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Pesquisa : G03.197.300 [Categoria DeCS]
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[PMID]:29203747
[Au] Autor:Mielczarek-Puta M; Chrzanowska A; Otto-Slusarczyk D; Grabon W; Baranczyk-Kuzma A
[Ad] Endereço:Katedra I Zaklad Biochemii, Warszawski Uniwersytet Medyczny, Warszawa, Polska.
[Ti] Título:[Effect of antioxidants on human primary and metastatic colon cancer cells at hypoxia and normoxia].
[So] Source:Wiad Lek;70(5):946-952, 2017.
[Is] ISSN:0043-5147
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:THE AIM: Evaluation of some antioxidants on human colon cancer cells viability and proliferation at various oxygen levels. MATERIAL AND METHODS: Human primary (SW480) and metastatic (SW620) colon cancer cells were cultured at hypoxia (1% oxygen), tissues (10% oxygen) and atmospheric (21% oxygen) normoxia with quercetin, epigallocatechin gallate, lipoic acid, hydroxycitric acid, their mixture, and without studied compounds (control). Antioxidants were used at physiological concentrations. The cell viability was determined by trypan blue dye exclusion and proliferation by MTT assay. RESULTS: The viability of each line ranged from 80% to 97%, and it was independent on the compound and oxygen availability. At hypoxia the cell count of both lines was lower than for the controls in the presence of each studied compound. At tissue normoxia the cell count of primary cancer cells was decreased only with epigallocatechin gallate, whereas metastatic cells were sensitive for each antioxidant. CONCLUSIONS: Our results indicated, that the studied antioxidants were not cytotoxic at physiological levels for both pirmary and metastatic colon cancer. Their cytostatic effect depend on the type of cell, oxygen availability and antioxidant concentration.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Hipóxia Celular/efeitos dos fármacos
Neoplasias do Colo/tratamento farmacológico
[Mh] Termos MeSH secundário: Catequina/análogos & derivados
Catequina/farmacologia
Linhagem Celular Tumoral/efeitos dos fármacos
Citratos/farmacologia
Neoplasias do Colo/patologia
Seres Humanos
Metástase Neoplásica
Oxigênio/farmacologia
Ácido Tióctico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Citrates); 73Y7P0K73Y (Thioctic Acid); 8R1V1STN48 (Catechin); 8W94T9026R (hydroxycitric acid); BQM438CTEL (epigallocatechin gallate); S88TT14065 (Oxygen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


  2 / 17208 MEDLINE  
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[PMID]:29362355
[Au] Autor:Maybin JA; Murray AA; Saunders PTK; Hirani N; Carmeliet P; Critchley HOD
[Ad] Endereço:MRC Centre for Reproductive Health, The Queen's Medical Research Centre, The University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, Scotland.
[Ti] Título:Hypoxia and hypoxia inducible factor-1α are required for normal endometrial repair during menstruation.
[So] Source:Nat Commun;9(1):295, 2018 01 23.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Heavy menstrual bleeding (HMB) is common and debilitating, and often requires surgery due to hormonal side effects from medical therapies. Here we show that transient, physiological hypoxia occurs in the menstrual endometrium to stabilise hypoxia inducible factor 1 (HIF-1) and drive repair of the denuded surface. We report that women with HMB have decreased endometrial HIF-1α during menstruation and prolonged menstrual bleeding. In a mouse model of simulated menses, physiological endometrial hypoxia occurs during bleeding. Maintenance of mice under hyperoxia during menses decreases HIF-1α induction and delays endometrial repair. The same effects are observed upon genetic or pharmacological reduction of endometrial HIF-1α. Conversely, artificial induction of hypoxia by pharmacological stabilisation of HIF-1α rescues the delayed endometrial repair in hypoxia-deficient mice. These data reveal a role for HIF-1 in the endometrium and suggest its pharmacological stabilisation during menses offers an effective, non-hormonal treatment for women with HMB.
[Mh] Termos MeSH primário: Hipóxia Celular
Endométrio/fisiologia
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
Menstruação/metabolismo
[Mh] Termos MeSH secundário: Animais
Endométrio/metabolismo
Feminino
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02375-6


  3 / 17208 MEDLINE  
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[PMID]:29378209
[Au] Autor:Zhu M; Tian Y; Zhang H; Ma X; Shang B; Zhang J; Jiao Y; Zhang Y; Hu J; Wang Y
[Ad] Endereço:Department of Psychiatry and Psychology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
[Ti] Título:Methylphenidate ameliorates hypoxia-induced mitochondrial damage in human neuroblastoma SH-SY5Y cells through inhibition of oxidative stress.
[So] Source:Life Sci;197:40-45, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Methylphenidate (MPH) is a dopamine-reuptake inhibitor approved for the treatment of attention-deficit/hyperactivity disorder (ADHD). Nonetheless, the cellular and molecular mechanisms of MPH are still unknown. We attempt to determine whether MPH protect neuron cells against oxidative stress by using human neuroblastoma SH-SY5Y cells. MAIN METHODS: The SH-SY5Y cells were cultured in normoxic and hypoxic conditions in the presence of different doses of MPH. Then, reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and adenosine triphosphate (ATP) production were quantitatively measured by using flow cytometry or spectrophotometry. The mitochondrial ultrastructure of the cells was observed by electron microscope, and the function of mitochondrial was evaluated by measuring mitochondrial membrane potential (MMP) using flow cytometry. The levels of SOD and heme oxygenase-1 (HO-1) proteins were detected by Western blot. KEY FINDINGS: We found that low doses of MPH treatment (50-500 ng/mL) led to decreased ROS and MDA production (P<0.05), increased GSH and SOD as well as ATP concentration (P<0.05) in hypoxic SH-SY5Y cells. Additionally, low doses of MPH significantly inhibited mitochondrial swelling and decreased the percentage of JC-1 monomer positive cells. However, we did not observe the same effects of MPH in normoxia. SIGNIFICANCE: Our results show that low doses of MPH play protective roles in maintaining mitochondrial homeostasis in response to hypoxia-induced oxidative stress. Our findings may provide novel insight into the mechanisms of MPH in the treatment of ADHD, and shed light on the disease mechanisms of ADHD.
[Mh] Termos MeSH primário: Metilfenidato/farmacologia
Mitocôndrias/metabolismo
Neuroblastoma/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Heme Oxigenase-1/metabolismo
Seres Humanos
Mitocôndrias/patologia
Proteínas de Neoplasias/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/patologia
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Reactive Oxygen Species); 207ZZ9QZ49 (Methylphenidate); 8L70Q75FXE (Adenosine Triphosphate); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.15.1.1 (Superoxide Dismutase)
[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:180130
[St] Status:MEDLINE


  4 / 17208 MEDLINE  
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[PMID]:29284117
[Au] Autor:Murata Y; Hashimoto T; Urushihara Y; Shiga S; Takeda K; Jingu K; Hosoi Y
[Ad] Endereço:Department of Radiation Biology, Tohoku University School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi-ken 980-8575, Japan.
[Ti] Título:Knockdown of AMPKα decreases ATM expression and increases radiosensitivity under hypoxia and nutrient starvation in an SV40-transformed human fibroblast cell line, LM217.
[So] Source:Biochem Biophys Res Commun;495(4):2566-2572, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Presence of unperfused regions containing cells under hypoxia and nutrient starvation contributes to radioresistance in solid human tumors. It is well known that hypoxia causes cellular radioresistance, but little is known about the effects of nutrient starvation on radiosensitivity. We have reported that nutrient starvation induced decrease of mTORC1 activity and decrease of radiosensitivity in an SV40-transformed human fibroblast cell line, LM217, and that nutrient starvation induced increase of mTORC1 activity and increase of radiosensitivity in human liver cancer cell lines, HepG2 and HuH6 (Murata et al., BBRC 2015). Knockdown of mTOR using small interfering RNA (siRNA) for mTOR suppressed radiosensitivity under nutrient starvation alone in HepG2 cells, which suggests that mTORC1 pathway regulates radiosensitivity under nutrient starvation alone. In the present study, effects of hypoxia and nutrient starvation on radiosensitivity were investigated using the same cell lines. METHODS: LM217 and HepG2 cells were used to examine the effects of hypoxia and nutrient starvation on cellular radiosensitivity, mTORC1 pathway including AMPK, ATM, and HIF-1α, which are known as regulators of mTORC1 activity, and glycogen storage, which is induced by HIF-1 and HIF-2 under hypoxia and promotes cell survival. RESULTS: Under hypoxia and nutrient starvation, AMPK activity and ATM expression were increased in LM217 cells and decreased in HepG2 cells compared with AMPK activity under nutrient starvation alone or ATM expression under hypoxia alone. Under hypoxia and nutrient starvation, radiosensitivity was decreased in LM217 cells and increased in HepG2 cells compared with radiosensitivity under hypoxia alone. Under hypoxia and nutrient starvation, knockdown of AMPK decreased ATM activity and increased radiation sensitivity in LM217 cells. In both cell lines, mTORC1 activity was decreased under hypoxia and nutrient starvation. Under hypoxia alone, knockdown of mTOR slightly increased ATM expression but did not affect radiosensitivity in LM217. Under hypoxia and nutrient starvation, HIF-1α expression was suppressed and glycogen storage was reduced. CONCLUSION: Our data suggest that AMPK regulates ATM expression and partially regulates radiosensitivity under hypoxia and nutrient starvation. The molecular mechanism underlying the induction of ATM expression by AMPK remains to be elucidated.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/genética
Proteínas Mutadas de Ataxia Telangiectasia/genética
Hipóxia Celular/efeitos da radiação
Meios de Cultura/metabolismo
Regulação para Baixo/genética
Neoplasias Experimentais/radioterapia
Tolerância a Radiação
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Apoptose/efeitos da radiação
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Linhagem Celular
Relação Dose-Resposta à Radiação
Regulação para Baixo/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Vetores Genéticos/genética
Células Hep G2
Seres Humanos
Neoplasias Experimentais/metabolismo
Neoplasias Experimentais/patologia
Dose de Radiação
Vírus 40 dos Símios/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[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:171229
[St] Status:MEDLINE


  5 / 17208 MEDLINE  
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[PMID]:29278702
[Au] Autor:Chen C; Ma X; Yang C; Nie W; Zhang J; Li H; Rong P; Yi S; Wang W
[Ad] Endereço:Cell Transplantation and Gene Therapy Institute, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China; Department of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
[Ti] Título:Hypoxia potentiates LPS-induced inflammatory response and increases cell death by promoting NLRP3 inflammasome activation in pancreatic ß cells.
[So] Source:Biochem Biophys Res Commun;495(4):2512-2518, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypoxia and islet inflammation are involved in ß-cell failure in type 2 diabetes (T2D). Elevated plasma LPS levels have been verified in patients with T2D, and hypoxia occurs in islets of diabetic mice. Activation of inflammasomes in ischemic or hypoxic conditions was identified in various tissues. Here, we investigated whether hypoxia activates the inflammasome in ß cells and the possible mechanisms involved. In mouse insulinoma cell line 6 (MIN6), hypoxia (1% O ) primes the NLRP3 inflammasome along with NF-κB signaling activation. Our results demonstrate that hypoxia can activate the NLRP3 inflammasome in LPS-primed MIN6 to result in initiating the ß cell inflammatory response and cell death in vitro. Reactive oxygen species (ROS) and the thioredoxin-interacting protein (TXNIP) are up-regulated in response to hypoxia. Finally, the role of the ROS-TXNIP axis in mediating the activation of the NLRP3 inflammasome and cell death was characterized by pretreating with the ROS scavenger N-acetylcysteine (NAC) and performing TXNIP knockdown experiments in MIN6. Our data indicate for the first time that the inflammasome is involved in the inflammatory response and cell death in hypoxia-induced ß cells through the ROS-TXNIP-NLRP3 axis in vitro. This provides new insight into the relationship between hypoxia and inflammation in T2D.
[Mh] Termos MeSH primário: Apoptose/imunologia
Proteínas de Transporte/imunologia
Hipóxia Celular/imunologia
Inflamassomos/imunologia
Células Secretoras de Insulina/imunologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia
Espécies Reativas de Oxigênio/imunologia
Tiorredoxinas/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular
Inflamassomos/efeitos dos fármacos
Células Secretoras de Insulina/efeitos dos fármacos
Lipopolissacarídeos
Camundongos
NF-kappa B/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Inflammasomes); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (Reactive Oxygen Species); 0 (Txnip protein, mouse); 52500-60-4 (Thioredoxins)
[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:171227
[St] Status:MEDLINE


  6 / 17208 MEDLINE  
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[PMID]:29254287
[Au] Autor:Jiang L; Li H; Zhao N
[Ad] Endereço:Department of Anesthesiology, No. 215 Hospital of Shaanxi Nuclear Industry, Xianyang, Shaanxi, China.
[Ti] Título:Thymoquinone protects against cobalt chloride-induced neurotoxicity via Nrf2/GCL-regulated glutathione homeostasis.
[So] Source:J Biol Regul Homeost Agents;31(4):843-853, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The prevalence of neurodegenerative diseases worldwide has increased dramatically in the last decades. Hypoxia and oxidative stress play a central role in the pathogenesis of neurodegenerative diseases. Thymoquinone (TQ) is a monoterpenoid hydrocarbon compound that possesses potent antioxidant activity. In the current study, we investigated the neuroprotective effects of TQ against CoCl2, a widely used hypoxia-inducing agent. We found that TQ inhibited CoCl2-indcued cytotoxicity in vitro, as reflected by an increase of cell viability and decrease of apoptosis in CoCl2-treated PC12 cells. TQ exhibited a potent protective effect against CoCl2-induced neurotoxicity in vivo, as evidenced by decreased time spent to find the platform site in the Probe trials, reduced escape latencies, decreased traveling distance and reduction of apoptotic cell death in brains in CoCl2-treated rats. CoCl2-resulted decrease of glutathione (GSH) and increase of malondialdehyde (MDA) levels were significantly inhibited by TQ. Inhibition of GSH synthesis by buthionine sulphoximine (BSO) significantly attenuated TQ-induced neuroprotective effects against CoCl2 in rats and in PC12 cells. TQ could upregulate nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/glutamate-cysteine ligase catalytic subunit (GCLc) and Nrf2/glutamate-cysteine ligase modifier subunit (GCLm) pathway which contributed to antioxidant and neuroprotective effects of TQ. In summary, we found that TQ exhibited protective effects against neurotoxicity via upregulation of Nrf2/GCL signaling. Upregulation of Nrf2/GCL signaling promoted the synthesis of GSH and contributed to attenuation of oxidative stress, neuronal cell apoptosis and neurotoxicity. These data have appointed a new path toward the understanding of the neuroprotective activities of TQ.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Benzoquinonas/farmacologia
Cobalto/farmacologia
Hipóxia/prevenção & controle
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Butionina Sulfoximina/antagonistas & inibidores
Butionina Sulfoximina/farmacologia
Hipóxia Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Comportamento Exploratório/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Glutamato-Cisteína Ligase/genética
Glutamato-Cisteína Ligase/metabolismo
Glutationa/agonistas
Glutationa/metabolismo
Seres Humanos
Hipóxia/induzido quimicamente
Hipóxia/genética
Hipóxia/patologia
Masculino
Malondialdeído/antagonistas & inibidores
Malondialdeído/metabolismo
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Células PC12
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzoquinones); 0 (NF-E2-Related Factor 2); 0 (Neuroprotective Agents); 0 (Nfe2l2 protein, rat); 3G0H8C9362 (Cobalt); 490-91-5 (thymoquinone); 4Y8F71G49Q (Malondialdehyde); 5072-26-4 (Buthionine Sulfoximine); EC 6.3.2.2 (GCLM protein, rat); EC 6.3.2.2 (Glutamate-Cysteine Ligase); EC 6.3.2.2. (GCLC protein, rat); EVS87XF13W (cobaltous chloride); GAN16C9B8O (Glutathione)
[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:171220
[St] Status:MEDLINE


  7 / 17208 MEDLINE  
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[PMID]:27776337
[Au] Autor:Chlenski A; Dobratic M; Salwen HR; Applebaum M; Guerrero LJ; Miller R; DeWane G; Solomaha E; Marks JD; Cohn SL
[Ad] Endereço:Department of Pediatrics, University of Chicago, Chicago, IL, USA.
[Ti] Título:Secreted protein acidic and rich in cysteine (SPARC) induces lipotoxicity in neuroblastoma by regulating transport of albumin complexed with fatty acids.
[So] Source:Oncotarget;7(47):77696-77706, 2016 Nov 22.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SPARC is a matrix protein that mediates interactions between cells and the microenvironment. In cancer, SPARC may either promote or inhibit tumor growth depending upon the tumor type. In neuroblastoma, SPARC is expressed in the stromal Schwannian cells and functions as a tumor suppressor. Here, we developed a novel in vivo model of stroma-rich neuroblastoma using non-tumorigenic SHEP cells with modulated levels of SPARC, mixed with tumorigenic KCNR cells. Tumors with stroma-derived SPARC displayed suppressed growth, inhibited angiogenesis and increased lipid accumulation. Based on the described chaperone function of SPARC, we hypothesized that SPARC binds albumin complexed with fatty acids and transports them to tumors. We show that SPARC binds albumin with Kd=18.9±2.3 uM, and enhances endothelial cell internalization and transendothelial transport of albumin in vitro. We also demonstrate that lipids induce toxicity in neuroblastoma cells and show that lipotoxicity is increased when cells are cultured in hypoxic conditions. Studies investigating the therapeutic potential of SPARC are warranted.
[Mh] Termos MeSH primário: Metabolismo dos Lipídeos/efeitos dos fármacos
Neuroblastoma/metabolismo
Osteonectina/genética
Osteonectina/metabolismo
Ácido Palmítico/farmacologia
Soroalbumina Bovina/metabolismo
[Mh] Termos MeSH secundário: Animais
Hipóxia Celular
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Feminino
Terapia Genética
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Camundongos
Modelos Biológicos
Neuroblastoma/genética
Neuroblastoma/terapia
Ácido Palmítico/química
Soroalbumina Bovina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Osteonectin); 0 (SPARC protein, human); 27432CM55Q (Serum Albumin, Bovine); 2V16EO95H1 (Palmitic Acid)
[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:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12773


  8 / 17208 MEDLINE  
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[PMID]:28493473
[Au] Autor:Tahrir FG; Shanmughapriya S; Ahooyi TM; Knezevic T; Gupta MK; Kontos CD; McClung JM; Madesh M; Gordon J; Feldman AM; Cheung JY; Khalili K
[Ad] Endereço:Department of Neuroscience, Center for Neurovirology, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania.
[Ti] Título:Dysregulation of mitochondrial bioenergetics and quality control by HIV-1 Tat in cardiomyocytes.
[So] Source:J Cell Physiol;233(2):748-758, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease remains a leading cause of morbidity and mortality in HIV-positive patients, even in those whose viral loads are well controlled with antiretroviral therapy. However, the underlying molecular events responsible for the development of cardiac disease in the setting of HIV remain unknown. The HIV-encoded Tat protein plays a critical role in the activation of HIV gene expression and profoundly impacts homeostasis in both HIV-infected cells and uninfected cells that have taken up released Tat via a bystander effect. Since cardiomyocyte function, including excitation-contraction coupling, greatly depends on energy provided by the mitochondria, in this study, we performed a series of experiments to assess the impact of Tat on mitochondrial function and bioenergetics pathways in a primary cell culture model derived from neonatal rat ventricular cardiomyocytes (NRVCs). Our results show that the presence of Tat in cardiomyocytes is accompanied by a decrease in oxidative phosphorylation, a decline in the levels of ATP, and an accumulation of reactive oxygen species (ROS). Tat impairs the uptake of mitochondrial Ca ([Ca ] ) and the electrophysiological activity of cardiomyocytes. Tat also affects the protein clearance pathway and autophagy in cardiomyocytes under stress due to hypoxia-reoxygenation conditions. A reduction in the level of ubiquitin along with dysregulated degradation of autophagy proteins including SQSTM1/p62 and a reduction of LC3 II were detected in cardiomyocytes harboring Tat. These results suggest that, by targeting mitochondria and protein quality control, Tat significantly impacts bioenergetics and autophagy resulting in dysregulation of cardiomyocyte health and homeostasis.
[Mh] Termos MeSH primário: Metabolismo Energético
HIV-1/metabolismo
Mitocôndrias Cardíacas/metabolismo
Miócitos Cardíacos/metabolismo
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Apoptose
Autofagia
Cálcio/metabolismo
Canais de Cálcio/metabolismo
Hipóxia Celular
Células Cultivadas
Interações Hospedeiro-Patógeno
Potenciais da Membrana
Proteínas Associadas aos Microtúbulos/metabolismo
Mitocôndrias Cardíacas/virologia
Degradação Mitocondrial
Miócitos Cardíacos/virologia
Fosforilação Oxidativa
Cultura Primária de Células
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Proteína Sequestossoma-1/metabolismo
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (LC3 protein, rat); 0 (Microtubule-Associated Proteins); 0 (Reactive Oxygen Species); 0 (Sequestosome-1 Protein); 0 (Sqstm1 protein, rat); 0 (mitochondrial calcium uniporter); 0 (tat Gene Products, Human Immunodeficiency Virus); 8L70Q75FXE (Adenosine Triphosphate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26002


  9 / 17208 MEDLINE  
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[PMID]:29307823
[Au] Autor:Kim J; Choi S; Kim JO; Kim KK
[Ad] Endereço:Department of Biochemistry, College of Natural Sciences, Chungnam National University, Daejeon, 34134, Republic of Korea.
[Ti] Título:Autophagy-mediated upregulation of cytoplasmic claudin 1 stimulates the degradation of SQSTM1/p62 under starvation.
[So] Source:Biochem Biophys Res Commun;496(1):159-166, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Claudin 1, a major tight junction protein, is highly expressed in various types of tumors such as thyroid, breast, and colorectal cancers. Moreover, claudin 1 is frequently found in the cytoplasm in various types of tumor cells. However, the cytoplasmic function of claudin 1 in tumors still remains largely unknown. Here, we investigated the novel function of cytoplasmic claudin 1 in autophagy. The mRNA expression level of claudin 1 was higher in several types of tumors than in normal tissues. Furthermore, colon tumor tissues showed increased autophagy compared with the adjacent normal tissues. Both endogenous and exogenous claudin 1 showed a cytoplasmic punctate staining pattern and were co-stained with the lysosome-associated membrane protein 1 (LAMP1). Importantly, autophagy-induced conditions, including starvation, increased the protein stability of claudin 1. Moreover, the increased level of claudin 1 stimulated autophagy by decreasing the level of the autophagy substrate, sequestosome1/p62 (SQSTM1), under autophagy-inducing conditions; activation of AMP-activated protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR). Taken together, we demonstrate that the novel function of cytoplasmic claudin 1 is related to autophagy. This study is the first to show a cytoplasmic function of claudin 1 as an autophagy regulator and provides the evidence that claudin 1-mediated autophagy regulation is an integral part of the mechanism by which claudin 1 regulates cancer progression.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Hipóxia Celular
Claudina-1/metabolismo
Glucose/metabolismo
Proteínas de Ligação a RNA/metabolismo
Proteína Sequestossoma-1/metabolismo
[Mh] Termos MeSH secundário: Citoplasma/metabolismo
Células HeLa
Seres Humanos
Células MCF-7
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CLDN1 protein, human); 0 (Claudin-1); 0 (P62 protein, human); 0 (RNA-Binding Proteins); 0 (SQSTM1 protein, human); 0 (Sequestosome-1 Protein); IY9XDZ35W2 (Glucose)
[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:180109
[St] Status:MEDLINE


  10 / 17208 MEDLINE  
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[PMID]:28459279
[Au] Autor:Obeidat M; Nie Y; Fishbane N; Li X; Bossé Y; Joubert P; Nickle DC; Hao K; Postma DS; Timens W; Sze MA; Shannon CP; Hollander Z; Ng RT; McManus B; Miller BE; Rennard S; Spira A; Hackett TL; Lam W; Lam S; Faner R; Agusti A; Hogg JC; Sin DD; Paré PD
[Ad] Endereço:1 The University of British Columbia Centre for Heart Lung Innovation, St. Paul's Hospital, Vancouver, British Columbia, Canada.
[Ti] Título:Integrative Genomics of Emphysema-Associated Genes Reveals Potential Disease Biomarkers.
[So] Source:Am J Respir Cell Mol Biol;57(4):411-418, 2017 10.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic obstructive pulmonary disease is the third leading cause of death worldwide. Gene expression profiling across multiple regions of the same lung identified genes significantly related to emphysema. We sought to determine whether the lung and epithelial expression of 127 emphysema-related genes was also related to lung function in independent cohorts, and whether any of these genes could be used as biomarkers in the peripheral blood of patients with chronic obstructive pulmonary disease. To that end, we examined whether the expression levels of these genes were under genetic control in lung tissue (n = 1,111). We then determined whether the mRNA levels of these genes in lung tissue (n = 727), small airway epithelial cells (n = 238), and peripheral blood (n = 620) were significantly related to lung function measurements. The expression of 63 of the 127 genes (50%) was under genetic control in lung tissue. The lung and epithelial mRNA expression of a subset of the emphysema-associated genes, including ASRGL1, LPHN2, and EDNRB, was strongly associated with lung function. In peripheral blood, the expression of 40 genes was significantly associated with lung function. Twenty-nine of these genes (73%) were also associated with lung function in lung tissue, but with the opposite direction of effect for 24 of the 29 genes, including those involved in hypoxia and B cell-related responses. The integrative genomics approach uncovered a significant overlap of emphysema genes associations with lung function between lung and blood with opposite directions between the two. These results support the use of peripheral blood to detect disease biomarkers.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Genômica
Pulmão/metabolismo
Enfisema Pulmonar/metabolismo
RNA Mensageiro/biossíntese
[Mh] Termos MeSH secundário: Linfócitos B/metabolismo
Linfócitos B/patologia
Biomarcadores/metabolismo
Hipóxia Celular
Feminino
Seres Humanos
Pulmão/patologia
Masculino
Enfisema Pulmonar/genética
Enfisema Pulmonar/patologia
RNA Mensageiro/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (RNA, Messenger)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0284OC



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