout of Atg7 (Atg7 EKO) was significantly decreased compared to wild-type control. Consistently, in vitro angiogenesis assays showed that Atg7 knockdown impaired angiogenesis in brain microvascular endothelial cells. Further results indicated that knockdown of Atg7 reduced interleukin-6 (IL-6) expression in brain microvascular endothelial cells, which is mediated by NF-κB-dependent transcriptional control. Interestingly, exogenous IL-6 restored the impaired angiogenesis and reduced cell motility caused by Atg7 knockdown. These results demonstrated that Atg7 has proangiogenic activity in brain angiogenesis which is mediated by IL-6 production in a NF-κB-dependent manner.
[Mh] Termos MeSH primário: Proteína 7 Relacionada à Autofagia/metabolismo
Encéfalo/irrigação sanguínea
Interleucina-6/metabolismo
NF-kappa B/metabolismo
Neovascularização Fisiológica/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Proteína 7 Relacionada à Autofagia/genética
Movimento Celular/fisiologia
Células Cultivadas
Modelos Animais de Doenças
Células Endoteliais
Seres Humanos
Camundongos
Camundongos Knockout
Microvasos/crescimento & desenvolvimento
Microvasos/metabolismo
Neovascularização Fisiológica/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atg7 protein, mouse); 0 (Interleukin-6); 0 (NF-kappa B); 0 (interleukin-6, mouse); EC 6.2.1.45 (Autophagy-Related Protein 7)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:27778439
[Au] Autor:Randi AM; Laffan MA
[Ad] Endereço:National Heart and Lung Institute, Imperial College, London, UK.
[Ti] Título:Von Willebrand factor and angiogenesis: basic and applied issues.
[So] Source:J Thromb Haemost;15(1):13-20, 2017 01.
[Is] ISSN:1538-7836
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The recent discovery that von Willebrand factor (VWF) regulates blood vessel formation has opened a novel perspective on the function of this complex protein. VWF was discovered as a key component of hemostasis, capturing platelets at sites of endothelial damage and synthesized in megakaryocytes and endothelial cells (EC). In recent years, novel functions and binding partners have been identified for VWF. The finding that loss of VWF in EC results in enhanced, possibly dysfunctional, angiogenesis is consistent with the clinical observations that in some patients with von Willebrand disease (VWD), vascular malformations can cause severe gastrointestinal (GI) bleeding. In vitro and in vivo studies indicate that VWF can regulate angiogenesis through multiple pathways, both intracellular and extracellular, although their relative importance is still unclear. Investigation of these pathways has been greatly facilitated by the ability to isolate EC from progenitors circulating in the peripheral blood of normal controls and patients with VWD. In the next few years, these will yield further evidence on the molecular pathways controlled by VWF and shed light on this novel and fascinating area of vascular biology. In this article, we will review the evidence supporting a role for VWF in blood vessel formation, the link between VWF dysfunction and vascular malformations causing GI bleeding and how they may be causally related. Finally, we will discuss how these findings point to novel therapeutic approaches to bleeding refractory to VWF replacement therapy in VWD.
[Mh] Termos MeSH primário: Neovascularização Fisiológica
Fator de von Willebrand/metabolismo
[Mh] Termos MeSH secundário: Angiodisplasia/metabolismo
Animais
Coagulação Sanguínea
Plaquetas/metabolismo
Células Endoteliais/metabolismo
Hemorragia Gastrointestinal/sangue
Glicoproteínas/metabolismo
Hemorragia
Hemostasia
Seres Humanos
Megacariócitos/metabolismo
Camundongos
Neovascularização Patológica
Transdução de Sinais
Células-Tronco/metabolismo
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo
Doenças de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glycoproteins); 0 (von Willebrand Factor); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/jth.13551


  9 / 21705 MEDLINE  
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[PMID]:29307655
[Au] Autor:Chang X; Li H; Li Y; He Q; Yao J; Duan T; Wang K
[Ad] Endereço:Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, 200040, PR China.
[Ti] Título:RhoA/MLC signaling pathway is involved in Δ9-tetrahydrocannabinol-impaired placental angiogenesis.
[So] Source:Toxicol Lett;285:148-155, 2018 Mar 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cannabis is a widely used illicit drug and its abuse during pregnancy has been related to adverse reproductive outcomes. In addition, placental angiogenesis is considered to be responsible for the transport of nutrients critical for placental development and fetal growth. The purpose of this study is to determine the effects of Δ9-tetrahydrocannabinol (THC), the major component of cannabis, on placental angiogenesis, involving endothelial cell (EC) proliferation, migration and tube formation. Here, we observe dramatic alterations in placental vascular network of cannabis users correlated with an impaired HUVE cell proliferation, migration and tube formation after treated with THC. Mechanistically, the activity of RhoA/MLC is involved in the THC-impaired EC migration and angiogenesis. To further analyze the role of cannabis in mice placental and embryonic development, we inject pregnant mice with THC daily. This treatment results in an altered placental microvasculature, accompanied by the decreased expression of CD31 and activity of RhoA/MLC. Taken together, these findings identify THC plays a pivotal role in impairing placental angiogenesis potentially via RhoA/MLC signaling nexus.
[Mh] Termos MeSH primário: Dronabinol/toxicidade
Cadeias Leves de Miosina/metabolismo
Neovascularização Fisiológica/efeitos dos fármacos
Placenta/efeitos dos fármacos
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Feminino
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Camundongos Endogâmicos C57BL
Microvasos/efeitos dos fármacos
Microvasos/metabolismo
Placenta/irrigação sanguínea
Placenta/metabolismo
Gravidez
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myosin Light Chains); 7J8897W37S (Dronabinol); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:28467985
[Au] Autor:Castillo-Melendez M; Yawno T; Sutherland A; Jenkin G; Wallace EM; Miller SL
[Ad] Endereço:The Ritchie Centre, The Hudson Institute of Medical Research, Clayton, VIC, Australia.
[Ti] Título:Effects of Antenatal Melatonin Treatment on the Cerebral Vasculature in an Ovine Model of Fetal Growth Restriction.
[So] Source:Dev Neurosci;39(1-4):323-337, 2017.
[Is] ISSN:1421-9859
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Chronic moderate hypoxia, such as occurs in fetal growth restriction (FGR) during gestation, compromises the blood-brain barrier (BBB) and results in structural abnormalities of the cerebral vasculature. We have previously determined the neuroprotective and antioxidant effects of maternal administration of melatonin (MLT) on growth-restricted newborn lambs. The potential of maternal MLT therapy for the treatment of cerebrovascular dysfunction-associated developmental hypoxia has also been demonstrated in newborn lambs. We assessed whether MLT had an effect on the previously reported structural and cerebral vascular abnormalities in chronically hypoxic FGR lambs. Single umbilical-artery ligation surgery was performed in fetuses at approximately 105 days of gestation (term: 147 days) to induce placental insufficiency and FGR, and treatment with either saline or an MLT infusion (0.1 mg/kg) was started 4 h after surgery. Ewes delivered naturally at term and lambs were euthanased 24 h later. We found a significant reduction in the number of laminin-positive blood vessels within the subcortical and periventricular white matter (SCWM and PVWM) and the subventricular zone (SVZ) in FGR (p < 0.0005) and FGR + MLT brains (p < 0.0005 vs. controls), with no difference found between FGR and FGR + MLT animals. This was associated with a significant decrease in VEGF immunoreactivity in FGR and FGR + MLT brains versus controls (p < 0.0005; SCWM and PVWM) and in the SVZ in FGR brains versus controls (p < 0.005) and also with significantly lower levels of proliferating blood vessels versus controls (p < 0.0005). Glucose transporter-1 immunoreactivity (vascular endothelium) was decreased in FGR versus control lambs (p < 0.0005) in SCWM, PVWM, and the SVZ; it was significantly increased in FGR + MLT lambs compared with FGR lambs in SCWM and PVWM (p < 0.005) and even more markedly in the SVZ (p < 0.0005). FGR brains showed a 72% reduction in pericyte coverage versus control lambs and 68% versus FGR + MLT in PVWM. In SCWM, we found a 77 and 73% reduction compared with control and FGR + MLT lambs, respectively, while in the SVZ, we observed a 68% reduction versus controls and a 70% reduction in FGR versus FGR + MLT lambs. Astrocyte end-feet coverage in the SCWM showed a significant 24% reduction in FGR versus control levels, a 42% decrease within the PVWM, and a 35% decrease within the SVZ versus controls. MLT normalized astrocyte attachment to blood vessels, with no difference seen between controls and FGR + MLT animals in any of the brain regions examined. We also observed a decrease in albumin extravasation and microhemorrhage in controls and FGR + MLT brains versus FGR lambs. Our results demonstrate that umbilicoplacental insufficiency is associated with FGR-produced vascular changes in the white matter and SVZ of FGR newborn brains and that maternal MLT prevented disruption of the BBB by protecting perivascular cells essential for the maintenance of vascular homeostasis and stability.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Encéfalo/efeitos dos fármacos
Melatonina/farmacologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Feminino
Retardo do Crescimento Fetal/patologia
Hipóxia-Isquemia Encefálica/etiologia
Neovascularização Fisiológica/efeitos dos fármacos
Gravidez
Ovinos
Carneiro Doméstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); JL5DK93RCL (Melatonin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1159/000471797



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