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  1 / 15007 MEDLINE  
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[PMID]:28457994
[Au] Autor:Kady N; Yan Y; Salazar T; Wang Q; Chakravarthy H; Huang C; Beli E; Navitskaya S; Grant M; Busik J
[Ad] Endereço:Department of Physiology, Michigan State University, East Lansing, MI, USA.
[Ti] Título:Increase in acid sphingomyelinase level in human retinal endothelial cells and CD34 circulating angiogenic cells isolated from diabetic individuals is associated with dysfunctional retinal vasculature and vascular repair process in diabetes.
[So] Source:J Clin Lipidol;11(3):694-703, 2017 May - Jun.
[Is] ISSN:1933-2874
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diabetic retinopathy is a microvascular disease that results from retinal vascular degeneration and defective repair due to diabetes-induced endothelial progenitor dysfunction. OBJECTIVE: Understanding key molecular factors involved in vascular degeneration and repair is paramount for developing effective diabetic retinopathy treatment strategies. We propose that diabetes-induced activation of acid sphingomyelinase (ASM) plays essential role in retinal endothelial and CD34 circulating angiogenic cell (CAC) dysfunction in diabetes. METHODS: Human retinal endothelial cells (HRECs) isolated from control and diabetic donor tissue and human CD34 CACs from control and diabetic patients were used in this study. ASM messenger RNA and protein expression were assessed by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. To evaluate the effect of diabetes-induced ASM on HRECs and CD34 CACs function, tube formation, CAC incorporation into endothelial tubes, and diurnal release of CD34 CACs in diabetic individuals were determined. RESULTS: ASM expression level was significantly increased in HRECs isolated from diabetic compared with control donor tissue, as well as CD34 CACs and plasma of diabetic patients. A significant decrease in tube area was observed in HRECs from diabetic donors compared with control HRECs. The tube formation deficiency was associated with increased expression of ASM in diabetic HRECs. Moreover, diabetic CD34 CACs with high ASM showed defective incorporation into endothelial tubes. Diurnal release of CD34 CACs was disrupted with the rhythmicity lost in diabetic patients. CONCLUSION: Collectively, these findings support that diabetes-induced ASM upregulation has a marked detrimental effect on both retinal endothelial cells and CACs.
[Mh] Termos MeSH primário: Retinopatia Diabética/enzimologia
Células Endoteliais/metabolismo
Neovascularização Patológica/patologia
Retina/patologia
Vasos Retinianos/fisiopatologia
Esfingomielina Fosfodiesterase/metabolismo
[Mh] Termos MeSH secundário: Idoso
Antígenos CD34/metabolismo
Ritmo Circadiano
Retinopatia Diabética/sangue
Retinopatia Diabética/patologia
Retinopatia Diabética/fisiopatologia
Células Endoteliais/patologia
Feminino
Regulação Enzimológica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Vasos Retinianos/metabolismo
Esfingomielina Fosfodiesterase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); EC 3.1.4.- (acid sphingomyelinase-1); EC 3.1.4.12 (Sphingomyelin Phosphodiesterase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  2 / 15007 MEDLINE  
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[PMID]:29360873
[Au] Autor:Xu SX; Leontyev D; Kaul R; Gray-Owen SD
[Ad] Endereço:Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:Neisseria gonorrhoeae co-infection exacerbates vaginal HIV shedding without affecting systemic viral loads in human CD34+ engrafted mice.
[So] Source:PLoS One;13(1):e0191672, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HIV synergy with sexually transmitted co-infections is well-documented in the clinic. Co-infection with Neisseria gonorrhoeae in particular, increases genital HIV shedding and mucosal transmission. However, no animal model of co-infection currently exists to directly explore this relationship or to bridge the gap in understanding between clinical and in vitro studies of this interaction. This study aims to test the feasibility of using a humanized mouse model to overcome this barrier. Combining recent in vivo modelling advancements in both HIV and gonococcal research, we developed a co-infection model by engrafting immunodeficient NSG mice with human CD34+ hematopoietic stem cells to generate humanized mice that permit both systemic HIV infection and genital N. gonorrhoeae infection. Systemic plasma and vaginal lavage titres of HIV were measured in order to assess the impact of gonococcal challenge on viral plasma titres and genital shedding. Engrafted mice showed human CD45+ leukocyte repopulation in blood and mucosal tissues. Systemic HIV challenge resulted in 104-105 copies/mL of viral RNA in blood by week 4 post-infection, as well as vaginal shedding of virus. Subsequent gonococcal challenge resulted in unchanged plasma HIV levels but higher viral shedding in the genital tract, which reflects published clinical observations. Thus, human CD34+ stem cell-transplanted NSG mice represent an experimentally tractable animal model in which to study HIV shedding during gonococcal co-infection, allowing dissection of molecular and immunological interactions between these pathogens, and providing a platform to assess future therapeutics aimed at reducing HIV transmission.
[Mh] Termos MeSH primário: Antígenos CD34/imunologia
Gonorreia/complicações
Infecções por HIV/complicações
HIV/fisiologia
Neisseria gonorrhoeae/isolamento & purificação
Vagina/virologia
Carga Viral
Eliminação de Partículas Virais
[Mh] Termos MeSH secundário: Animais
Feminino
Infecções por HIV/virologia
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD34)
[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:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191672


  3 / 15007 MEDLINE  
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[PMID]:28457753
[Au] Autor:Sadovnik I; Herrmann H; Eisenwort G; Blatt K; Hoermann G; Mueller N; Sperr WR; Valent P
[Ad] Endereço:Department of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Expression of CD25 on leukemic stem cells in BCR-ABL1 CML: Potential diagnostic value and functional implications.
[So] Source:Exp Hematol;51:17-24, 2017 07.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic myeloid leukemia (CML) is a stem cell-derived leukemia in which neoplastic cells exhibit the Philadelphia chromosome and the related oncoprotein BCR-ABL1. The disease is characterized by an accumulation of myeloid precursor cells in the peripheral blood and bone marrow (BM). A small fraction of neoplastic cells in the CML clone supposedly exhibits self-renewal and thus long-term disease-propagating ability. However, so far, little is known about the phenotype, function, and target expression profiles of these leukemic stem cells (LSCs). Recent data suggest that CML LSCs aberrantly express the interleukin-2 receptor alpha chain CD25. Whereas normal CD34 /CD38 BM stem cells display only low amounts of CD25 or lack CD25 altogether, CD34 /CD38 LSCs express CD25 strongly in more than 90% of all patients with untreated CML. As a result, CD25 can be used to identify and quantify CML LSCs. In addition, it has been shown that CD25 serves as a negative growth regulator of CML LSCs. Here, we review the value of CD25 as a novel marker and potential drug target in CML LSCs.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Proteínas de Fusão bcr-abl/metabolismo
Regulação Leucêmica da Expressão Gênica
Subunidade alfa de Receptor de Interleucina-2/biossíntese
Leucemia Mielogênica Crônica BCR-ABL Positiva/diagnóstico
Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo
Proteínas de Neoplasias/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Antígenos CD34/metabolismo
Células da Medula Óssea/metabolismo
Seres Humanos
Glicoproteínas de Membrana/metabolismo
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  4 / 15007 MEDLINE  
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[PMID]:29205259
[Au] Autor:Mainardi C; Ebinger M; Enkel S; Feuchtinger T; Teltschik HM; Eyrich M; Schumm M; Rabsteyn A; Schlegel P; Seitz C; Schwarze CP; Müller I; Greil J; Bader P; Schlegel PG; Martin D; Holzer U; Döring M; Handgretinger R; Lang P
[Ad] Endereço:Department of Paediatric Oncology, Children's University Hospital, University of Padova, Padova, Italy.
[Ti] Título:CD34 selected stem cell boosts can improve poor graft function after paediatric allogeneic stem cell transplantation.
[So] Source:Br J Haematol;180(1):90-99, 2018 01.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Poor graft function (PGF) is a severe complication of haematopoietic stem cell transplantation (HSCT) and administration of donor stem cell boosts (SCBs) represents a therapeutic option. We report 50 paediatric patients with PGF who received 61 boosts with CD34 selected peripheral blood stem cells (PBSC) after transplantation from matched unrelated (n = 25) or mismatched related (n = 25) donors. Within 8 weeks, a significant increase in median neutrophil counts (0·6 vs. 1·516 × 10 /l, P < 0·05) and a decrease in red blood cell and platelet transfusion requirement (median frequencies 1 and 7 vs. 0, P < 0·0001 and <0·001), were observed, and 78·8% of patients resolved one or two of their cytopenias. 36·5% had a complete haematological response. Median lymphocyte counts for CD3 , CD3 CD4 , CD19 and CD56 increased 8·3-, 14·2-, 22.- and 1·6-fold. The rate of de novo acute graft-versus-host disease (GvHD) grade I-III was only 6% and resolved completely. No GvHD grade IV or chronic GvHD occurred. Patients who responded to SCB displayed a trend toward better overall survival (OS) (P = 0·07). Thus, administration of CD34 selected SCBs from alternative donors is safe and effective. Further studies are warranted to clarify the impact on immune reconstitution and survival.
[Mh] Termos MeSH primário: Sobrevivência de Enxerto
Transplante de Células-Tronco Hematopoéticas
Células-Tronco Hematopoéticas
[Mh] Termos MeSH secundário: Adolescente
Adulto
Antígenos CD34/metabolismo
Linhagem da Célula
Criança
Pré-Escolar
Estudos de Coortes
Feminino
Doença Enxerto-Hospedeiro/etiologia
Hematopoese
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Transplante de Células-Tronco Hematopoéticas/métodos
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Lactente
Masculino
Prognóstico
Retratamento
Estudos Retrospectivos
Quimeras de Transplante
Condicionamento Pré-Transplante
Transplante Homólogo
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34)
[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:171206
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.15012


  5 / 15007 MEDLINE  
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[PMID]:29309785
[Au] Autor:Pathak V; Colah R; Ghosh K
[Ad] Endereço:Department of Haematogenetics, National Institute of Immunohaematology (ICMR), KEM Hospital, Parel 400012, Mumbai, India.
[Ti] Título:Plasmodium falciparum malaria skews globin gene expression balance in in-vitro haematopoietic stem cell culture system: Its implications in malaria associated anemia.
[So] Source:Exp Parasitol;185:29-38, 2018 Feb.
[Is] ISSN:1090-2449
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding the pathophysiology and associated host parasite interactions of the malaria infection is the prerequisite for developing effective prevention and treatment strategies. The exact mechanism underlying malaria associated ineffective and dyserythropoiesis is not yet fully understood. Being an important protein, haemoglobin serves as the main amino acid reservoir available to the intra-erythrocytic plasmodium. It is important to check the expression profiling of globin genes which may help us to understand host parasite interactions and its potential contribution to both infection and disease. Here, an in-vitro culture system was used to study the effect of different doses of Plasmodium falciparum on haematopoietic stem cell expansion, differentiation and expression of globin genes. Upon exposure to the different doses of P. falciparum parasites of strains 3D7, Dd2 and RKL9 (intact and lysed form) at different stages of erythroid development, cells demonstrated suppression in growth and differentiation. At almost all stages of erythroid development upon parasite exposure, the γ globin gene was found to be downregulated and the α/ß as well as α/non- α globin mRNA ratios in late stage erythroid cells were found to be reduced (p < .01) compared to the untreated controls. The imbalance in globin chain expression might be considered as one of the factors involved in malaria associated inappropriate erythropoietic responses.
[Mh] Termos MeSH primário: Anemia/etiologia
Regulação da Expressão Gênica/genética
Globinas/genética
Células-Tronco Hematopoéticas/parasitologia
Malária Falciparum/genética
[Mh] Termos MeSH secundário: Anemia/genética
Anemia/metabolismo
Antígenos CD34/sangue
Biomarcadores/metabolismo
Células Cultivadas
Eritrócitos/parasitologia
Eritrócitos/patologia
Células Eritroides/imunologia
Sangue Fetal/citologia
Globinas/metabolismo
Células-Tronco Hematopoéticas/metabolismo
Hemólise
Interações Hospedeiro-Parasita/genética
Seres Humanos
Malária Falciparum/complicações
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Biomarkers); 9004-22-2 (Globins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


  6 / 15007 MEDLINE  
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[PMID]:29324880
[Au] Autor:Zhao K; Zheng WW; Dong XM; Yin RH; Gao R; Li X; Liu JF; Zhan YQ; Yu M; Chen H; Ge CH; Ning HM; Yang XM; Li CY
[Ad] Endereço:State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
[Ti] Título:EDAG promotes the expansion and survival of human CD34+ cells.
[So] Source:PLoS One;13(1):e0190794, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:EDAG is multifunctional transcriptional regulator primarily expressed in the linloc-kit+Sca-1+ hematopoietic stem cells (HSC) and CD34+ progenitor cells. Previous studies indicate that EDAG is required for maintaining hematopoietic lineage commitment balance. Here using ex vivo culture and HSC transplantation models, we report that EDAG enhances the proliferative potential of human cord blood CD34+ cells, increases survival, prevents cell apoptosis and promotes their repopulating capacity. Moreover, EDAG overexpression induces rapid entry of CD34+ cells into the cell cycle. Gene expression profile analysis indicate that EDAG knockdown leads to down-regulation of various positive cell cycle regulators including cyclin A, B, D, and E. Together these data provides novel insights into EDAG in regulation of expansion and survival of human hematopoietic stem/progenitor cells.
[Mh] Termos MeSH primário: Antígenos CD34/metabolismo
Proliferação Celular/fisiologia
Sobrevivência Celular/fisiologia
Sangue Fetal/metabolismo
Células-Tronco Hematopoéticas/metabolismo
Proteínas Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Ciclo Celular/fisiologia
Células Cultivadas
Transplante de Células-Tronco de Sangue do Cordão Umbilical
Ciclinas/metabolismo
Feminino
Sangue Fetal/citologia
Células-Tronco Hematopoéticas/química
Seres Humanos
Subunidade gama Comum de Receptores de Interleucina/deficiência
Subunidade gama Comum de Receptores de Interleucina/genética
Camundongos Endogâmicos NOD
Camundongos Knockout
Camundongos SCID
Proteínas Nucleares/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Cyclins); 0 (HEMGN protein, human); 0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Nuclear Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190794


  7 / 15007 MEDLINE  
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[PMID]:29325250
[Au] Autor:Fu Y; Guan WY; Wu HY; Wu HY; Fan ZW; Ye Q; Meng FQ
[Ad] Endereço:Department of Pathology, Affiliated Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
[Ti] Título:[Myofibroma/myofibromatosis: a clinicopathologic analysis of 9 cases].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):45-50, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the clinical and histological features, diagnosis and differential diagnosis of myofibroma/myofibromatosis. The clinical data and pathology features of nine cases of myofibroma/myofibromatosis were collected from August 2011 to November 2016 in Affiliated Drum Tower Hospital, Nanjing University Medical School and Children's Hospital of Nanjing Medical University. Immunohistochemistry(IHC), PDGFRB molecular analysis and ETV6-NTRK3 gene fusion were performed and relevant literature reviewed. There were 7 males and 2 females, with age ranging from 3 days to 18 years (mean 5 years). The tumors were located in head and neck (eight cases) and trunk (one case). Clinically, the tumors presented as freely movable nodules. Microscopically, they appeared biphasic with alternating light- and dark-staining areas. The light-staining area consisted mainly of plump myoid spindle cells with eosinophilic cytoplasm arranged in nodules, short fascicles, or whorls.The dark-staining area was composed of round or polygonal cells with slightly hyperchromatic nuclei or small spindle cells arranged around a distinct hemangiopericytoma-like vascular pattern. IHC showed the tumor cells in the light-staining area were strongly positive for vimentin and SMA, while cells in dark-staining area were strongly positive for vimentin, and weakly for SMA. Tumor cells were negative for desmin, S-100 protein, h-Caldesmon, CD34 and STAT6. Analysis of PDGFRB mutations was performed in seven cases. Two cases showed 12 exon point mutation c. 1681 c>T(p.R561C), one case showed 14 exon point mutation c. 1998C>G (p.N666K). ETV6-NTRK3 gene fusion was not detected by fluorescence in situ hybridization in four patients under three years old. All cases were followed for 6 to 68 months, with two recurrences. Myofibroma/myofibromatosis is an uncommon benign myofibroblastic tumor of infancy and childhood. The tumor can appear biphasic, and may show PDGFRB point mutation which is of potential diagnostic value.
[Mh] Termos MeSH primário: Miofibroma
Miofibromatose
[Mh] Termos MeSH secundário: Adolescente
Antígenos CD34/análise
Proteínas de Ligação a Calmodulina/análise
Criança
Pré-Escolar
Desmina/análise
Diagnóstico Diferencial
Éxons
Feminino
Hemangiopericitoma/irrigação sanguínea
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Masculino
Mutação
Miofibroma/diagnóstico
Miofibroma/genética
Miofibroma/patologia
Miofibromatose/diagnóstico
Miofibromatose/genética
Miofibromatose/patologia
Receptor beta de Fator de Crescimento Derivado de Plaquetas/análise
Receptor beta de Fator de Crescimento Derivado de Plaquetas/genética
Proteínas S100/análise
Fator de Transcrição STAT6/análise
Vimentina/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Calmodulin-Binding Proteins); 0 (Desmin); 0 (S100 Proteins); 0 (STAT6 Transcription Factor); 0 (STAT6 protein, human); 0 (Vimentin); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.009


  8 / 15007 MEDLINE  
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[PMID]:29190781
[Au] Autor:Abe SI; Abe K; Zhang J; Harada T; Mizumoto G; Oshikawa H; Akiyama H; Shimamura K
[Ad] Endereço:Center for General Education, Kumamoto Health Science University, Kumamoto, Japan.
[Ti] Título:Roles of CD34+ cells and ALK5 signaling in the reconstruction of seminiferous tubule-like structures in 3-D re-aggregate culture of dissociated cells from neonatal mouse testes.
[So] Source:PLoS One;12(11):e0188705, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue reconstruction in vitro can provide, if successful, a refined and simple system to analyze the underlying mechanisms that drive the morphogenesis and maintain the ordered structure. We have recently succeeded in reconstruction of seminiferous cord-like and tubule-like structures using 3-D re-aggregate culture of dissociated testicular cells. In testis formation, endothelial cells that migrated from mesonephroi to embryonic gonads have been shown to be critical for development of testis cords, but how endothelial cells contribute to testis cord formation remains unknown. To decipher the roles of endothelial and peritubular cells in the reconstruction of cord-like and tubule-like structures, we investigated the behavior of CD34+ endothelial and p75+ cells, and peritubular myoid cells (PTMCs) in 3-D re-aggregate cultures of testicular cells. The results showed that these 3 types of cells had the capacity of re-aggregation on their own and with each other, and of segregation into 3 layers in a re-aggregate, which were very similar to interstitial and peritubular tissues in vivo. Observation of behaviors of fluorescent Sertoli cells and other non-fluorescent types of cells using testes from Sox9-EGFP transgenic mice showed dynamic cell movement and segregation in re-aggregate cultures. Cultures of testicular cells deprived of interstitial and peritubular cells resulted in dysmorphic structures, but re-addition of them restored tubule-like structures. Purified CD34+ cells in culture differentiated into p75+ cells and PTMCs. These results indicate that CD34+ cells differentiate into p75+ cells, which then differentiate into PTMCs. TGFß signaling inhibitors, SB431542 and ALK5i, disturbed the reconstruction of cord-like and tubule-like structures, and the latter compromised re-construction of interstitial-like and peritubular-like structures, as well as the proliferation of CD34+, p75+, PTMCs, and Sertoli cells, and their movement and differentiation. These results indicate that CD34+ cells and signaling through ALK5 play pivotal roles in the morphogenesis of interstitial-like, peritubular-like and cord-like structures.
[Mh] Termos MeSH primário: Antígenos CD34/imunologia
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Túbulos Seminíferos/anatomia & histologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Proliferação Celular
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Túbulos Seminíferos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Receptors, Transforming Growth Factor beta); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188705


  9 / 15007 MEDLINE  
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[PMID]:28110587
[Au] Autor:Giordano D; Loddo S; Laganà AS; Coppolino G; Zoccali G; Di Benedetto A; Santamaria A; Buemi M; D'Anna R
[Ad] Endereço:a Unit of Gynecology and Obstetrics, Department of Human Pathology in Adulthood and Childhood "G. Barresi" , University of Messina , Messina , Italy.
[Ti] Título:Peripheral blood CD34 cells as a novel and noninvasive early marker of first trimester miscarriage: results from a case-control analysis.
[So] Source:J Matern Fetal Neonatal Med;31(2):258-260, 2018 Jan.
[Is] ISSN:1476-4954
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To evaluate the levels of peripheral blood CD34 cells in women who subsequently had a spontaneous miscarriage (SM). MATERIALS AND METHODS: We enrolled 11 women who had SM, matching them for age, BMI and gestational age with 33 healthy pregnancies (controls). From a blood sample at 9th-11th weeks of pregnancy, we evaluated PAPP-A, free ß-hCG, T (suppressor and helper), NK, B, CD34 cells. RESULTS: In peripheral blood of women who had SM, PAPP-A and CD34 cells were significantly lower (p < 0.001) compared to control group. CONCLUSIONS: CD34 cell low level in peripheral blood is associated with increased risk of SM.
[Mh] Termos MeSH primário: Aborto Espontâneo/sangue
Antígenos CD34/sangue
Biomarcadores/sangue
Primeiro Trimestre da Gravidez/sangue
Proteína Plasmática A Associada à Gravidez/análise
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Feminino
Seres Humanos
Gravidez
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Biomarkers); EC 3.4.24.- (Pregnancy-Associated Plasma Protein-A)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1080/14767058.2016.1277703


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[PMID]:28976817
[Au] Autor:Eichler F; Duncan C; Musolino PL; Orchard PJ; De Oliveira S; Thrasher AJ; Armant M; Dansereau C; Lund TC; Miller WP; Raymond GV; Sankar R; Shah AJ; Sevin C; Gaspar HB; Gissen P; Amartino H; Bratkovic D; Smith NJC; Paker AM; Shamir E; O'Meara T; Davidson D; Aubourg P; Williams DA
[Ad] Endereço:From Massachusetts General Hospital and Harvard Medical School (F.E., P.L.M.), Dana-Farber and Boston Children's Cancer and Blood Disorders Center (C. Duncan, M.A., C. Dansereau, D.A.W.), and Boston Children's Hospital, Harvard Medical School, and Harvard Stem-Cell Institute (D.A.W.), Boston, and Bl
[Ti] Título:Hematopoietic Stem-Cell Gene Therapy for Cerebral Adrenoleukodystrophy.
[So] Source:N Engl J Med;377(17):1630-1638, 2017 10 26.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In X-linked adrenoleukodystrophy, mutations in ABCD1 lead to loss of function of the ALD protein. Cerebral adrenoleukodystrophy is characterized by demyelination and neurodegeneration. Disease progression, which leads to loss of neurologic function and death, can be halted only with allogeneic hematopoietic stem-cell transplantation. METHODS: We enrolled boys with cerebral adrenoleukodystrophy in a single-group, open-label, phase 2-3 safety and efficacy study. Patients were required to have early-stage disease and gadolinium enhancement on magnetic resonance imaging (MRI) at screening. The investigational therapy involved infusion of autologous CD34+ cells transduced with the elivaldogene tavalentivec (Lenti-D) lentiviral vector. In this interim analysis, patients were assessed for the occurrence of graft-versus-host disease, death, and major functional disabilities, as well as changes in neurologic function and in the extent of lesions on MRI. The primary end point was being alive and having no major functional disability at 24 months after infusion. RESULTS: A total of 17 boys received Lenti-D gene therapy. At the time of the interim analysis, the median follow-up was 29.4 months (range, 21.6 to 42.0). All the patients had gene-marked cells after engraftment, with no evidence of preferential integration near known oncogenes or clonal outgrowth. Measurable ALD protein was observed in all the patients. No treatment-related death or graft-versus-host disease had been reported; 15 of the 17 patients (88%) were alive and free of major functional disability, with minimal clinical symptoms. One patient, who had had rapid neurologic deterioration, had died from disease progression. Another patient, who had had evidence of disease progression on MRI, had withdrawn from the study to undergo allogeneic stem-cell transplantation and later died from transplantation-related complications. CONCLUSIONS: Early results of this study suggest that Lenti-D gene therapy may be a safe and effective alternative to allogeneic stem-cell transplantation in boys with early-stage cerebral adrenoleukodystrophy. Additional follow-up is needed to fully assess the duration of response and long-term safety. (Funded by Bluebird Bio and others; STARBEAM ClinicalTrials.gov number, NCT01896102 ; ClinicalTrialsRegister.eu number, 2011-001953-10 .).
[Mh] Termos MeSH primário: Transportadores de Cassetes de Ligação de ATP/uso terapêutico
Adrenoleucodistrofia/terapia
Terapia Genética
Vetores Genéticos
Transplante de Células-Tronco Hematopoéticas
Lentivirus
[Mh] Termos MeSH secundário: Membro 1 da Subfamília D de Transportadores de Cassetes de Ligação de ATP
Transportadores de Cassetes de Ligação de ATP/genética
Adolescente
Adrenoleucodistrofia/genética
Antígenos CD34/sangue
Biomarcadores/sangue
Criança
Terapia Combinada
Vetores Genéticos/sangue
Fator Estimulador de Colônias de Granulócitos/uso terapêutico
Células-Tronco Hematopoéticas/imunologia
Seres Humanos
Masculino
Reação em Cadeia da Polimerase
Transplante Autólogo
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (ABCD1 protein, human); 0 (ATP Binding Cassette Transporter, Sub-Family D, Member 1); 0 (Antigens, CD34); 0 (Biomarkers); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1700554



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