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Pesquisa : A11.872.620.510 [Categoria DeCS]
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[PMID]:27965937
[Au] Autor:Li L; Liu M; Kang L; Li Y; Dai Z; Wang B; Liu S; Chen L; Tan Y; Wu G
[Ad] Endereço:Department of Vasculocardiology, Xiangya Hospital, Central South University Changsha, China.
[Ti] Título:HHEX: A Crosstalker between HCMV Infection and Proliferation of VSMCs.
[So] Source:Front Cell Infect Microbiol;6:169, 2016.
[Is] ISSN:2235-2988
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The study was designed to evaluate the role of Human cytomegalovirus (HCMV) infection on homebox (HOX) gene expression and the effects of overexpression of HOX genes on proliferation and apoptosis of vascular smooth muscle cells (VSMCs). Viral infection was verified by observation of cytopathic effects through inverted microscopy, viral particles by electron microscopy and HCMV IE gene amplification by RT-PCR. cDNA profiling technology was used to screen expression of HOX genes after HCMV infection in VSMCs. Abnormal expression of Haematopoietically-expressed homeobox (HHEX) was selected to construct over-expressed vector and transfected into VSMCs. The effects of over expression of HHEX on cell proliferation and apoptosis of VSMCs were assayed by flow cytometry. Apoptosis and proliferation-associated genes were also assayed by RT-PCR. Multiple HOX gene expression levels had obvious changes after HCMV infection, among which expression of HHEX gene increased obviously at 24, 48, and 72 h after infection. Over expression of HHEX can promote VSMCs proliferation by promoting G0/G1 phase cells into S phase and inhibit VSMCs apoptosis. HHEX inhibited the expression of apoptosis-associated caspase 2 and caspase3 and promoted the expression of cell cycle-related genes such as CDK2 and CDK6, CyclinB2 and CyclinD2. HHEX over expression induced by HCMV infection closely associated with vascular proliferative diseases.
[Mh] Termos MeSH primário: Apoptose
Proliferação Celular
Citomegalovirus/patogenicidade
Proteínas de Homeodomínio/biossíntese
Interações Hospedeiro-Patógeno
Músculo Liso Vascular/patologia
Mioblastos de Músculo Liso/fisiologia
Fatores de Transcrição/biossíntese
[Mh] Termos MeSH secundário: Células Cultivadas
Perfilação da Expressão Gênica
Proteínas de Homeodomínio/genética
Seres Humanos
Mioblastos de Músculo Liso/virologia
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HHEX protein, human); 0 (Homeodomain Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161215
[St] Status:MEDLINE


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[PMID]:25858065
[Au] Autor:Psaltis PJ; Simari RD
[Ad] Endereço:From the Department of Medicine, University of Adelaide and Heart Health Theme, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia (P.J.P.); Monash Cardiovascular Research Centre, Monash University, Clayton, Victoria, Australia (P.J.P.); and Department of Internal Medicine, University of Kansas School of Medicine (R.D.S.).
[Ti] Título:Vascular wall progenitor cells in health and disease.
[So] Source:Circ Res;116(8):1392-412, 2015 Apr 10.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The vasculature plays an indispensible role in organ development and maintenance of tissue homeostasis, such that disturbances to it impact greatly on developmental and postnatal health. Although cell turnover in healthy blood vessels is low, it increases considerably under pathological conditions. The principle sources for this phenomenon have long been considered to be the recruitment of cells from the peripheral circulation and the re-entry of mature cells in the vessel wall back into cell cycle. However, recent discoveries have also uncovered the presence of a range of multipotent and lineage-restricted progenitor cells in the mural layers of postnatal blood vessels, possessing high proliferative capacity and potential to generate endothelial, smooth muscle, hematopoietic or mesenchymal cell progeny. In particular, the tunica adventitia has emerged as a progenitor-rich compartment with niche-like characteristics that support and regulate vascular wall progenitor cells. Preliminary data indicate the involvement of some of these vascular wall progenitor cells in vascular disease states, adding weight to the notion that the adventitia is integral to vascular wall pathogenesis, and raising potential implications for clinical therapies. This review discusses the current body of evidence for the existence of vascular wall progenitor cell subpopulations from development to adulthood and addresses the gains made and significant challenges that lie ahead in trying to accurately delineate their identities, origins, regulatory pathways, and relevance to normal vascular structure and function, as well as disease.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/patologia
Células Progenitoras Endoteliais/patologia
Músculo Liso Vascular/patologia
Mioblastos de Músculo Liso/patologia
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/cirurgia
Diferenciação Celular
Linhagem da Célula
Proliferação Celular
Células Progenitoras Endoteliais/metabolismo
Células Progenitoras Endoteliais/transplante
Seres Humanos
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/transplante
Mioblastos de Músculo Liso/metabolismo
Mioblastos de Músculo Liso/transplante
Neovascularização Patológica
Neovascularização Fisiológica
Regeneração
Medicina Regenerativa/métodos
Nicho de Células-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150410
[Lr] Data última revisão:
150410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150411
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.116.305368


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[PMID]:24475076
[Au] Autor:Chen ZH; Zhang YC; Jiang WF; Yang C; Zou GM; Kong Y; Cai W
[Ad] Endereço:Shanghai Institute for Pediatric Research, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P. R. China.
[Ti] Título:Characterization of interstitial Cajal progenitors cells and their changes in Hirschsprung's disease.
[So] Source:PLoS One;9(1):e86100, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interstitial cells of Cajal (ICC) are critical to gastrointestinal motility. The phenotypes of ICC progenitors have been observed in the mouse gut, but whether they exist in the human colon and what abnormal changes in their quantity and ultrastructure are present in Hirschsprung's disease (HSCR) colon remains uncertain. In this study, we collected the surgical resection of colons, both proximal and narrow segments, from HSCR patients and normal controls. First, we identified the progenitor of ICC in normal adult colon using immunofluorescent localization techniques with laser confocal microscopy. Next, the progenitors were sorted to observe their morphology. We further applied flow cytometry to examine the content of ICC progenitors in these fresh samples. The ultrastructural changes in the narrow and proximal parts of the HSCR colon were observed using transmission electron microscopy (TEM) and were compared with the normal adult colon. The presumed early progenitor (c-Kit(low)CD34(+)Igf1r(+)) and committed progenitor (c-Kit(+)CD34(+)Igf1r(+)) of ICC exist in adult normal colon as well as in the narrow and proximal parts of the HSCR colon. However, the proportions of mature, early and committed progenitors of ICC were dramatically reduced in the narrow segment of the HSCR colon. The proportions of mature and committed progenitors of ICC in the proximal segment of the HSCR colon were lower than in the adult normal colon. Ultrastructurally, ICC, enteric nerves, and smooth muscle in the narrow segment of the HSCR colon showed severe injury, including swollen vacuola or ted mitochondria, disappearance of mitochondrial cristae, dilated rough endoplasmic reticulum, vesiculation and degranulation, and disappearance of the caveolae on the ICC membrane surface. The contents of ICC and its progenitors in the narrow part of the HSCR colon were significantly decreased than those of adult colon, which may be associated with HSCR pathogenesis.
[Mh] Termos MeSH primário: Doença de Hirschsprung/metabolismo
Células Intersticiais de Cajal/metabolismo
Mioblastos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Estudos de Casos e Controles
Células Cultivadas
Pré-Escolar
Feminino
Seres Humanos
Imunofenotipagem
Lactente
Células Intersticiais de Cajal/citologia
Células Intersticiais de Cajal/ultraestrutura
Masculino
Meia-Idade
Mioblastos de Músculo Liso/citologia
Mioblastos de Músculo Liso/ultraestrutura
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1410
[Cu] Atualização por classe:150515
[Lr] Data última revisão:
150515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0086100


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[PMID]:24197586
[Au] Autor:Janeczek A; Zimna A; Rozwadowska N; Fraczek M; Kucharzewska P; Rucinski M; Mietkiewski T; Kolanowski T; Malcher A; Kurpisz M
[Ad] Endereço:Institute of Human Genetics, Polish Academy of Sciences. kurpimac@man.poznan.pl.
[Ti] Título:Genetically modified human myoblasts with eNOS may improve regenerative ability of myogenic stem cells to infarcted heart.
[So] Source:Kardiol Pol;71(10):1048-58, 2013.
[Is] ISSN:1897-4279
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Modern therapies of post infarcted heart failure are focused on perfusion improvement of the injured myocardium. This effect can be achieved by, among other means, implanting stem cells which could be genetically modified with factors inducing the formation of new blood vessels in the post infarction scar area. Combined stem cell and gene therapy seems to be a promising strategy to heal an impaired myocardium. The creation of new blood vessels can be indirectly stimulated via factors inducing vascular endothelial growth factor synthesis, for example endothelial nitric oxide synthase (eNOS). The product of this enzyme, nitric oxide, is a molecule that can influence numerous physiological activities; it can contribute to vasodilation, stimulation of endothelial cell growth, prevention of platelet aggregation and leukocyte adhesion to the endothelium. AIM: To verify the pro-angiogenic and regenerative potential of human primary myoblasts and murine myoblast cell line C2C12 transiently transfected with eNOS gene. METHODS: Stem cells (either human or murine) were maintained in standard in vitro conditions. Next, both types of myoblasts were modified using electroporation and lipofection (human and murine cells), respectively. The efficacy of the transfection method was evaluated using flow cytometry. The concentration of eNOS protein was measured by ELISA immunoassay. The biological properties of modified cells were assessed using an MTT proliferation test and DAPI cell cycle analysis. To verify the influence of oxidative stress on myoblasts, cytometric tests using Annexin V and propidium iodide were applied. To check possible alterations in myogenic gene expression of stem cells transduced by genetic modification, the myogenic regulatory factors were evaluated by real-time PCR. The function of genetic modification was confirmed by a HUVEC capillary sprouting test using myoblasts supernatants. RESULTS: Electroporation turned out to be an efficient transfection method. High amounts of secreted protein were obtained (in the range 2,000 pg/mL) in both cell types studied. Moreover, the functionality of gene overexpression product was confirmed in capillary development assay. Human myoblasts did not exhibit any changes in cell cycle; however, eNOS transfected murine myoblasts revealed a statistically significant reduction in cell cycle ratio compared to controls (p < 0.001). In the case of myogenic gene expression, a decrease in Myogenin level was only detected in the human transfected myoblast population (p < 0.05). CONCLUSIONS: The results of our study may suggest that transplantation of myoblasts overexpressing eNOS could be promising for cell therapy in regenerating the post infarction heart.
[Mh] Termos MeSH primário: Terapia Genética
Mioblastos Esqueléticos/transplante
Mioblastos de Músculo Liso/transplante
Infarto do Miocárdio/terapia
Óxido Nítrico Sintase Tipo III/genética
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Ciclo Celular/genética
Proliferação Celular
Células Cultivadas
Eletroporação
Células Endoteliais/citologia
Seres Humanos
Camundongos
Mioblastos Esqueléticos/citologia
Mioblastos Esqueléticos/metabolismo
Mioblastos de Músculo Liso/citologia
Mioblastos de Músculo Liso/metabolismo
Neovascularização Fisiológica/genética
Estresse Oxidativo/genética
Regeneração/genética
Transplante de Células-Tronco
Transfecção
Veias Umbilicais/citologia
Fator A de Crescimento do Endotélio Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Vascular Endothelial Growth Factor A); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III)
[Em] Mês de entrada:1403
[Cu] Atualização por classe:131107
[Lr] Data última revisão:
131107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131108
[St] Status:MEDLINE
[do] DOI:10.5603/KP.2013.0260


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[PMID]:22925499
[Au] Autor:Tan B; Wei RQ; Tan MY; Luo JC; Deng L; Chen XH; Hou JL; Li XQ; Yang ZM; Xie HQ
[Ad] Endereço:Laboratory of Stem Cell and Tissue Engineering, Regenerative Medicine Research Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, PR China.
[Ti] Título:Tissue engineered esophagus by mesenchymal stem cell seeding for esophageal repair in a canine model.
[So] Source:J Surg Res;182(1):40-8, 2013 Jun 01.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Acellular porcine small intestinal submucosa (SIS) has been successfully used for esophagoplasty in dogs. However, this has not led to complete epithelialization and muscular regeneration. We undertook the present study to assess the effect of tissue-engineered esophagus generated by seeding bone marrow mesenchymal stem cells (BMSCs) onto an SIS scaffold (BMSCs-SIS) in a canine model. METHODS: We cultured, passaged, and measured autologous BMSCs and myoblasts with cell proliferation and immunohistochemical assays. We labeled the third passage of BMSCs with PKH-26, a fluorescent dye, before seeded it onto the SIS. We resected canine cervical esophagus to generate a defect 5 cm in length and 50% in circumference, which we repaired with BMSCs-SIS or SIS alone. RESULTS: Four weeks later, barium esophagram demonstrated that esophageal lumen surface of the patch graft was smoother in the BMSCs-SIS group compared with the SIS group. Histological examination suggested a strong similarity between BMSCs and esophageal myoblasts in terms of morphology and function. Although both BMSCs-SIS and SIS repaired the esophageal defects, we noted complete re-epithelialization with almost no inflammation only in the former group. By 12 wk after the surgery, we observed long bundles of skeletal muscles only in the BMSCs-SIS group, where the microvessel density was also much greater. CONCLUSIONS: Bone marrow mesenchymal stem cells on an SIS scaffold can promote re-epithelialization, revascularization, and muscular regeneration. This approach may provide an attractive option for esophageal regeneration.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Esôfago/citologia
Células Mesenquimais Estromais/citologia
Modelos Animais
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Células da Medula Óssea/citologia
Células da Medula Óssea/metabolismo
Proliferação Celular
Células Cultivadas
Cães
Esôfago/fisiologia
Masculino
Células Mesenquimais Estromais/fisiologia
Mioblastos de Músculo Liso/citologia
Mioblastos de Músculo Liso/metabolismo
Regeneração/fisiologia
Tecidos Suporte
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:130426
[Lr] Data última revisão:
130426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120829
[St] Status:MEDLINE


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[PMID]:22833126
[Au] Autor:Trowe MO; Airik R; Weiss AC; Farin HF; Foik AB; Bettenhausen E; Schuster-Gossler K; Taketo MM; Kispert A
[Ad] Endereço:Institut für Molekularbiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany.
[Ti] Título:Canonical Wnt signaling regulates smooth muscle precursor development in the mouse ureter.
[So] Source:Development;139(17):3099-108, 2012 Sep.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Smooth muscle cells (SMCs) are a key component of many visceral organs, including the ureter, yet the molecular pathways that regulate their development from mesenchymal precursors are insufficiently understood. Here, we identified epithelial Wnt7b and Wnt9b as possible ligands of Fzd1-mediated ß-catenin (Ctnnb1)-dependent (canonical) Wnt signaling in the adjacent undifferentiated ureteric mesenchyme. Mice with a conditional deletion of Ctnnb1 in the ureteric mesenchyme exhibited hydroureter and hydronephrosis at newborn stages due to functional obstruction of the ureter. Histological analysis revealed that the layer of undifferentiated mesenchymal cells directly adjacent to the ureteric epithelium did not undergo characteristic cell shape changes, exhibited reduced proliferation and failed to differentiate into SMCs. Molecular markers for prospective SMCs were lost, whereas markers of the outer layer of the ureteric mesenchyme fated to become adventitial fibroblasts were expanded to the inner layer. Conditional misexpression of a stabilized form of Ctnnb1 in the prospective ureteric mesenchyme resulted in the formation of a large domain of cells that exhibited histological and molecular features of prospective SMCs and differentiated along this lineage. Our analysis suggests that Wnt signals from the ureteric epithelium pattern the ureteric mesenchyme in a radial fashion by suppressing adventitial fibroblast differentiation and initiating smooth muscle precursor development in the innermost layer of mesenchymal cells.
[Mh] Termos MeSH primário: Hipoxantina Fosforribosiltransferase/genética
Mioblastos de Músculo Liso/fisiologia
Proteínas Proto-Oncogênicas/metabolismo
Ureter/embriologia
Proteínas Wnt/metabolismo
Via de Sinalização Wnt/fisiologia
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Cruzamentos Genéticos
Fluorescência
Técnicas de Introdução de Genes
Hibridização In Situ
Camundongos
Mioblastos de Músculo Liso/metabolismo
Ureter/citologia
Ureter/metabolismo
beta Catenina/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CTNNB1 protein, mouse); 0 (Proto-Oncogene Proteins); 0 (Wnt Proteins); 0 (Wnt7b protein, mouse); 0 (Wnt9b protein, mouse); 0 (beta Catenin); EC 2.4.2.8 (Hypoxanthine Phosphoribosyltransferase)
[Em] Mês de entrada:1210
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120727
[St] Status:MEDLINE
[do] DOI:10.1242/dev.077388


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[PMID]:22652098
[Au] Autor:Gittenberger-de Groot AC; Winter EM; Bartelings MM; Goumans MJ; DeRuiter MC; Poelmann RE
[Ad] Endereço:Department of Cardiology, Leiden University Medical Center, Postal zone: S-5-24, P.O. Box 9600, 2300 RC Leiden, The Netherlands. acgitten@lumc.nl
[Ti] Título:The arterial and cardiac epicardium in development, disease and repair.
[So] Source:Differentiation;84(1):41-53, 2012 Jul.
[Is] ISSN:1432-0436
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The importance of the epicardium covering the heart and the intrapericardial part of the great arteries has reached a new summit. It has evolved as a major cellular component with impact both in development, disease and more recently also repair potential. The role of the epicardium in development, its differentiation from a proepicardial organ at the venous pole (vPEO) and the differentiation capacities of the vPEO initiating cardiac epicardium (cEP) into epicardium derived cells (EPDCs) have been extensively described in recent reviews on growth and transcription factor pathways. In short, the epicardium is the source of the interstitial, the annulus fibrosus and the adventitial fibroblasts, and differentiates into the coronary arterial smooth muscle cells. Furthermore, EPDCs induce growth of the compact myocardium and differentiation of the Purkinje fibers. This review includes an arterial pole located PEO (aPEO) that provides the epicardium covering the intrapericardial great vessels. In avian and mouse models disturbance of epicardial outgrowth and maturation leads to a broad spectrum of cardiac anomalies with main focus on non-compaction of the myocardium, deficient annulus fibrosis, valve malformations and coronary artery abnormalities. The discovery that in disease both arterial and cardiac epicardium can again differentiate into EPDCs and thus reactivate its embryonic program and potential has highly broadened the scope of research interest. This reactivation is seen after myocardial infarction and also in aneurysm formation of the ascending aorta. Use of EPDCs for cell therapy show their positive function in paracrine mediated repair processes which can be additive when combined with the cardiac progenitor stem cells that probably share the same embryonic origin with EPDCs. Research into the many cell-autonomous and cell-cell-based capacities of the adult epicardium will open up new realistic therapeutic avenues.
[Mh] Termos MeSH primário: Linhagem da Célula
Cardiopatias Congênitas/embriologia
Pericárdio/citologia
Pericárdio/embriologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Transplante de Células
Embrião de Galinha
Células-Tronco Embrionárias/citologia
Células Endoteliais/citologia
Fibroblastos/citologia
Cardiopatias Congênitas/terapia
Seres Humanos
Camundongos
Mioblastos Cardíacos/citologia
Mioblastos de Músculo Liso/citologia
Miócitos Cardíacos/citologia
Miócitos de Músculo Liso/citologia
Pericárdio/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1211
[Cu] Atualização por classe:120703
[Lr] Data última revisão:
120703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120602
[St] Status:MEDLINE
[do] DOI:10.1016/j.diff.2012.05.002


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[PMID]:22609551
[Au] Autor:Zeng L; Childs SJ
[Ad] Endereço:Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, AB, Canada T2N 4N1.
[Ti] Título:The smooth muscle microRNA miR-145 regulates gut epithelial development via a paracrine mechanism.
[So] Source:Dev Biol;367(2):178-86, 2012 Jul 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs are potent modulators of cellular differentiation. miR-145 is expressed in, and promotes the differentiation of vascular and visceral smooth muscle cells (SMCs). Interestingly, we have observed that miR-145 also promotes differentiation of the gut epithelium in the developing zebrafish, a cell type where it is not expressed. Here we identify that a paracrine pathway involving the morphogens Sonic hedgehog (Shh) in epithelium and bone morphogenic protein 4 (Bmp4) in SMCs is modulated by miR-145. We show that expression of miR-145 in visceral SMCs normally represses the expression of the morphogen bmp4, as loss of miR-145 leads to upregulation of bmp4 in SMCs. We show that bmp4 in turn controls expression of Shh in the visceral epithelium. Conversely, in miR-145 morphants where bmp4 expression is increased, expression of sonic hedgehog a (shha) is strongly increased in gut epithelium. We show that expression of bmp4 is modulated by the miR-145 direct target gata6 but not a second potential direct target, klf5a. Thus although miR-145 is a tissue-restricted microRNA, it plays an essential role in promoting the patterning of both gut layers during gut development via a paracrine mechanism.
[Mh] Termos MeSH primário: MicroRNAs/genética
Peixe-Zebra/embriologia
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Sequência de Bases
Proteína Morfogenética Óssea 4/genética
Proteína Morfogenética Óssea 4/metabolismo
Diferenciação Celular
Proliferação Celular
Sistema Digestório/embriologia
Sistema Digestório/metabolismo
Fatores de Transcrição GATA/genética
Regulação da Expressão Gênica no Desenvolvimento
Técnicas de Silenciamento de Genes
Proteínas Hedgehog/genética
Proteínas Hedgehog/metabolismo
Fatores de Transcrição Kruppel-Like/genética
Morfolinos/genética
Músculo Liso/embriologia
Músculo Liso/metabolismo
Mioblastos de Músculo Liso/citologia
Mioblastos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/metabolismo
Comunicação Parácrina
Peixe-Zebra/metabolismo
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 4); 0 (GATA Transcription Factors); 0 (Gata6 protein, zebrafish); 0 (Hedgehog Proteins); 0 (Kruppel-Like Transcription Factors); 0 (MicroRNAs); 0 (Mirn145 microRNA, zebrafish); 0 (Morpholinos); 0 (Shha protein, zebrafish); 0 (Zebrafish Proteins); 0 (bmp4 protein, zebrafish)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:120612
[Lr] Data última revisão:
120612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120522
[St] Status:MEDLINE
[do] DOI:10.1016/j.ydbio.2012.05.009


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[PMID]:22509029
[Au] Autor:Chang L; Noseda M; Higginson M; Ly M; Patenaude A; Fuller M; Kyle AH; Minchinton AI; Puri MC; Dumont DJ; Karsan A
[Ad] Endereço:Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 1L3.
[Ti] Título:Differentiation of vascular smooth muscle cells from local precursors during embryonic and adult arteriogenesis requires Notch signaling.
[So] Source:Proc Natl Acad Sci U S A;109(18):6993-8, 2012 May 01.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular smooth muscle cells (VSMC) have been suggested to arise from various developmental sources during embryogenesis, depending on the vascular bed. However, evidence also points to a common subpopulation of vascular progenitor cells predisposed to VSMC fate in the embryo. In the present study, we use binary transgenic reporter mice to identify a Tie1(+)CD31(dim)vascular endothelial (VE)-cadherin(-)CD45(-) precursor that gives rise to VSMC in vivo in all vascular beds examined. This precursor does not represent a mature endothelial cell, because a VE-cadherin promoter-driven reporter shows no expression in VSMC during murine development. Blockade of Notch signaling in the Tie1(+) precursor cell, but not the VE-cadherin(+) endothelial cell, decreases VSMC investment of developing arteries, leading to localized hemorrhage in the embryo at the time of vascular maturation. However, Notch signaling is not required in the Tie1(+) precursor after establishment of a stable artery. Thus, Notch activity is required in the differentiation of a Tie1(+) local precursor to VSMC in a spatiotemporal fashion across all vascular beds.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Mioblastos de Músculo Liso/citologia
Mioblastos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/metabolismo
Neovascularização Fisiológica
Receptores Notch/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Artérias/embriologia
Artérias/crescimento & desenvolvimento
Artérias/metabolismo
Sequência de Bases
Caderinas/deficiência
Caderinas/genética
Diferenciação Celular/genética
Primers do DNA/genética
Feminino
Antígenos Comuns de Leucócito/deficiência
Antígenos Comuns de Leucócito/genética
Camundongos
Camundongos Transgênicos
Neovascularização Fisiológica/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Gravidez
Receptor de TIE-1/metabolismo
Receptores Notch/antagonistas & inibidores
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cadherins); 0 (DNA Primers); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Receptors, Notch); 0 (cadherin 5); EC 2.7.10.1 (Receptor, TIE-1); EC 3.1.3.48 (Leukocyte Common Antigens); EC 3.1.3.48 (Ptprc protein, mouse)
[Em] Mês de entrada:1207
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120418
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1118512109


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[PMID]:22173975
[Au] Autor:Delacroix S; Simari RD
[Ti] Título:Tissue factor-thrombin-PAR-1 pathway: a novel link between bone marrow and blood vessel.
[So] Source:Arterioscler Thromb Vasc Biol;32(1):3-4, 2012 Jan.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Actinas/metabolismo
Lesões das Artérias Carótidas/metabolismo
Mioblastos de Músculo Liso/metabolismo
Receptores de Trombina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMMENT; EDITORIAL
[Nm] Nome de substância:
0 (Actins); 0 (Receptors, Thrombin); 0 (alpha-smooth muscle actin, mouse)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:111216
[Lr] Data última revisão:
111216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111217
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.111.240507



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