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  1 / 2651 MEDLINE  
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[PMID]:29352318
[Au] Autor:William D; Walther M; Schneider B; Linnebacher M; Classen CF
[Ad] Endereço:University Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.
[Ti] Título:Temozolomide-induced increase of tumorigenicity can be diminished by targeting of mitochondria in in vitro models of patient individual glioblastoma.
[So] Source:PLoS One;13(1):e0191511, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor with a dismal prognosis. Development of resistance towards cytostatic drugs like the GBM standard drug temozolomide is a severe problem in GBM treatment. One potential source of GBM relapse could be so called cancer stem like cells (CSCs). These represent an undifferentiated subpopulation of cells with high potential for tumor initiation. Furthermore, it has been shown that differentiated GBM cells can regain CSC properties when exposed to continuous temozolomide treatment in vitro. In this study, treatment of several primary GBM cell lines with clinically relevant doses of temozolomide increased their tumorigenicity as determined by colony formation assays in soft agar. Increased tumorigenicity is a known property of CSCs. Hence, therapy options that specifically target CSCs are under investigation. CSCs appear to be particularly dependent on mitochondria biogenesis which may represent a useful target for CSC elimination. Toxicity towards mitochondria is a known side effect of several antibiotics. Thus, addition of antibiotics like doxycycline may represent a useful tool to inhibit CSCs in GBM. Here, we show that combining temozolomide treatment of primary GBM cells with doxycycline could counteract the increase of tumorigenicity induced by temozolomide treatment.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/efeitos adversos
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/patologia
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/patologia
[Mh] Termos MeSH secundário: Antibacterianos/administração & dosagem
Antineoplásicos Alquilantes/administração & dosagem
Biomarcadores Tumorais/metabolismo
Neoplasias Encefálicas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Metilases de Modificação do DNA/genética
Enzimas Reparadoras do DNA/genética
Dacarbazina/administração & dosagem
Dacarbazina/efeitos adversos
Doxiciclina/administração & dosagem
Resistência a Medicamentos Antineoplásicos
Fucosiltransferases/metabolismo
Glioblastoma/metabolismo
Seres Humanos
Antígeno Lewis X/metabolismo
Mitocôndrias/efeitos dos fármacos
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Nestina/metabolismo
Ensaio Tumoral de Célula-Tronco
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antineoplastic Agents, Alkylating); 0 (Biomarkers, Tumor); 0 (Lewis X Antigen); 0 (NES protein, human); 0 (Nestin); 0 (Tumor Suppressor Proteins); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases); EC 6.5.1.- (DNA Repair Enzymes); N12000U13O (Doxycycline); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191511


  2 / 2651 MEDLINE  
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[PMID]:29375111
[Au] Autor:Xie D; Liao Y; Wu B; Chen Y; Lin W; Lu D; Gao S; Zhu S; Peng C; Jiang MH
[Ad] Endereço:Department of Cardiology, The Third Affiliated Hospital, Sun Yat-sen University.
[Ti] Título:Cardiac Nestin Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells.
[So] Source:Int Heart J;59(1):180-189, 2018.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Dilated cardiomyopathy (DCM), as one of the common cardiomyopathies, is a disease of the heart muscle; however, the etiology and pathogenesis of DCM were still poorly understood. Nestin has been reported a special marker of stem/progenitor cells in various tissues, and the tissue resident Nestin cells could promote the wound healing and tissue remodeling. However, it remains unclear whether Nestin cells participate in the protection of cardiomyocytes during the pathogenesis of DCM. Here the model of mice DCM was induced by doxorubicin (DOX) intraperitoneal injection and observed heart failure and ventricular enlargement via echocardiography and histologic analysis, respectively. During DCM pathogenesis, the number of Nestin cells showed a significant peak on day 6 after DOX treatment, which then gradually decreases to lower than normal levels after day 30 in the total population of the heart. Furthermore, we found that the isolated increased heart-derived Nestin cells are mesenchymal property and could protect DOX-induced HL-1 cells toxicity in vitro by promoting their proliferation and inhibiting their apoptosis. Collectively, our results showed that Nestin cells increased during DCM pathogenesis and played an important role in protecting against the DOX-induced HL-1 cells loss via regulating proliferation and apoptosis. Thus, the loss of Nestin cells might be an etiology to DCM pathogenesis, and these cells could be a promising candidate cell source for study and treatment of DCM patients.
[Mh] Termos MeSH primário: Apoptose
Cardiomiopatia Dilatada/genética
Regulação da Expressão Gênica
Ventrículos do Coração/metabolismo
Nestina/genética
RNA/genética
Função Ventricular Esquerda/fisiologia
[Mh] Termos MeSH secundário: Animais
Cardiomiopatia Dilatada/patologia
Cardiomiopatia Dilatada/fisiopatologia
Células Cultivadas
Modelos Animais de Doenças
Doxorrubicina/toxicidade
Ecocardiografia
Citometria de Fluxo
Ventrículos do Coração/patologia
Ventrículos do Coração/fisiopatologia
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Miócitos Cardíacos/patologia
Nestina/biossíntese
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nestin); 63231-63-0 (RNA); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.17-014


  3 / 2651 MEDLINE  
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[PMID]:28805814
[Au] Autor:Wojcinski A; Lawton AK; Bayin NS; Lao Z; Stephen DN; Joyner AL
[Ad] Endereço:Developmental Biology Program, Sloan Kettering Institute, New York, New York, USA.
[Ti] Título:Cerebellar granule cell replenishment postinjury by adaptive reprogramming of Nestin progenitors.
[So] Source:Nat Neurosci;20(10):1361-1370, 2017 Oct.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regeneration of several organs involves adaptive reprogramming of progenitors, but the intrinsic capacity of the developing brain to replenish lost cells remains largely unknown. Here we found that the developing cerebellum has unappreciated progenitor plasticity, since it undergoes near full growth and functional recovery following acute depletion of granule cells, the most plentiful neuron population in the brain. We demonstrate that following postnatal ablation of granule cell progenitors, Nestin-expressing progenitors, specified during mid-embryogenesis to produce astroglia and interneurons, switch their fate and generate granule neurons in mice. Moreover, Hedgehog signaling in two Nestin-expressing progenitor populations is crucial not only for the compensatory replenishment of granule neurons but also for scaling interneuron and astrocyte numbers. Thus, we provide insights into the mechanisms underlying robustness of circuit formation in the cerebellum and speculate that adaptive reprogramming of progenitors in other brain regions plays a greater role than appreciated in developmental regeneration.
[Mh] Termos MeSH primário: Cerebelo/fisiologia
Nestina/fisiologia
Células-Tronco Neurais/fisiologia
Neurogênese/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/fisiologia
Cerebelo/efeitos da radiação
Feminino
Proteínas Hedgehog/fisiologia
Interneurônios/fisiologia
Masculino
Camundongos
Camundongos Transgênicos
Nestina/metabolismo
Células-Tronco Neurais/metabolismo
Neurônios/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (Nestin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4621


  4 / 2651 MEDLINE  
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[PMID]:28771552
[Au] Autor:Chen J; Mao S; Li H; Zheng M; Yi L; Lin JM; Lin ZX
[Ad] Endereço:Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
[Ti] Título:The pathological structure of the perivascular niche in different microvascular patterns of glioblastoma.
[So] Source:PLoS One;12(8):e0182183, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The perivascular niche is critical for intercellular communication between resident cell types in glioblastoma (GBM), and it plays a vital role in maintaining the glioma stem cell (GSC) microenvironment. It is shown in abundant research that different microvascular patterns exist in GBM; and it can be implied that different microvascular patterns are associated with different pathological structures in the perivascular niche. However, the pathological structure of the perivascular niche is still not clear. Here, we investigated the distribution and biological characteristics of different microvascular pattern niches (MVPNs) in GBM by detecting the expression of CD34, CD133, Nestin, α-SMA, GFAP and CD14 in the perivascular niche using multiple -fluorescence. The four basic microvascular patterns are microvascular sprouting (MS), vascular cluster (VC), vascular garland (VG), and glomeruloid vascular proliferation (GVP). By analyzing the proportion of the area of each marker in four types of formations, the results indicated that the expression of CD34, CD133 and Nestin in MS and VC was significantly lower than that in VG and GVP (P<0.05). Furthermore, the results showed that α-SMA expression different in the MS, VC, VG and GVP (P<0.05). However, the expression of GFAP and CD14 in each type of formation exhibited no significant difference (P>0.05). According to the area distributions of different markers, we mapped four precise simulation diagrams to provide an effective foundation for the accurate simulation of glioblastoma in vitro.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia
Glioblastoma/patologia
Microvasos/patologia
[Mh] Termos MeSH secundário: Antígeno AC133/metabolismo
Actinas/metabolismo
Adolescente
Adulto
Idoso
Antígenos CD34/metabolismo
Feminino
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Receptores de Lipopolissacarídeos/metabolismo
Masculino
Microscopia de Fluorescência
Microvasos/metabolismo
Meia-Idade
Nestina/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (ACTA2 protein, human); 0 (Actins); 0 (Antigens, CD34); 0 (Glial Fibrillary Acidic Protein); 0 (Lipopolysaccharide Receptors); 0 (Nestin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182183


  5 / 2651 MEDLINE  
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[PMID]:28758904
[Au] Autor:Balani DH; Ono N; Kronenberg HM
[Ad] Endereço:Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:Parathyroid hormone regulates fates of murine osteoblast precursors in vivo.
[So] Source:J Clin Invest;127(9):3327-3338, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Teriparatide, a recombinant form of parathyroid hormone (PTH), is the only approved treatment for osteoporosis that increases the rate of bone formation. Teriparatide increases osteoblast numbers by suppressing osteoblast apoptosis and activating bone-lining cells. No direct evidence for teriparatide's actions on early cells of the osteoblast lineage has been demonstrated. Here, we have employed a lineage-tracing strategy that uses a tamoxifen-dependent, promoter-driven cre to mark early cells of the osteoblast lineage in adult mice. We show that teriparatide increases the numbers of osteoblast precursors and drives their differentiation into mature osteoblasts. Unexpectedly, following withdrawal of teriparatide therapy, bone marrow adipocytes increased dramatically in number. Some of these adipocytes derived from cells marked by Sox9-cre expression weeks earlier. Continued therapy with teriparatide prevented the appearance of adipocytes. Selective, inducible deletion of the PTH receptor in Sox9-cre cells demonstrated that PTH receptor expression is required for teriparatide-mediated increases in early osteoblast precursors. The increase in early precursors after teriparatide administration was associated with robust suppression of precursor apoptosis without affecting their rate of proliferation. Thus, teriparatide increases the numbers of early cells of the osteoblast lineage, hastens their differentiation into osteoblasts, and suppresses their differentiation into adipocytes in vivo.
[Mh] Termos MeSH primário: Linhagem da Célula
Osteoblastos/citologia
Hormônio Paratireóideo/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adipócitos/metabolismo
Animais
Apoptose
Diferenciação Celular
Proliferação Celular
Genes Reporter
Proteínas de Fluorescência Verde/genética
Camundongos
Camundongos Transgênicos
Nestina/genética
Osteoblastos/metabolismo
Osteócitos/citologia
Osteócitos/metabolismo
Osteogênese
Osteoporose/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Transcrição SOX9/genética
Teriparatida/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nes protein, mouse); 0 (Nestin); 0 (Parathyroid Hormone); 0 (SOX9 Transcription Factor); 0 (Sox9 protein, mouse); 10T9CSU89I (Teriparatide); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE


  6 / 2651 MEDLINE  
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[PMID]:28728846
[Au] Autor:Du Z; Cai C; Sims M; Boop FA; Davidoff AM; Pfeffer LM
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Center for Cancer Research, Memphis, TN, USA.
[Ti] Título:The effects of type I interferon on glioblastoma cancer stem cells.
[So] Source:Biochem Biophys Res Commun;491(2):343-348, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastomas (GBMs) are highly invasive brain tumors that are extremely deadly. The highly aggressive nature of GBM as well as its heterogeneity at the molecular and cellular levels has been attributed to a rare subpopulation of GBM stem-like cells (GSCs). Interferons (IFNs) are a family of endogenous antiviral proteins that have anticancer activity in vitro, and have been used clinically to treat GBM. IFN inhibits the proliferation of various established GBM cell lines, but the effects of IFNs on GSCs remain relatively unknown. The present study explored the effects of IFN on the proliferation and the differentiation capacity of GSCs isolated from GBM patient-derived xenolines (PDXs) grown as xenografts in immunocompromised mice. We show that IFN inhibits the proliferation of GSCs, inhibits the sphere forming capacity of GSCs that is a hallmark of cancer stem cells, and inhibits the ability of GSCs to differentiate into astrocytic cells. In addition, we show that IFN induces transient STAT3 activation in GSCs, while induction of astrocytic differentiation in GSCs results in sustained STAT3 activation.
[Mh] Termos MeSH primário: Astrócitos/efeitos dos fármacos
Interferon Tipo I/farmacologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Esferoides Celulares/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antígeno AC133/genética
Antígeno AC133/metabolismo
Animais
Astrócitos/metabolismo
Astrócitos/patologia
Biomarcadores/metabolismo
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/cirurgia
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Citocinas/genética
Citocinas/metabolismo
Expressão Gênica
Proteína Glial Fibrilar Ácida
Glioblastoma/genética
Glioblastoma/metabolismo
Glioblastoma/patologia
Glioblastoma/cirurgia
Xenoenxertos/crescimento & desenvolvimento
Xenoenxertos/metabolismo
Xenoenxertos/patologia
Seres Humanos
Camundongos
Camundongos Endogâmicos NOD
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Nestina/genética
Nestina/metabolismo
Fatores de Transcrição SOXB1/genética
Fatores de Transcrição SOXB1/metabolismo
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Esferoides Celulares/metabolismo
Esferoides Celulares/patologia
Ubiquitinas/genética
Ubiquitinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Biomarkers); 0 (Cytokines); 0 (Glial Fibrillary Acidic Protein); 0 (Interferon Type I); 0 (NES protein, human); 0 (Nestin); 0 (PROM1 protein, human); 0 (SOX2 protein, human); 0 (SOXB1 Transcription Factors); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Ubiquitins); 60267-61-0 (ISG15 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


  7 / 2651 MEDLINE  
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[PMID]:28683107
[Au] Autor:Coste C; Neirinckx V; Sharma A; Agirman G; Rogister B; Foguenne J; Lallemend F; Gothot A; Wislet S
[Ad] Endereço:GIGA Neurosciences, University of Liège, Liège, Belgium.
[Ti] Título:Human bone marrow harbors cells with neural crest-associated characteristics like human adipose and dermis tissues.
[So] Source:PLoS One;12(7):e0177962, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adult neural crest stem-derived cells (NCSC) are of extraordinary high plasticity and promising candidates for use in regenerative medicine. Several locations such as skin, adipose tissue, dental pulp or bone marrow have been described in rodent, as sources of NCSC. However, very little information is available concerning their correspondence in human tissues, and more precisely for human bone marrow. The main objective of this study was therefore to characterize NCSC from adult human bone marrow. In this purpose, we compared human bone marrow stromal cells to human adipose tissue and dermis, already described for containing NCSC. We performed comparative analyses in terms of gene and protein expression as well as functional characterizations. It appeared that human bone marrow, similarly to adipose tissue and dermis, contains NESTIN+ / SOX9+ / TWIST+ / SLUG+ / P75NTR+ / BRN3A+/ MSI1+/ SNAIL1+ cells and were able to differentiate into melanocytes, Schwann cells and neurons. Moreover, when injected into chicken embryos, all those cells were able to migrate and follow endogenous neural crest migration pathways. Altogether, the phenotypic characterization and migration abilities strongly suggest the presence of neural crest-derived cells in human adult bone marrow.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Células da Medula Óssea/citologia
Derme/citologia
Células Mesenquimais Estromais/citologia
Crista Neural/citologia
Células-Tronco Neurais/citologia
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Adulto
Animais
Biomarcadores/metabolismo
Células da Medula Óssea/metabolismo
Diferenciação Celular
Embrião de Galinha
Derme/metabolismo
Feminino
Expressão Gênica
Seres Humanos
Melanócitos/citologia
Melanócitos/metabolismo
Transplante de Células-Tronco Mesenquimais
Células Mesenquimais Estromais/metabolismo
Microinjeções
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Nestina/genética
Nestina/metabolismo
Crista Neural/crescimento & desenvolvimento
Crista Neural/metabolismo
Células-Tronco Neurais/metabolismo
Neurônios/citologia
Neurônios/metabolismo
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Proteínas de Ligação a RNA/genética
Proteínas de Ligação a RNA/metabolismo
Receptores de Fator de Crescimento Neural/genética
Receptores de Fator de Crescimento Neural/metabolismo
Fatores de Transcrição SOX9/genética
Fatores de Transcrição SOX9/metabolismo
Células de Schwann/citologia
Células de Schwann/metabolismo
Fatores de Transcrição da Família Snail/genética
Fatores de Transcrição da Família Snail/metabolismo
Fator de Transcrição Brn-3A/genética
Fator de Transcrição Brn-3A/metabolismo
Proteína 1 Relacionada a Twist/genética
Proteína 1 Relacionada a Twist/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (MSI1 protein, human); 0 (NES protein, human); 0 (NGFR protein, human); 0 (Nerve Tissue Proteins); 0 (Nestin); 0 (Nuclear Proteins); 0 (POU4F1 protein, human); 0 (RNA-Binding Proteins); 0 (Receptors, Nerve Growth Factor); 0 (SNAI1 protein, human); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); 0 (Snail Family Transcription Factors); 0 (TWIST1 protein, human); 0 (Transcription Factor Brn-3A); 0 (Twist-Related Protein 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177962


  8 / 2651 MEDLINE  
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[PMID]:28647374
[Au] Autor:Pan M; Weng Y; Sun Y
[Ad] Endereço:Department of Implantology, School & Hospital of Stomatology, Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai 200072, China.
[Ti] Título:Overexpression of Dentin matrix protein 1 in Nestin cells causes bone loss in mouse long bone.
[So] Source:Biochem Biophys Res Commun;490(2):356-363, 2017 Aug 19.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The well-known matrix protein Dentin matrix protein 1 (DMP1) is expressed by osteoblasts and osteocytes in bone, and it controls bone mineralization. Recently, it has been found that DMP1 is also expressed in other cell types, such as chondrocytes. Nestin cells are one important type of progenitor cell in bone marrow and are associated with bone remodeling. In our preliminary experiment, DMP1 could also be detected in Nestin cells in bone marrow. This study was designed to explore the effect on bone of DMP1 in Nestin cells. A transgenic mouse model with DMP1 expression driven by the Nestin promoter was generated. In vivo and in vitro experiments revealed that overexpression of DMP1 in Nestin cells could limit the proliferation and osteogenic differentiation of BMMSCs, subsequently leading to decreased bone mass. Lower expression of bone matrix protein and a lower bone deposition rate were also observed. Meanwhile, overexpression of DMP1 in Nestin cells had no influence on osteoclast activity. These data indicate that DMP1 plays negative roles in differentiation of Nestin cells and bone formation.
[Mh] Termos MeSH primário: Osso e Ossos/fisiopatologia
Proteínas da Matriz Extracelular/genética
Nestina/genética
Osteogênese
[Mh] Termos MeSH secundário: Animais
Densidade Óssea
Remodelação Óssea
Osso e Ossos/metabolismo
Osso e Ossos/patologia
Proliferação Celular
Proteínas da Matriz Extracelular/metabolismo
Regulação da Expressão Gênica
Masculino
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Células Mesenquimais Estromais/patologia
Camundongos
Camundongos Transgênicos
Nestina/metabolismo
Regiões Promotoras Genéticas
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dmp1 protein, mouse); 0 (Extracellular Matrix Proteins); 0 (Nes protein, mouse); 0 (Nestin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170626
[St] Status:MEDLINE


  9 / 2651 MEDLINE  
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[PMID]:28642362
[Au] Autor:Renault-Mihara F; Mukaino M; Shinozaki M; Kumamaru H; Kawase S; Baudoux M; Ishibashi T; Kawabata S; Nishiyama Y; Sugai K; Yasutake K; Okada S; Nakamura M; Okano H
[Ad] Endereço:Department of Physiology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan frenaultpro@yahoo.fr.
[Ti] Título:Regulation of RhoA by STAT3 coordinates glial scar formation.
[So] Source:J Cell Biol;216(8):2533-2550, 2017 Aug 07.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding how the transcription factor signal transducer and activator of transcription-3 (STAT3) controls glial scar formation may have important clinical implications. We show that astrocytic STAT3 is associated with greater amounts of secreted MMP2, a crucial protease in scar formation. Moreover, we report that STAT3 inhibits the small GTPase RhoA and thereby controls actomyosin tonus, adhesion turnover, and migration of reactive astrocytes, as well as corralling of leukocytes in vitro. The inhibition of RhoA by STAT3 involves ezrin, the phosphorylation of which is reduced in STAT3-CKO astrocytes. Reduction of phosphatase and tensin homologue (PTEN) levels in STAT3-CKO rescues reactive astrocytes dynamics in vitro. By specific targeting of lesion-proximal, reactive astrocytes in - mice, we show that reduction of PTEN rescues glial scar formation in mice. These findings reveal novel intracellular signaling mechanisms underlying the contribution of reactive astrocyte dynamics to glial scar formation.
[Mh] Termos MeSH primário: Astrócitos/enzimologia
Cicatriz/enzimologia
Neuroglia/enzimologia
Fator de Transcrição STAT3/metabolismo
Traumatismos da Medula Espinal/enzimologia
Medula Espinal/enzimologia
Ferimentos Perfurantes/enzimologia
Proteínas rho de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Actomiosina/metabolismo
Animais
Animais Recém-Nascidos
Astrócitos/patologia
Adesão Celular
Movimento Celular
Células Cultivadas
Cicatriz/genética
Cicatriz/patologia
Técnicas de Cocultura
Proteínas do Citoesqueleto/genética
Proteínas do Citoesqueleto/metabolismo
Modelos Animais de Doenças
Genótipo
Integrases/genética
Macrófagos/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
MicroRNAs/genética
MicroRNAs/metabolismo
Nestina/genética
Neuroglia/patologia
PTEN Fosfo-Hidrolase/genética
PTEN Fosfo-Hidrolase/metabolismo
Fenótipo
Fosforilação
Proteólise
Fator de Transcrição STAT3/deficiência
Fator de Transcrição STAT3/genética
Transdução de Sinais
Medula Espinal/patologia
Traumatismos da Medula Espinal/genética
Traumatismos da Medula Espinal/patologia
Transfecção
Ferimentos Perfurantes/genética
Ferimentos Perfurantes/patologia
Proteínas rho de Ligação ao GTP/genética
Quinases Associadas a rho/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (MIRN21 microRNA, mouse); 0 (MicroRNAs); 0 (Nes protein, mouse); 0 (Nestin); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (ezrin); 9013-26-7 (Actomyosin); EC 2.7.11.1 (rho-Associated Kinases); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201610102


  10 / 2651 MEDLINE  
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[PMID]:28552558
[Au] Autor:Jossin Y; Lee M; Klezovitch O; Kon E; Cossard A; Lien WH; Fernandez TE; Cooper JA; Vasioukhin V
[Ad] Endereço:Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA; Mammalian Development & Cell Biology Unit, Institute of Neuroscience, Université Catholique de Louvain, 1200 Brussels, Belgium. Electronic address: yves.jossin@uclouvain.be.
[Ti] Título:Llgl1 Connects Cell Polarity with Cell-Cell Adhesion in Embryonic Neural Stem Cells.
[So] Source:Dev Cell;41(5):481-495.e5, 2017 Jun 05.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malformations of the cerebral cortex (MCCs) are devastating developmental disorders. We report here that mice with embryonic neural stem-cell-specific deletion of Llgl1 (Nestin-Cre/Llgl1 ), a mammalian ortholog of the Drosophila cell polarity gene lgl, exhibit MCCs resembling severe periventricular heterotopia (PH). Immunohistochemical analyses and live cortical imaging of PH formation revealed that disruption of apical junctional complexes (AJCs) was responsible for PH in Nestin-Cre/Llgl1 brains. While it is well known that cell polarity proteins govern the formation of AJCs, the exact mechanisms remain unclear. We show that LLGL1 directly binds to and promotes internalization of N-cadherin, and N-cadherin/LLGL1 interaction is inhibited by atypical protein kinase C-mediated phosphorylation of LLGL1, restricting the accumulation of AJCs to the basolateral-apical boundary. Disruption of the N-cadherin-LLGL1 interaction during cortical development in vivo is sufficient for PH. These findings reveal a mechanism responsible for the physical and functional connection between cell polarity and cell-cell adhesion machineries in mammalian cells.
[Mh] Termos MeSH primário: Encéfalo/anormalidades
Adesão Celular/fisiologia
Polaridade Celular/fisiologia
Células-Tronco Embrionárias/fisiologia
Proteínas de Homeodomínio/fisiologia
Células-Tronco Neurais/fisiologia
Heterotopia Nodular Periventricular/patologia
Proteínas Supressoras de Tumor/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Encéfalo/metabolismo
Encéfalo/patologia
Caderinas/genética
Caderinas/metabolismo
Proliferação Celular
Células Cultivadas
Células-Tronco Embrionárias/citologia
Feminino
Camundongos
Camundongos Transgênicos
Nestina/genética
Nestina/metabolismo
Células-Tronco Neurais/citologia
Heterotopia Nodular Periventricular/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Homeodomain Proteins); 0 (Llgl1 protein, mouse); 0 (Nes protein, mouse); 0 (Nestin); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE



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