Base de dados : MEDLINE
Pesquisa : G04.085.600 [Categoria DeCS]
Referências encontradas : 3525 [refinar]
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[PMID]:29173353
[Au] Autor:Ratajczak MZ; Ratajczak J
[Ad] Endereço:Department of Medicine, Stem Cell Institute at James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky. Electronic address: mzrata01@louisville.edu.
[Ti] Título:Extracellular Microvesicles as Game Changers in Better Understanding the Complexity of Cellular Interactions-From Bench to Clinical Applications.
[So] Source:Am J Med Sci;354(5):449-452, 2017 11.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent research has led to wide acceptance and better understanding of a novel mechanism for cell-cell communication that employs a network of extracellular microvesicles (ExMVs). Derived from the plasma membrane or the endosomal membrane compartment, these small, spherical membrane fragments are secreted from the cell surface or in the process of exocytosis from endosomal membrane compartment and (1) with ligands expressed on their surface directly stimulate target cells in a paracrine manner, (2) transfer cell membrane receptors to target cells or (3) deliver encapsulated messenger RNA, microRNA, proteins and bioactive lipids to target cells. This represents an evolutionarily ancient mechanism by which cells signal their presence in the microenvironment, communicate with each other and affect the biology of neighboring cells. Evidence suggests the pivotal role of ExMVs in almost all biological processes within the body as well as their involvement in certain pathologies. Moreover, liquid biopsies based on deciphering the molecular signature of ExMVs promise to revolutionize laboratory diagnostics. At the same time, there are ongoing attempts to employ them as delivery vehicles for drugs as well as therapeutics in regenerative medicine, oncology and immunotherapy.
[Mh] Termos MeSH primário: Comunicação Celular
Vesículas Extracelulares/metabolismo
MicroRNAs/metabolismo
Comunicação Parácrina
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Ligantes
Proteínas/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ligands); 0 (MicroRNAs); 0 (Proteins); 0 (RNA, Messenger); 0 (Receptors, Cytoplasmic and Nuclear)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:28468971
[Au] Autor:Olson MR; Ulrich BJ; Hummel SA; Khan I; Meuris B; Cherukuri Y; Dent AL; Janga SC; Kaplan MH
[Ad] Endereço:Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; olsonmr@iupui.edu mkaplan2@iupui.edu.
[Ti] Título:Paracrine IL-2 Is Required for Optimal Type 2 Effector Cytokine Production.
[So] Source:J Immunol;198(11):4352-4359, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-2 is a pleiotropic cytokine that promotes the differentiation of Th cell subsets, including Th1, Th2, and Th9 cells, but it impairs the development of Th17 and T follicular helper cells. Although IL-2 is produced by all polarized Th subsets to some level, how it impacts cytokine production when effector T cells are restimulated is unknown. We show in this article that Golgi transport inhibitors (GTIs) blocked IL-9 production. Mechanistically, GTIs blocked secretion of IL-2 that normally feeds back in a paracrine manner to promote STAT5 activation and IL-9 production. IL-2 feedback had no effect on Th1- or Th17-signature cytokine production, but it promoted Th2- and Th9-associated cytokine expression. These data suggest that the use of GTIs results in an underestimation of the presence of type 2 cytokine-secreting cells and highlight IL-2 as a critical component in optimal cytokine production by Th2 and Th9 cells in vitro and in vivo.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Interleucina-2/metabolismo
Interleucina-9/biossíntese
Comunicação Parácrina
Células Th2/imunologia
[Mh] Termos MeSH secundário: Animais
Brefeldina A/farmacologia
Diferenciação Celular
Citocinas/imunologia
Interleucina-2/secreção
Interleucina-9/antagonistas & inibidores
Interleucina-9/imunologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Monensin/farmacologia
Inibidores da Síntese de Proteínas/farmacologia
Ionóforos de Próton/farmacologia
Fator de Transcrição STAT5/metabolismo
Células Th1/imunologia
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-2); 0 (Interleukin-9); 0 (Protein Synthesis Inhibitors); 0 (Proton Ionophores); 0 (STAT5 Transcription Factor); 20350-15-6 (Brefeldin A); 906O0YJ6ZP (Monensin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601792


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[PMID]:28460416
[Au] Autor:Fairfield H; Falank C; Harris E; Demambro V; McDonald M; Pettitt JA; Mohanty ST; Croucher P; Kramer I; Kneissel M; Rosen CJ; Reagan MR
[Ad] Endereço:Center for Clinical and Translational Research, Maine Medical Center Research Institute, Scarborough, Maine.
[Ti] Título:The skeletal cell-derived molecule sclerostin drives bone marrow adipogenesis.
[So] Source:J Cell Physiol;233(2):1156-1167, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The bone marrow niche is a dynamic and complex microenvironment that can both regulate, and be regulated by the bone matrix. Within the bone marrow (BM), mesenchymal stromal cell (MSC) precursors reside in a multi-potent state and retain the capacity to differentiate down osteoblastic, adipogenic, or chondrogenic lineages in response to numerous biochemical cues. These signals can be altered in various pathological states including, but not limited to, osteoporotic-induced fracture, systemic adiposity, and the presence of bone-homing cancers. Herein we provide evidence that signals from the bone matrix (osteocytes) determine marrow adiposity by regulating adipogenesis in the bone marrow. Specifically, we found that physiologically relevant levels of Sclerostin (SOST), which is a Wnt-inhibitory molecule secreted from bone matrix-embedded osteocytes, can induce adipogenesis in 3T3-L1 cells, mouse ear- and BM-derived MSCs, and human BM-derived MSCs. We demonstrate that the mechanism of SOST induction of adipogenesis is through inhibition of Wnt signaling in pre-adipocytes. We also demonstrate that a decrease of sclerostin in vivo, via both genetic and pharmaceutical methods, significantly decreases bone marrow adipose tissue (BMAT) formation. Overall, this work demonstrates a direct role for SOST in regulating fate determination of BM-adipocyte progenitors. This provides a novel mechanism for which BMAT is governed by the local bone microenvironment, which may prove relevant in the pathogenesis of certain diseases involving marrow adipose. Importantly, with anti-sclerostin therapy at the forefront of osteoporosis treatment and a greater recognition of the role of BMAT in disease, these data are likely to have important clinical implications.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Adipogenia
Tecido Adiposo/metabolismo
Células da Medula Óssea/metabolismo
Glicoproteínas/metabolismo
Células Mesenquimais Estromais/metabolismo
Osteócitos/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Tecido Adiposo/citologia
Adiposidade
Animais
Meios de Cultivo Condicionados/metabolismo
Glicoproteínas/deficiência
Glicoproteínas/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Comunicação Parácrina
Fenótipo
Nicho de Células-Tronco
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Glycoproteins); 0 (Sost protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25976


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[PMID]:28743804
[Au] Autor:Tachibana A; Santoso MR; Mahmoudi M; Shukla P; Wang L; Bennett M; Goldstone AB; Wang M; Fukushi M; Ebert AD; Woo YJ; Rulifson E; Yang PC
[Ad] Endereço:From the Division of Cardiovascular Medicine (A.T., M.R.S., M.M., P.S., L.W., M.W., A.D.E., E.R., P.C.Y.), Division of Neonatal and Developmental Medicine (M.B.), and Department of Cardiothoracic Surgery (A.B.G., Y.J.W.), Stanford University, CA; Department of Radiological Sciences, Tokyo Metropolit
[Ti] Título:Paracrine Effects of the Pluripotent Stem Cell-Derived Cardiac Myocytes Salvage the Injured Myocardium.
[So] Source:Circ Res;121(6):e22-e36, 2017 Sep 01.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Cardiac myocytes derived from pluripotent stem cells have demonstrated the potential to mitigate damage of the infarcted myocardium and improve left ventricular ejection fraction. However, the mechanism underlying the functional benefit is unclear. OBJECTIVE: To evaluate whether the transplantation of cardiac-lineage differentiated derivatives enhance myocardial viability and restore left ventricular ejection fraction more effectively than undifferentiated pluripotent stem cells after a myocardial injury. Herein, we utilize novel multimodality evaluation of human embryonic stem cells (hESCs), hESC-derived cardiac myocytes (hCMs), human induced pluripotent stem cells (iPSCs), and iPSC-derived cardiac myocytes (iCMs) in a murine myocardial injury model. METHODS AND RESULTS: Permanent ligation of the left anterior descending coronary artery was induced in immunosuppressed mice. Intramyocardial injection was performed with (1) hESCs (n=9), (2) iPSCs (n=8), (3) hCMs (n=9), (4) iCMs (n=14), and (5) PBS control (n=10). Left ventricular ejection fraction and myocardial viability, measured by cardiac magnetic resonance imaging and manganese-enhanced magnetic resonance imaging, respectively, was significantly improved in hCM- and iCM-treated mice compared with pluripotent stem cell- or control-treated mice. Bioluminescence imaging revealed limited cell engraftment in all treated groups, suggesting that the cell secretions may underlie the repair mechanism. To determine the paracrine effects of the transplanted cells, cytokines from supernatants from all groups were assessed in vitro. Gene expression and immunohistochemistry analyses of the murine myocardium demonstrated significant upregulation of the promigratory, proangiogenic, and antiapoptotic targets in groups treated with cardiac lineage cells compared with pluripotent stem cell and control groups. CONCLUSIONS: This study demonstrates that the cardiac phenotype of hCMs and iCMs salvages the injured myocardium effectively than undifferentiated stem cells through their differential paracrine effects.
[Mh] Termos MeSH primário: Células-Tronco Pluripotentes Induzidas/transplante
Infarto do Miocárdio/terapia
Miócitos Cardíacos/transplante
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Cultivadas
Citocinas/genética
Citocinas/metabolismo
Células-Tronco Embrionárias/citologia
Células-Tronco Embrionárias/metabolismo
Células-Tronco Embrionárias/transplante
Seres Humanos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Camundongos
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Comunicação Parácrina
Transplante de Células-Tronco/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.310803


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[PMID]:28600879
[Au] Autor:Andreeva ER; Udartseva OO; Zhidkova OV; Buravkov SV; Ezdakova MI; Buravkova LB
[Ad] Endereço:Cell Physiology Laboratory, Institute of Biomedical Problems, Russian Academy of Sciences, Moscow, Russia.
[Ti] Título:IFN-gamma priming of adipose-derived stromal cells at "physiological" hypoxia.
[So] Source:J Cell Physiol;233(2):1535-1547, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multipotent mesenchymal stromal cells (MSCs) are considered cue regulators of tissue remodeling. Their activity is strongly governed by local milieu, where O level is most important. The elevation of inflammatory mediators and acute O lowering may additionally modulate MSC activity. In present paper the priming effects of IFN-gamma on adipose tissue-derived MSCs (ASCs) at tissue-related O level (5%) and acute hypoxic stress (0.1% O ) were assessed as alterations of ASCs' CFU-F, proliferation, migration, osteo-commitment. IFN-gamma priming provoked ROS elevation, cell growth slowdown, attenuation of both spontaneous and induced osteodifferentiation of tissue O -adapted ASCs. The prominent changes in ASC cytoskeleton-related gene transcription was detected. IFN-gamma exposure shifted the ASC paracrine profile, suppressing the production of VEGF and IL-8, while MCP-1 and IL-6 were stimulated. Conditioned medium of IFN-gamma-primed ASCs did not activate vessel growth in the CAM assay, but induced endothelial cell migration in "wound closure." Short-term hypoxia suppressed CFU-F number, IFN-gamma-induced elevation of IL-6 and endothelial cell migration, while it abolished IFN-gamma-provoked VEGF inhibition. After N-acetyl cysteine treatment ROS level was partly abolished providing additional enhancement of IL-6 and suppression of IL-8 and VEGF production. These findings demonstrated that paracrine activity of ASCs in part may be governed by ROS level. Thus, this study first demonstrated that IFN-gamma priming itself and in combination with acute O deprivation could supply dual effects on ASC functions providing both stimulatory and hampering effects. The equilibrium of these factors is a substantial requirement for the execution of MSC remodeling functions.
[Mh] Termos MeSH primário: Tecido Adiposo/efeitos dos fármacos
Interferon gama/farmacologia
Células Mesenquimais Estromais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Tecido Adiposo/citologia
Tecido Adiposo/metabolismo
Animais
Hipóxia Celular
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Técnicas de Cocultura
Coturnix
Meios de Cultivo Condicionados/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Células Mesenquimais Estromais/metabolismo
Neovascularização Fisiológica
Osteogênese/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Comunicação Parácrina/efeitos dos fármacos
Fenótipo
Espécies Reativas de Oxigênio/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Reactive Oxygen Species); 82115-62-6 (Interferon-gamma)
[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:170611
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26046


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[PMID]:29020068
[Au] Autor:Cai C; Zhou J; Sun X; Sun T; Xie W; Cui J
[Ad] Endereço:Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
[Ti] Título:Integrated modeling and analysis of intracellular and intercellular mechanisms in shaping the interferon response to viral infection.
[So] Source:PLoS One;12(10):e0186105, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interferons (IFNs) responses to viral infection are heterogeneous, while the underlying mechanisms for variability among cells are still not clear. In this study, we developed a hybrid model to systematically identify the sources of IFN induction heterogeneity. The experiment-integrated simulation demonstrated that the viral dose/type, the diversity in transcriptional factors activation and the intercellular paracrine signaling could strikingly shape the heterogeneity of IFN expression. We further determined that the IFNß and IFNλ1 induced diverse dynamics of IFN-stimulated genes (ISGs) production. Collectively, our findings revealed the intracellular and intercellular mechanisms contributing to cell-to-cell variation in IFN induction, and further demonstrated the significant effects of IFN heterogeneity on antagonizing viruses.
[Mh] Termos MeSH primário: Espaço Extracelular/metabolismo
Interferons/farmacologia
Espaço Intracelular/metabolismo
Modelos Biológicos
Estomatite Vesicular/metabolismo
[Mh] Termos MeSH secundário: Células A549
Forma Celular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Células HEK293
Seres Humanos
Comunicação Parácrina/efeitos dos fármacos
Fatores de Tempo
Fatores de Transcrição/metabolismo
Ativação Transcricional/efeitos dos fármacos
Ativação Transcricional/genética
Estomatite Vesicular/genética
Estomatite Vesicular/patologia
Vesiculovirus/efeitos dos fármacos
Vesiculovirus/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transcription Factors); 9008-11-1 (Interferons)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186105


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[PMID]:28947496
[Au] Autor:Vaahtomeri K; Karaman S; Mäkinen T; Alitalo K
[Ad] Endereço:Wihuri Research Institute, Translational Cancer Biology Program, Biomedicum Helsinki, University of Helsinki, FI-00014 Helsinki, Finland.
[Ti] Título:Lymphangiogenesis guidance by paracrine and pericellular factors.
[So] Source:Genes Dev;31(16):1615-1634, 2017 Aug 15.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lymphatic vessels are important for tissue fluid homeostasis, lipid absorption, and immune cell trafficking and are involved in the pathogenesis of several human diseases. The mechanisms by which the lymphatic vasculature network is formed, remodeled, and adapted to physiological and pathological challenges are controlled by an intricate balance of growth factor and biomechanical cues. These transduce signals for the readjustment of gene expression and lymphatic endothelial migration, proliferation, and differentiation. In this review, we describe several of these cues and how they are integrated for the generation of functional lymphatic vessel networks.
[Mh] Termos MeSH primário: Linfangiogênese
[Mh] Termos MeSH secundário: Animais
Membrana Basal/fisiologia
Carcinogênese
Inflamação/fisiopatologia
Integrinas/fisiologia
Peptídeos e Proteínas de Sinalização Intercelular/fisiologia
Vasos Linfáticos/embriologia
Camundongos
Comunicação Parácrina
Fator C de Crescimento do Endotélio Vascular/fisiologia
Receptor 3 de Fatores de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Integrins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Vascular Endothelial Growth Factor C); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171029
[Lr] Data última revisão:
171029
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1101/gad.303776.117


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[PMID]:28916678
[Au] Autor:Li P; Wuthrick E; Rappaport JA; Kraft C; Lin JE; Marszalowicz G; Snook AE; Zhan T; Hyslop TM; Waldman SA
[Ad] Endereço:Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, The University of Florida, Gainesville, Florida.
[Ti] Título:GUCY2C Signaling Opposes the Acute Radiation-Induced GI Syndrome.
[So] Source:Cancer Res;77(18):5095-5106, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High doses of ionizing radiation induce acute damage to epithelial cells of the gastrointestinal (GI) tract, mediating toxicities restricting the therapeutic efficacy of radiation in cancer and morbidity and mortality in nuclear disasters. No approved prophylaxis or therapy exists for these toxicities, in part reflecting an incomplete understanding of mechanisms contributing to the acute radiation-induced GI syndrome (RIGS). Guanylate cyclase C (GUCY2C) and its hormones guanylin and uroguanylin have recently emerged as one paracrine axis defending intestinal mucosal integrity against mutational, chemical, and inflammatory injury. Here, we reveal a role for the GUCY2C paracrine axis in compensatory mechanisms opposing RIGS. Eliminating GUCY2C signaling exacerbated RIGS, amplifying radiation-induced mortality, weight loss, mucosal bleeding, debilitation, and intestinal dysfunction. Durable expression of GUCY2C, guanylin, and uroguanylin mRNA and protein by intestinal epithelial cells was preserved following lethal irradiation inducing RIGS. Oral delivery of the heat-stable enterotoxin (ST), an exogenous GUCY2C ligand, opposed RIGS, a process requiring p53 activation mediated by dissociation from MDM2. In turn, p53 activation prevented cell death by selectively limiting mitotic catastrophe, but not apoptosis. These studies reveal a role for the GUCY2C paracrine hormone axis as a novel compensatory mechanism opposing RIGS, and they highlight the potential of oral GUCY2C agonists (Linzess; Trulance) to prevent and treat RIGS in cancer therapy and nuclear disasters. .
[Mh] Termos MeSH primário: Raios gama/efeitos adversos
Trato Gastrointestinal/efeitos da radiação
Síndrome do Intestino Irritável/prevenção & controle
Lesões Experimentais por Radiação/prevenção & controle
Receptores Acoplados a Guanilato Ciclase/metabolismo
Receptores de Peptídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos da radiação
Proliferação Celular/efeitos da radiação
Neoplasias do Colo/enzimologia
Neoplasias do Colo/patologia
Neoplasias do Colo/radioterapia
Feminino
Hormônios Gastrointestinais/metabolismo
Seres Humanos
Síndrome do Intestino Irritável/enzimologia
Síndrome do Intestino Irritável/etiologia
Linfoma/enzimologia
Linfoma/patologia
Linfoma/radioterapia
Masculino
Melanoma Experimental/enzimologia
Melanoma Experimental/patologia
Melanoma Experimental/radioterapia
Camundongos
Camundongos Endogâmicos C57BL
Peptídeos Natriuréticos/metabolismo
Comunicação Parácrina/efeitos da radiação
Lesões Experimentais por Radiação/enzimologia
Lesões Experimentais por Radiação/etiologia
Receptores de Enterotoxina
Transdução de Sinais/efeitos da radiação
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gastrointestinal Hormones); 0 (Natriuretic Peptides); 0 (Receptors, Peptide); 140653-38-9 (guanylin); 152175-68-3 (uroguanylin); EC 4.6.1.2 (GUCY2C protein, human); EC 4.6.1.2 (Gucy2c protein, mouse); EC 4.6.1.2 (Receptors, Enterotoxin); EC 4.6.1.2 (Receptors, Guanylate Cyclase-Coupled)
[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:170917
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0859


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[PMID]:28886382
[Au] Autor:Zepp JA; Zacharias WJ; Frank DB; Cavanaugh CA; Zhou S; Morley MP; Morrisey EE
[Ad] Endereço:Department of Medicine, Division of Pediatric Cardiology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Penn Center for Pulmonary Biology, University of Pennsylvania, Philadelphia, PA 19104, USA; Penn Cardiovascular Institute, University of Pennsylvania, Philadelphia, PA 19104, U
[Ti] Título:Distinct Mesenchymal Lineages and Niches Promote Epithelial Self-Renewal and Myofibrogenesis in the Lung.
[So] Source:Cell;170(6):1134-1148.e10, 2017 Sep 07.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The lung is an architecturally complex organ comprising a heterogeneous mixture of various epithelial and mesenchymal lineages. We use single-cell RNA sequencing and signaling lineage reporters to generate a spatial and transcriptional map of the lung mesenchyme. We find that each mesenchymal lineage has a distinct spatial address and transcriptional profile leading to unique niche regulatory functions. The mesenchymal alveolar niche cell is Wnt responsive, expresses Pdgfrα, and is critical for alveolar epithelial cell growth and self-renewal. In contrast, the Axin2+ myofibrogenic progenitor cell preferentially generates pathologically deleterious myofibroblasts after injury. Analysis of the secretome and receptome of the alveolar niche reveals functional pathways that mediate growth and self-renewal of alveolar type 2 progenitor cells, including IL-6/Stat3, Bmp, and Fgf signaling. These studies define the cellular and molecular framework of lung mesenchymal niches and reveal the functional importance of developmental pathways in promoting self-renewal versus a pathological response to tissue injury.
[Mh] Termos MeSH primário: Pulmão/citologia
Mesoderma/citologia
[Mh] Termos MeSH secundário: Algoritmos
Animais
Células Epiteliais/metabolismo
Fibrose/metabolismo
Perfilação da Expressão Gênica
Pulmão/patologia
Pulmão/fisiologia
Lesão Pulmonar/patologia
Camundongos
Organoides/citologia
Comunicação Parácrina
Regeneração
Transdução de Sinais
Análise de Célula Única
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28846077
[Au] Autor:Koukourakis MI; Kalamida D; Mitrakas AG; Liousia M; Pouliliou S; Sivridis E; Giatromanolaki A
[Ad] Endereço:Department of Radiotherapy/Oncology, Democritus University of Thrace, Alexandroupolis, Greece.
[Ti] Título:Metabolic cooperation between co-cultured lung cancer cells and lung fibroblasts.
[So] Source:Lab Invest;97(11):1321-1331, 2017 Nov.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cooperation of cancer cells with stromal cells, such as cancer-associated fibroblasts (CAFs), has been revealed as a mechanism sustaining cancer cell survival and growth. In the current study, we focus on the metabolic interactions of MRC5 lung fibroblasts with lung cancer cells (A549 and H1299) using co-culture experiments and studying changes of the metabolic protein expression profile and of their growth and migration abilities. Using western blotting, confocal microscopy and RT-PCR, we observed that in co-cultures MRC5 respond by upregulating pyruvate dehydrogenase (PDH) and the monocarboxylate transporter MCT1. In contrast, cancer cells increase the expression of glucose transporters (GLUT1), LDH5, PDH kinase and the levels of phosphorylated/inactivated pPDH. H1299 cells growing in the same culture medium with fibroblasts exhibit a 'metastasis-like' phenomenon by forming nests within the fibroblast area. LDH5 and pPDH were drastically upregulated in these nests. The growth rate of both MRC5 and cancer cells increased in co-cultures. Suppression of LDHA or PDK1 in cancer cells abrogates the stimulatory signal from cancer cells to fibroblasts. Incubation of MRC5 fibroblasts with lactate resulted in an increase of LDHB and of PDH expression. Silencing of PDH gene in fibroblasts, or silencing of PDK1 or LDHA gene in tumor cells, impedes cancer cell's migration ability. Overall, a metabolic cooperation between lung cancer cells and fibroblasts has been confirmed in the context of direct Warburg effect, thus the fibroblasts reinforce aerobic metabolism to support the intensified anaerobic glycolytic pathways exploited by cancer cells.
[Mh] Termos MeSH primário: Fibroblastos Associados a Câncer/metabolismo
Metabolismo Energético
Regulação Neoplásica da Expressão Gênica
Neoplasias Pulmonares/metabolismo
Pulmão/metabolismo
Proteínas de Neoplasias/metabolismo
Comunicação Parácrina
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Fibroblastos Associados a Câncer/patologia
Linhagem Celular
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Técnicas de Cocultura
Perfilação da Expressão Gênica
Seres Humanos
Pulmão/patologia
Neoplasias Pulmonares/patologia
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/genética
Fosforilação
Processamento de Proteína Pós-Traducional
Interferência de RNA
Esferoides Celulares
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neoplasm Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2017.79



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