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Pesquisa : A11.284.295.588.750 [Categoria DeCS]
Referências encontradas : 3026 [refinar]
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[PMID]:29348617
[Au] Autor:Miranda AM; Lasiecka ZM; Xu Y; Neufeld J; Shahriar S; Simoes S; Chan RB; Oliveira TG; Small SA; Di Paolo G
[Ad] Endereço:Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, 10032, USA.
[Ti] Título:Neuronal lysosomal dysfunction releases exosomes harboring APP C-terminal fragments and unique lipid signatures.
[So] Source:Nat Commun;9(1):291, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Defects in endolysosomal and autophagic functions are increasingly viewed as key pathological features of neurodegenerative disorders. A master regulator of these functions is phosphatidylinositol-3-phosphate (PI3P), a phospholipid synthesized primarily by class III PI 3-kinase Vps34. Here we report that disruption of neuronal Vps34 function in vitro and in vivo impairs autophagy, lysosomal degradation as well as lipid metabolism, causing endolysosomal membrane damage. PI3P deficiency also promotes secretion of unique exosomes enriched for undigested lysosomal substrates, including amyloid precursor protein C-terminal fragments (APP-CTFs), specific sphingolipids, and the phospholipid bis(monoacylglycero)phosphate (BMP), which normally resides in the internal vesicles of endolysosomes. Secretion of these exosomes requires neutral sphingomyelinase 2 and sphingolipid synthesis. Our results reveal a homeostatic response counteracting lysosomal dysfunction via secretion of atypical exosomes eliminating lysosomal waste and define exosomal APP-CTFs and BMP as candidate biomarkers for endolysosomal dysfunction associated with neurodegenerative disorders.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Exossomos/metabolismo
Lipídeos/análise
Lisossomos/metabolismo
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/química
Animais
Autofagia/genética
Biomarcadores/metabolismo
Linhagem Celular Tumoral
Classe III de Fosfatidilinositol 3-Quinases/genética
Classe III de Fosfatidilinositol 3-Quinases/metabolismo
Células HEK293
Seres Humanos
Lisofosfolipídeos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monoglicerídeos/metabolismo
Doenças Neurodegenerativas/diagnóstico
Doenças Neurodegenerativas/metabolismo
Fragmentos de Peptídeos/metabolismo
Fosfatos de Fosfatidilinositol/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (Biomarkers); 0 (Lipids); 0 (Lysophospholipids); 0 (Monoglycerides); 0 (Peptide Fragments); 0 (Phosphatidylinositol Phosphates); 0 (bis(monoacylglyceryl)phosphate); 0 (phosphatidylinositol 3-phosphate); EC 2.7.1.137 (Class III Phosphatidylinositol 3-Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02533-w


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


  3 / 3026 MEDLINE  
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[PMID]:29295981
[Au] Autor:Kimura K; Hohjoh H; Fukuoka M; Sato W; Oki S; Tomi C; Yamaguchi H; Kondo T; Takahashi R; Yamamura T
[Ad] Endereço:Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502, Japan.
[Ti] Título:Circulating exosomes suppress the induction of regulatory T cells via let-7i in multiple sclerosis.
[So] Source:Nat Commun;9(1):17, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Multiple sclerosis (MS) is a T cell-mediated autoimmune disease of the central nervous system. Foxp3 regulatory T (Treg) cells are reduced in frequency and dysfunctional in patients with MS, but the underlying mechanisms of this deficiency are unclear. Here, we show that induction of human IFN-γ IL-17A Foxp3 CD4 T cells is inhibited in the presence of circulating exosomes from patients with MS. The exosomal miRNA profile of patients with MS differs from that of healthy controls, and let-7i, which is markedly increased in patients with MS, suppresses induction of Treg cells by targeting insulin like growth factor 1 receptor (IGF1R) and transforming growth factor beta receptor 1 (TGFBR1). Consistently, the expression of IGF1R and TGFBR1 on circulating naive CD4 T cells is reduced in patients with MS. Thus, our study shows that exosomal let-7i regulates MS pathogenesis by blocking the IGF1R/TGFBR1 pathway.
[Mh] Termos MeSH primário: Exossomos/imunologia
MicroRNAs/imunologia
Esclerose Múltipla/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Adulto
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Exossomos/genética
Exossomos/metabolismo
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Seres Humanos
Interleucina-17/genética
Interleucina-17/imunologia
Interleucina-17/metabolismo
Masculino
MicroRNAs/genética
Meia-Idade
Esclerose Múltipla/sangue
Esclerose Múltipla/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/imunologia
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Somatomedina/genética
Receptores de Somatomedina/imunologia
Receptores de Somatomedina/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/imunologia
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Linfócitos T Reguladores/metabolismo
Transcriptoma/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (IGF1R protein, human); 0 (IL17A protein, human); 0 (Interleukin-17); 0 (MicroRNAs); 0 (Receptors, Somatomedin); 0 (Receptors, Transforming Growth Factor beta); 0 (mirnlet7 microRNA, human); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02406-2


  4 / 3026 MEDLINE  
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[PMID]:29184401
[Au] Autor:Pillay P; Moodley K; Moodley J; Mackraj I
[Ad] Endereço:Discipline of Human Physiology, Nelson R Mandela School of Medicine, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.
[Ti] Título:Placenta-derived exosomes: potential biomarkers of preeclampsia.
[So] Source:Int J Nanomedicine;12:8009-8023, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Preeclampsia remains a leading cause of maternal and fetal mortality, due to ineffective treatment and diagnostic strategies, compounded by the lack of clarity on the etiology of the disorder. Although several clinical and biological markers of preeclampsia have been evaluated, they have proven to be ineffective in providing a definitive diagnosis during the various stages of the disorder. Exosomes have emerged as ideal biomarkers of pathological states, such as cancer, and have more recently gained interest in pregnancy-related complications, due to their role in cellular communication in normal and complicated pregnancies. This occurs as a result of the specific placenta-derived exosomal molecular cargo, which may be involved in normal pregnancy-associated immunological events, such as the maintenance of maternal-fetal tolerance. This review provides perspectives on placenta-derived exosomes as possible biomarkers for the diagnosis/prognosis of preeclampsia. Using keywords, online databases were searched to identify relevant publications to review the potential use of placenta-derived exosomes as biomarkers of preeclampsia.
[Mh] Termos MeSH primário: Biomarcadores/análise
Exossomos/patologia
Placenta/citologia
Pré-Eclâmpsia/patologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Placenta/patologia
Pré-Eclâmpsia/diagnóstico
Gravidez
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S142732


  5 / 3026 MEDLINE  
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[PMID]:28460630
[Au] Autor:Moen A; Jacobsen D; Phuyal S; Legfeldt A; Haugen F; Røe C; Gjerstad J
[Ad] Endereço:National Institute of Occupational Health, Pb 8149 Dep., 0033, Oslo, Norway.
[Ti] Título:MicroRNA-223 demonstrated experimentally in exosome-like vesicles is associated with decreased risk of persistent pain after lumbar disc herniation.
[So] Source:J Transl Med;15(1):89, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previous findings have demonstrated that lumbar radicular pain after disc herniation may be associated with up-regulation of inflammatory mediators. In the present study we examined the possible role of extracellular microRNAs (miRs) in this process. METHODS: Single unit recordings, isolation of exosome-like vesicles, electron microscopy, nanoparticle tracking analysis, western blot analysis and qPCR were used in rats to demonstrate the effect of nucleus pulposus (NP) applied onto the dorsal nerve roots. ELISA and qPCR were used to measure the level of circulating IL-6 and miRs in a 1-year observational study in patients after disc herniation. RESULTS: In the rats, enhanced spinal cord nociceptive responses were displayed after NP applied onto the dorsal nerve roots. An increased release of small non-coding RNAs, including miR-223, miR-760 and miR-145, from NP in exosome-like vesicles was demonstrated. In particular, the NP expression of miR-223, which inhibited the nociceptive spinal signalling, was increased. In the patients, increased extracellular miR-223 was also verified in the acute phase after disc herniation. The increased miR-223 expression was, however, only observed in those who recovered (sex, age and smoking were included as covariates). CONCLUSIONS: Our findings suggest that miR-223, which can be released from the NP after disc herniation, attenuates the neuronal activity in the pain pathways. Dysregulation of miR-223 may predict chronic lumbar radicular pain. Trial registration/ethics REK 2014/1725.
[Mh] Termos MeSH primário: Exossomos/metabolismo
Deslocamento do Disco Intervertebral/complicações
Vértebras Lombares/patologia
MicroRNAs/metabolismo
Dor/etiologia
Dor/genética
[Mh] Termos MeSH secundário: Adulto
Animais
Exossomos/ultraestrutura
Feminino
Seres Humanos
Deslocamento do Disco Intervertebral/patologia
Deslocamento do Disco Intervertebral/fisiopatologia
Vértebras Lombares/fisiopatologia
Masculino
MicroRNAs/genética
Meia-Idade
Ratos Endogâmicos Lew
Recuperação de Função Fisiológica
Fatores de Risco
Regulação para Cima/genética
Escala Visual Analógica
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (MIRN223 microRNA, human); 0 (MIRN223 microRNA, rat); 0 (MicroRNAs)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1194-8


  6 / 3026 MEDLINE  
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[PMID]:29421439
[Au] Autor:Li B; Mao R; Liu C; Zhang W; Tang Y; Guo Z
[Ad] Endereço:Department of Interventional Therapy, Tianjin Medical University Cancer Institute and Hospital, Chinese National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China. Electronic address: libao_gr6688@163.com.
[Ti] Título:LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells.
[So] Source:Life Sci;197:122-129, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Long non-coding RNAs (LncRNAs) have been demonstrated to play crucial role in tumor growth and metastasis for hepatocellular carcinoma (HCC). LncRNA FAL1 has been indicated to promote the progression of various cancers. However, the role of lncRNA FAL1 in HCC was poorly understood. METHODS: The expression levels of lncRNA FAL1 in HCC tissues and cells were determined by RT-qPCR. The roles of lncRNA FAL1 on HCC cells were investigated by MTT, colony formation, transwell, RT-qPCR, and Western blotting. The miRNA binding sites of lncRNA FAL1 was predicted using RegRNA 2.0 and miR-1236 was validated to target lncRNA FAL1 by luciferase reporter assays and RT-qPCR. Finally, the expression levels of lncRNA FAL1 in serum exosome of HCC patients was also investigated and the role of exosome-mediated lncRNA FAL1 was further investigated by co-culturing with HCC cells. RESULTS: This study first showed that lncRNA FAL1 was up-regulated in HCC tissues and functioned as an oncogene in HCC. LncRNA FAL1 could accelerate cell proliferation and metastasis as a ceRNA mechanism by competitively binding to miR-1236. Moreover, lncRNA FAL1 was also up-regulated in serum exosome of HCC patients and could transfer lncRNA FAL1 to HCC cells to increase their abilities of cell proliferation and migration. CONCLUSIONS: Taken together, this study indicated that lncRNA FAL1 functions as an oncogenic in HCC and may be a novel diagnostic biomarker or a novel target for the treatment of HCC in future.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Movimento Celular
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/metabolismo
MicroRNAs/biossíntese
RNA Longo não Codificante/biossíntese
RNA Neoplásico/biossíntese
Regulação para Cima
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Exossomos/genética
Exossomos/metabolismo
Exossomos/patologia
Feminino
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Masculino
MicroRNAs/genética
RNA Longo não Codificante/genética
RNA Neoplásico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN1236 microRNA, human); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, Neoplasm); 0 (focally amplified long noncoding RNA on chromosome 1, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


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[PMID]:29335551
[Au] Autor:Fang T; Lv H; Lv G; Li T; Wang C; Han Q; Yu L; Su B; Guo L; Huang S; Cao D; Tang L; Tang S; Wu M; Yang W; Wang H
[Ad] Endereço:International Co-operation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, 200438, China.
[Ti] Título:Tumor-derived exosomal miR-1247-3p induces cancer-associated fibroblast activation to foster lung metastasis of liver cancer.
[So] Source:Nat Commun;9(1):191, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The communication between tumor-derived elements and stroma in the metastatic niche has a critical role in facilitating cancer metastasis. Yet, the mechanisms tumor cells use to control metastatic niche formation are not fully understood. Here we report that in the lung metastatic niche, high-metastatic hepatocellular carcinoma (HCC) cells exhibit a greater capacity to convert normal fibroblasts to cancer-associated fibroblasts (CAFs) than low-metastatic HCC cells. We show high-metastatic HCC cells secrete exosomal miR-1247-3p that directly targets B4GALT3, leading to activation of ß1-integrin-NF-κB signaling in fibroblasts. Activated CAFs further promote cancer progression by secreting pro-inflammatory cytokines, including IL-6 and IL-8. Clinical data show high serum exosomal miR-1247-3p levels correlate with lung metastasis in HCC patients. These results demonstrate intercellular crosstalk between tumor cells and fibroblasts is mediated by tumor-derived exosomes that control lung metastasis of HCC, providing potential targets for prevention and treatment of cancer metastasis.
[Mh] Termos MeSH primário: Fibroblastos Associados a Câncer/metabolismo
Carcinoma Hepatocelular/metabolismo
Exossomos/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/metabolismo
Neoplasias Pulmonares/metabolismo
MicroRNAs/genética
N-Acetil-Lactosamina Sintase/genética
[Mh] Termos MeSH secundário: Animais
Fibroblastos Associados a Câncer/patologia
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/secundário
Comunicação Celular
Linhagem Celular Tumoral
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Exossomos/química
Seres Humanos
Integrina beta1/genética
Integrina beta1/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/secundário
Masculino
Camundongos
Camundongos Nus
MicroRNAs/secreção
N-Acetil-Lactosamina Sintase/metabolismo
Invasividade Neoplásica
Transplante de Neoplasias
Células Neoplásicas Circulantes/metabolismo
Células Neoplásicas Circulantes/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Integrin beta1); 0 (Interleukin-6); 0 (Interleukin-8); 0 (MIRN1247 microRNA, human); 0 (MicroRNAs); EC 2.4.1.90 (N-Acetyllactosamine Synthase)
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02583-0


  8 / 3026 MEDLINE  
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[PMID]:28468249
[Au] Autor:Santos TG; Martins VR; Hajj GNM
[Ad] Endereço:International Research Center, A.C. Camargo Cancer Center, São Paulo 01508-010, Brazil. tsantos@cipe.accamargo.org.br.
[Ti] Título:Unconventional Secretion of Heat Shock Proteins in Cancer.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 29.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Heat shock proteins (HSPs) are abundant cellular proteins involved with protein homeostasis. They have both constitutive and inducible isoforms, whose expression levels are further increased by stress conditions, such as temperature elevation, reduced oxygen levels, infection, inflammation and exposure to toxic substances. In these situations, HSPs exert a pivotal role in offering protection, preventing cell death and promoting cell recovery. Although the majority of HSPs functions are exerted in the cytoplasm and organelles, several lines of evidence reveal that HSPs are able to induce cell responses in the extracellular milieu. HSPs do not possess secretion signal peptides, and their secretion was subject to widespread skepticism until the demonstration of the role of unconventional secretion forms such as exosomes. Secretion of HSPs may confer immune system modulation and be a cell-to-cell mediated form of increasing stress resistance. Thus, there is a wide potential for secreted HSPs in resistance of cancer therapy and in the development new therapeutic strategies.
[Mh] Termos MeSH primário: Exossomos/metabolismo
Proteínas de Choque Térmico/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Animais
Exossomos/imunologia
Exossomos/patologia
Proteínas de Choque Térmico/análise
Proteínas de Choque Térmico/imunologia
Seres Humanos
Imunomodulação
Neoplasias/imunologia
Neoplasias/patologia
Neoplasias/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Heat-Shock Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  9 / 3026 MEDLINE  
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[PMID]:29223394
[Au] Autor:Zhang A; Li D; Liu Y; Li J; Zhang Y; Zhang CY
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, Nanjing Advanced Institute for Life Sciences, Nanjing University School of Life Sciences, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, Nanjing University, Nanjing, China; Department of Gerontology, The First Affilia
[Ti] Título:Islet ß cell: An endocrine cell secreting miRNAs.
[So] Source:Biochem Biophys Res Commun;495(2):1648-1654, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pancreas is an important endocrine organ. Pancreatic beta (ß) cells secrete insulin to regulate the metabolism of glucose and maintain the stability of blood glucose. MicroRNAs (miRNAs), small (20-25 nt) non-coding RNA molecules, function in target gene silencing through post-transcriptional patterns, and multiple miRNAs regulate insulin secretion, insulin signaling pathways in pancreatic ß cells and islet activity. In recent years, it has been found that many types of cells can secrete regulatory miRNA, but whether islet cells can secrete miRNA has not been clarified yet. In this study, we detected miRNA expressions in cell culture medium of primary mouse islet cells and islet cell line MIN6. And we found that islet cells can selectively and actively secrete miRNAs, mainly through the way of exosome package, and that miRNA secretion profiling patterns vary according to different insulin secretion stimulating conditions (high Glucose, high Kcl, high Arginine and high Free fat acid (FFA)). Additionally, we found that these miRNAs secreted by islet cells can be transported and have gene-regulating functions on recipient tissue cells, such as liver and muscles. In conclusion, we find another secretory function of the islet ß cells: not only insulin, but also miRNAs.
[Mh] Termos MeSH primário: Células Secretoras de Insulina/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Animais
Comunicação Celular
Linhagem Celular
Células Cultivadas
Exossomos/metabolismo
Regulação da Expressão Gênica
Glucose/metabolismo
Insulina/secreção
Células Secretoras de Insulina/secreção
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
MicroRNAs/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insulin); 0 (MicroRNAs); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


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[PMID]:29293592
[Au] Autor:Lankford KL; Arroyo EJ; Nazimek K; Bryniarski K; Askenase PW; Kocsis JD
[Ad] Endereço:Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
[Ti] Título:Intravenously delivered mesenchymal stem cell-derived exosomes target M2-type macrophages in the injured spinal cord.
[So] Source:PLoS One;13(1):e0190358, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In a previous report we showed that intravenous infusion of bone marrow-derived mesenchymal stem cells (MSCs) improved functional recovery after contusive spinal cord injury (SCI) in the non-immunosuppressed rat, although the MSCs themselves were not detected at the spinal cord injury (SCI) site [1]. Rather, the MSCs lodged transiently in the lungs for about two days post-infusion. Preliminary studies and a recent report [2] suggest that the effects of intravenous (IV) infusion of MSCs could be mimicked by IV infusion of exosomes isolated from conditioned media of MSC cultures (MSCexos). In this study, we assessed the possible mechanism of MSCexos action on SCI by investigating the tissue distribution and cellular targeting of DiR fluorescent labeled MSCexos at 3 hours and 24 hours after IV infusion in rats with SCI. The IV delivered MSCexos were detected in contused regions of the spinal cord, but not in the noninjured region of the spinal cord, and were also detected in the spleen, which was notably reduced in weight in the SCI rat, compared to control animals. DiR "hotspots" were specifically associated with CD206-expressing M2 macrophages in the spinal cord and this was confirmed by co-localization with anti-CD63 antibodies labeling a tetraspanin characteristically expressed on exosomes. Our findings that MSCexos specifically target M2-type macrophages at the site of SCI, support the idea that extracellular vesicles, released by MSCs, may mediate at least some of the therapeutic effects of IV MSC administration.
[Mh] Termos MeSH primário: Transplante de Células
Exossomos/metabolismo
Macrófagos/patologia
Células Mesenquimais Estromais
Traumatismos da Medula Espinal/patologia
[Mh] Termos MeSH secundário: Animais
Meios de Cultivo Condicionados
Meios de Cultura Livres de Soro
Tamanho do Órgão
Ratos
Ratos Sprague-Dawley
Baço/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Culture Media, Serum-Free)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190358



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