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[PMID]:29351567
[Au] Autor:Ghandhi SA; Turner HC; Shuryak I; Dugan GO; Bourland JD; Olson JD; Tooze JA; Morton SR; Batinic-Haberle I; Cline JM; Amundson SA
[Ad] Endereço:Center for Radiological Research, Columbia University Medical Center, New York, New York, United States of America.
[Ti] Título:Whole thorax irradiation of non-human primates induces persistent nuclear damage and gene expression changes in peripheral blood cells.
[So] Source:PLoS One;13(1):e0191402, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated the cytogenetic and gene expression responses of peripheral blood cells of non-human primates (NHP, Macaca mulatta) that were whole-thorax irradiated with a single dose of 10 Gy. In this model, partial irradiation of NHPs in the thoracic region (Whole Thorax Lung Irradiation, WTLI) allows the study of late radiation-induced lung injury, while avoiding acute radiation syndromes related to hematopoietic and gastrointestinal injury. A transient drop in circulating lymphocytes and platelets was seen by 9 days, followed by elevations in respiratory rate, circulating neutrophils, lymphocytes, and monocytes at 60-100 days, corresponding to computed tomography (CT) and histologic evidence of pneumonitis, and elective euthanasia of four animals. To evaluate long-term DNA damage in NHP peripheral blood lymphocytes after 10 Gy WTLI, we used the cytokinesis-block micronucleus (CBMN) assay to measure chromosomal aberrations as post-mitotic micronuclei in blood samples collected up to 8 months after irradiation. Regression analysis showed significant induction of micronuclei in NHP blood cells that persisted with a gradual decline over the 8-month study period, suggesting long-term DNA damage in blood lymphocytes after WTLI. We also report transcriptomic changes in blood up to 30 days after WTLI. We isolated total RNA from peripheral blood at 3 days before and then at 2, 5 and 30 days after irradiation. We identified 1187 transcripts that were significantly changed across the 30-day time course. From changes in gene expression, we identified biological processes related to immune responses, which persisted across the 30-day study. Response to oxygen-containing compounds and bacteria were implicated by gene-expression changes at the earliest day 2 and latest, day 30 time-points. Gene expression changes suggest a persistent altered state of the immune system, specifically response to infection, for at least a month after WTLI.
[Mh] Termos MeSH primário: Células Sanguíneas/metabolismo
Células Sanguíneas/efeitos da radiação
Dano ao DNA
Expressão Gênica/efeitos da radiação
[Mh] Termos MeSH secundário: Animais
Contagem de Células Sanguíneas
Aberrações Cromossômicas
Relação Dose-Resposta à Radiação
Ontologia Genética
Seres Humanos
Lesão Pulmonar/sangue
Lesão Pulmonar/etiologia
Lesão Pulmonar/genética
Macaca mulatta/sangue
Macaca mulatta/genética
Masculino
Testes para Micronúcleos
Lesões Experimentais por Radiação/sangue
Lesões Experimentais por Radiação/genética
Tórax/efeitos da radiação
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191402


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[PMID]:28464871
[Au] Autor:Aksoy MO; Kim V; Cornwell WD; Rogers TJ; Kosmider B; Bahmed K; Barrero C; Merali S; Shetty N; Kelsen SG
[Ad] Endereço:Department of Thoracic Medicine and Surgery, Temple University School of Medicine, Philadelphia, PA, 19140, USA. mark.aksoy@temple.edu.
[Ti] Título:Secretion of the endoplasmic reticulum stress protein, GRP78, into the BALF is increased in cigarette smokers.
[So] Source:Respir Res;18(1):78, 2017 May 02.
[Is] ISSN:1465-993X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Identification of biomarkers of cigarette smoke -induced lung damage and early COPD is an area of intense interest. Glucose regulated protein of 78 kD (i.e., GRP78), a multi-functional protein which mediates cell responses to oxidant stress, is increased in the lungs of cigarette smokers and in the serum of subjects with COPD. We have suggested that secretion of GRP78 by lung cells may explain the increase in serum GRP78 in COPD. To assess GRP78 secretion by the lung, we assayed GRP78 in bronchoalveolar lavage fluid (BALF) in chronic smokers and non-smokers. We also directly assessed the acute effect of cigarette smoke material on GRP78 secretion in isolated human airway epithelial cells (HAEC). METHODS: GRP78 was measured in BALF of smokers (S; n = 13) and non-smokers (NS; n = 11) by Western blotting. GRP78 secretion by HAEC was assessed by comparing its concentration in cell culture medium and cell lysates. Cells were treated for 24 h with either the volatile phase of cigarette smoke (cigarette smoke extract (CSE) or the particulate phase (cigarette smoke condensate (CSC)). RESULTS: GRP78 was present in the BALF of both NS and S but levels were significantly greater in S (p = 0.04). GRP78 was secreted constitutively in HAEC. CSE 15% X 24 h increased GRP78 in cell-conditioned medium without affecting its intracellular concentration. In contrast, CSC X 24 h increased intracellular GRP78 expression but did not affect GRP78 secretion. Brefeldin A, an inhibitor of classical Golgi secretion pathways, did not inhibit GRP78 secretion indicating that non-classical pathways were involved. CONCLUSION: The present study indicates that GRP78 is increased in BALF in cigarette smokers; that HAEC secrete GRP78; and that GRP78 secretion by HAEC is augmented by cigarette smoke particulates. Enhanced secretion of GRP78 by lung cells makes it a potential biomarker of cigarette smoke-induced lung injury.
[Mh] Termos MeSH primário: Líquido da Lavagem Broncoalveolar/química
Retículo Endoplasmático/secreção
Proteínas de Choque Térmico/secreção
Lesão Pulmonar/metabolismo
Fumar/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores/análise
Biomarcadores/química
Feminino
Seres Humanos
Masculino
Meia-Idade
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Heat-Shock Proteins); 0 (molecular chaperone GRP78)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12931-017-0561-6


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[PMID]:29286857
[Au] Autor:Svendsen ER
[Ad] Endereço:1 Medical University of South Carolina Charleston, South Carolina.
[Ti] Título:Chlorine Countermeasures: Supplemental Oxygen Equals Supplemental Lung Injury?
[So] Source:Am J Respir Cell Mol Biol;58(1):10-11, 2018 01.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Substâncias para a Guerra Química/toxicidade
Guerra Química
Cloro/toxicidade
Lesão Pulmonar
Oxigênio/uso terapêutico
[Mh] Termos MeSH secundário: Seres Humanos
Lesão Pulmonar/induzido quimicamente
Lesão Pulmonar/terapia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Chemical Warfare Agents); 4R7X1O2820 (Chlorine); S88TT14065 (Oxygen)
[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:171230
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0320ED


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[PMID]:29286855
[Au] Autor:McQuattie-Pimentel AC; Budinger GRS; Ballinger MN
[Ad] Endereço:1 Division of Pulmonary and Critical Care Northwestern University Chicago, Illinois and.
[Ti] Título:Monocyte-derived Alveolar Macrophages: The Dark Side of Lung Repair?
[So] Source:Am J Respir Cell Mol Biol;58(1):5-6, 2018 01.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Lesão Pulmonar/metabolismo
Pulmão/metabolismo
Macrófagos Alveolares/metabolismo
Monócitos/metabolismo
Fibrose Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Pulmão/patologia
Lesão Pulmonar/patologia
Lesão Pulmonar/fisiopatologia
Macrófagos Alveolares/patologia
Monócitos/patologia
Fibrose Pulmonar/patologia
Fibrose Pulmonar/fisiopatologia
[Pt] Tipo de publicação:EDITORIAL
[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:171230
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0328ED


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[PMID]:29242152
[Au] Autor:Hou C; Peng D; Gao L; Tian D; Dai J; Luo Z; Liu E; Chen H; Zou L; Fu Z
[Ad] Endereço:Pediatrics Research Institute, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing 400014, China; Chongqing Key Laboratory of Pediatrics, China; China International Science and Technology Cooperation Base of Child De
[Ti] Título:Human umbilical cord-derived mesenchymal stem cells protect from hyperoxic lung injury by ameliorating aberrant elastin remodeling in the lung of O -exposed newborn rat.
[So] Source:Biochem Biophys Res Commun;495(2):1972-1979, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incidence and mortality rates of bronchopulmonary dysplasia (BPD) remain very high. Therefore, novel therapies are imminently needed to improve the outcome of this disease. Human umbilical cord-derived mesenchymal stem cells (UC-MSCs) show promising therapeutic effects on oxygen-induced model of BPD. In our experiment, UC-MSCs were intratracheally delivered into the newborn rats exposed to hyperoxia, a well-established BPD model. This study demonstrated that UC-MSCs reduce elastin expression stimulated by 90% O in human lung fibroblasts-a (HLF-a), and inhibit HLF-a transdifferentiation into myofibroblasts. In addition, the therapeutic effects of UC-MSCs in neonatal rats with BPD, UC-MSCs could inhibit lung elastase activity and reduce aberrant elastin expression and deposition in the lung of BPD rats. Overall, this study suggested that UC-MSCs could ameliorate aberrant elastin expression in the lung of hyperoxia-induced BPD model which may be associated with suppressing increased TGFß1 activation.
[Mh] Termos MeSH primário: Displasia Broncopulmonar/imunologia
Displasia Broncopulmonar/patologia
Transplante de Células-Tronco de Sangue do Cordão Umbilical/métodos
Elastina/metabolismo
Pulmão/imunologia
Pulmão/patologia
Transplante de Células-Tronco Mesenquimais/métodos
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Seres Humanos
Oxigenação Hiperbárica
Hiperóxia/metabolismo
Hiperóxia/patologia
Hiperóxia/prevenção & controle
Lesão Pulmonar/imunologia
Lesão Pulmonar/patologia
Lesão Pulmonar/prevenção & controle
Ratos
Ratos Sprague-Dawley
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9007-58-3 (Elastin)
[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:171216
[St] Status:MEDLINE


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[PMID]:28460177
[Au] Autor:Patel BK; Wolfe KS; Hall JB; Kress JP
[Ad] Endereço:1 University of Chicago Chicago, Illinois.
[Ti] Título:A Word of Caution Regarding Patient Self-inflicted Lung Injury and Prophylactic Intubation.
[So] Source:Am J Respir Crit Care Med;196(7):936, 2017 10 01.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Intubação
Lesão Pulmonar
[Mh] Termos MeSH secundário: Seres Humanos
Comportamento Autodestrutivo
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201702-0410LE


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[PMID]:29237485
[Au] Autor:Maruhashi T; Minehara H; Takeuchi I; Kataoka Y; Asari Y
[Ad] Endereço:Department of Emergency and Critical Care Medicine, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa, 252-0375, Japan. tmaruhasi119@gmail.com.
[Ti] Título:Resuscitative endovascular balloon occlusion of the aorta may increase the bleeding of minor thoracic injury in severe multiple trauma patients: a case report.
[So] Source:J Med Case Rep;11(1):347, 2017 Dec 14.
[Is] ISSN:1752-1947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The resuscitative endovascular balloon occlusion of the aorta, because of its efficacy and feasibility, has been widely used in treating patients with severe torso trauma. However, complications developing around the site proximal to the occlusion by resuscitative endovascular balloon occlusion of the aorta have almost never been studied. CASE PRESENTATION: A 50-year-old Japanese woman fell from a height of approximately 10 m. At initial arrival, her respiratory rate was 24 breaths/minute, her blood oxygen saturation was 95% under 10 L/minute oxygenation, her pulse rate was 90 beats per minute, and her blood pressure was 180/120 mmHg. Mild lung contusion, hemopneumothorax, unstable pelvic fracture, and retroperitoneal bleeding with extravasation of contrast media were observed in initial computed tomography. As her vital signs had deteriorated during computed tomography, a 7-French aortic occlusion catheter (RESCUE BALLOON®, Tokai Medical Products, Aichi, Japan) was inserted and inflated for aortic occlusion at the first lumbar vertebra level and transcatheter arterial embolization was performed for the pelvic fracture. Her bilateral internal iliac arteries were embolized with a gelatin sponge; however, the embolized sites presented recanalization as coagulopathy appeared. Her bilateral internal iliac arteries were re-embolized by n-butyl-2-cyanoacrylate. The balloon was deflated 18 minutes later. After embolization, repeat computed tomography was performed and a massive hemothorax, which had not been captured on arrival, had appeared in her left pleural cavity. Thoracotomy hemostasis was performed and a hemothorax of approximately 2500 ml was aspirated to search for the source of bleeding. However, clear active bleeding was not captured; resuscitative endovascular balloon occlusion of the aorta may have been the cause of the increased bleeding of the thoracic injury at the proximal site of the aorta occlusion. CONCLUSIONS: It is necessary to note that the use of resuscitative endovascular balloon occlusion of the aorta may increase bleeding in sites proximal to occlusions, even in the case of minor injuries without active bleeding at the initial diagnosis.
[Mh] Termos MeSH primário: Aorta
Oclusão com Balão/efeitos adversos
Embolização Terapêutica/métodos
Procedimentos Endovasculares/efeitos adversos
Hemopneumotórax/diagnóstico por imagem
Hemotórax/etiologia
Traumatismo Múltiplo/terapia
Ressuscitação/efeitos adversos
Choque Hemorrágico/terapia
Traumatismos Torácicos/terapia
[Mh] Termos MeSH secundário: Meios de Contraste
Contusões/diagnóstico por imagem
Progressão da Doença
Drenagem
Feminino
Fraturas Ósseas/diagnóstico por imagem
Hemorragia/diagnóstico por imagem
Seres Humanos
Artéria Ilíaca
Lesão Pulmonar/diagnóstico por imagem
Meia-Idade
Ossos Pélvicos/lesões
Espaço Retroperitoneal
Toracotomia
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contrast Media)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1186/s13256-017-1511-0


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[PMID]:29233668
[Au] Autor:Tang W; Huang S; Du L; Sun W; Yu Z; Zhou Y; Chen J; Li X; Li X; Yu B; Chen D
[Ad] Endereço:Department of Obstetrics and Gynecology, Third Affiliated Hospital of Guangzhou Medical University, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Guangzhou, 510150, China; Department of Obstetrics and Gynecology, Dongguan People's Hospital, Dongguan, 523000 China.
[Ti] Título:Expression of HMGB1 in maternal exposure to fine particulate air pollution induces lung injury in rat offspring assessed with micro-CT.
[So] Source:Chem Biol Interact;280:64-69, 2018 Jan 25.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Maternal particulate matter with less than 2.5 µm in diameter (PM2.5) is associated with an increased risk for acute lower respiratory infections and allergic airway inflammation; however, its effect on the developing lung remains unclear. The aim of this study is to determine the effect of maternal PM2.5 during pregnancy on lung development in offspring. METHODS: Timed pregnant Sprague-Dawley rats were treated with PM2.5 (0.1, 0.5, 2.5, or 7.5 mg/kg) once every 3 days from day 0-18 of pregnancy and delivered at term. Lungs were obtained on postnatal day 0, the structure of the lung was analyzed by quantitative micro-computed tomography (CT) and the levels of proinflammatory cytokines were analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of high mobility group box-1 (HMGB1) was also detected by immunohistochemistry, Western blotting, and quantitative RT-PCR. RESULTS: Ground-glass opacity and high-density volumes in CT slice images of maternal PM2.5-exposure rats were observed. The concentrations of IL-1, IL-6 and TNF-α were significantly increased by 2.36-, 3.91- and 4.36-fold, respectively, in the rats of the PM-7.5 group compared with the rats in the control group. The PM2.5-treated rats showed a significant upregulated expression of HMGB1 in lungs. CONCLUSIONS: PM2.5 exposure during pregnancy results in lung inflammation in offspring mediated by increased HMGB1 expression, followed by upregulated IL-1, IL-6 and TNF-α secretions, which may contribute to the development of inflammatory lung diseases in later life.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/efeitos dos fármacos
Proteína HMGB1/genética
Pulmão/efeitos dos fármacos
Exposição Materna
Material Particulado/toxicidade
[Mh] Termos MeSH secundário: Animais
Citocinas/análise
Ensaio de Imunoadsorção Enzimática
Feminino
Proteína HMGB1/metabolismo
Imuno-Histoquímica
Pulmão/diagnóstico por imagem
Pulmão/patologia
Lesão Pulmonar/diagnóstico por imagem
Lesão Pulmonar/etiologia
Lesão Pulmonar/patologia
Tamanho da Partícula
Material Particulado/química
Gravidez
Efeitos Tardios da Exposição Pré-Natal
Ratos
Ratos Sprague-Dawley
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (HMGB1 Protein); 0 (Particulate Matter)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE


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[PMID]:29183009
[Au] Autor:Li B; Li C; Zhu M; Zhang Y; Du J; Xu Y; Liu B; Gao F; Liu H; Cai J; Yang Y
[Ad] Endereço:Department of Radiation Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
[Ti] Título:Hypoxia-Induced Mesenchymal Stromal Cells Exhibit an Enhanced Therapeutic Effect on Radiation-Induced Lung Injury in Mice due to an Increased Proliferation Potential and Enhanced Antioxidant Ability.
[So] Source:Cell Physiol Biochem;44(4):1295-1310, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Radiation therapy is an important treatment for thoracic cancer; however, side effects accompanied with radiotherapy lead to limited tumor control and a decline in patient quality of life. Among these side effects, radiation-induced lung injury (RILI) is the most serious and common. Hence, an effective remedy for RILI is needed. Mesenchymal stromal cells (MSCs) are multipotent adult stem cells that have been demonstrated to be an effective treatment in some disease caused by tissue damage. However, unlike other injuries, RILI received limited therapeutic effects from implanted MSCs due to local hypoxia and extensive reactive oxygen species (ROS) in irradiated lungs. Since the poor survival of MSCs is primarily due to hypoxia and ROS generation, we hypothesize that persistent and adaptive hypoxia treatment induces enhanced resistance to hypoxic stress in implanted MSC. The aim of this study is to investigate whether persistent and adaptive hypoxia treatment of bmMSCs prior to their transplantation in injured mice enhanced survival and improved curative effects in RILI. METHODS: Primary bmMSCs were obtained from the marrow of six-week-old male C57BL6/J mice and were cultured either under normoxic conditions (21% O2) or hypoxic conditions (2.5% O2). Mice were injected with normoxia/hypoxia MSCs after thoracic irradiation (20 Gy). The therapeutic effects of MSCs on RILI were assessed by pathological examinations that included H&E staining, Masson staining and α-SMA staining; meanwhile, inflammatory factors were measured using an ELISA. The morphology of MSCs in vitro was recorded using a microscope and identified by flow cytometry, cell viability was measured using the CCK-8 assay, the potential for proliferation was detected by the EdU assay, and ROS levels were measured using a ROS fluorogenic probe. In addition, HIF-1α and several survival pathway proteins (Akt, p-Akt, Caspase-3) were also detected by western blotting. RESULTS: Implanted MSCs alleviated both early radiation-induced pneumonia and late pulmonary fibrosis. However, hypoxia MSCs displayed a more pronounced therapeutic effect compared to normoxia MSCs. Compared to normoxia MSCs, the hypoxia MSCs demonstrated greater cell viability, an enhanced proliferation potential, decreased ROS levels and increased resistance to hypoxia and ROS stress. In addition, hypoxia MSCs achieved higher activation levels of HIF-1α and Akt, and HIF-1α played a critical role in the development of resistance. CONCLUSION: Hypoxia enhances the therapeutic effect of mesenchymal stromal cells on radiation-induced lung injury by promoting MSC proliferation and improving their antioxidant ability, mediated by HIF-1α.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Hipóxia Celular
Lesão Pulmonar/terapia
Transplante de Células-Tronco Mesenquimais
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Apoptose/efeitos da radiação
Células da Medula Óssea/citologia
Caspase 3/metabolismo
Proliferação Celular
Sobrevivência Celular
Células Cultivadas
Raios gama
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Lesão Pulmonar/patologia
Masculino
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Tecido Parenquimatoso/citologia
Tecido Parenquimatoso/metabolismo
Tecido Parenquimatoso/efeitos da radiação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Fator de Crescimento Transformador beta/análise
Fator de Crescimento Transformador beta/metabolismo
Fator de Necrose Tumoral alfa/análise
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antioxidants); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Reactive Oxygen Species); 0 (Transforming Growth Factor beta); 0 (Tumor Necrosis Factor-alpha); 0 (alpha-smooth muscle actin, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1159/000485490


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[PMID]:29227075
[Au] Autor:Soni S; Basu M; Agrawal P; Kumar N; Bhatnagar A; Chhillar N
[Ti] Título:Multiple parametric approaches to assess acute radiation lung injury of rats radiation lung injury of rats.
[So] Source:Ukr Biochem J;88(1):22-30, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The effect of whole body gamma irradiation (WBI) in single fraction was studied, as well as its influence on the secretion of various biochemical markers and cellular component that could be used as acute radiation lung injury marker. Sprague dawley rats were treated with WBI (60Co) of radiation dose from 1 Gy to 5 Gy (dose rate - 0.95 Gy/min). Bronchoalveolar lavage fluid was retrieved from all animals in control and radiation treated groups up to 72 h post radiation. Bronchoalveolar lavage fluid (BALF) was analyzed for lactate dehydrogenase (LDH ), acid phosphatase (AP ), alkaline phosphatase (ALP ), cell count and total protein. Intragroup and intergroup comparison of BALF parameters at different radiation doses showed significant difference. LDH was significantly increased as the dose increased from 1Gy to 5Gy (P = 0.00) after 2 h with effect size of difference (r > 0.3). ALP was significantly altered after 3Gy and 4Gy (P < 0.05). AP was significantly altered at 2Gy-5Gy (p < 0.05). Total protein level changed significantly from 1Gy to 5Gy (P < 0.00). Cellular content of BALF showed significant changes after radiation exposure. BALF parameters like LDH, AP, ALP, neutrophils, lymphocytes, total leukocyte count and total protein were sensitive to radiation exposure and their levels vary significantly up to 72 h after single whole body radiation exposure in Sprague dawley rats. It can be concluded that the biochemical indices in BALF have more wide application in evaluation of acute radiation induced lung injury.
[Mh] Termos MeSH primário: Raios gama/efeitos adversos
Lesão Pulmonar/patologia
Lesões Experimentais por Radiação/patologia
[Mh] Termos MeSH secundário: Fosfatase Ácida/imunologia
Fosfatase Ácida/metabolismo
Fosfatase Alcalina/imunologia
Fosfatase Alcalina/metabolismo
Animais
Biomarcadores/análise
Líquido da Lavagem Broncoalveolar/química
Líquido da Lavagem Broncoalveolar/citologia
Líquido da Lavagem Broncoalveolar/imunologia
Relação Dose-Resposta à Radiação
L-Lactato Desidrogenase/imunologia
L-Lactato Desidrogenase/metabolismo
Contagem de Leucócitos
Lesão Pulmonar/enzimologia
Lesão Pulmonar/imunologia
Linfócitos/imunologia
Linfócitos/patologia
Masculino
Neutrófilos/imunologia
Neutrófilos/patologia
Lesões Experimentais por Radiação/enzimologia
Lesões Experimentais por Radiação/imunologia
Ratos
Ratos Sprague-Dawley
Irradiação Corporal Total
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.1.3.2 (Acid Phosphatase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.022



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