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[PMID]:28467316
[Au] Autor:Chen R; Cai X; Ma K; Zhou Y; Wang Y; Jiang T
[Ad] Endereço:The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
[Ti] Título:The fabrication of double-layered chitosan/gelatin/genipin nanosphere coating for sequential and controlled release of therapeutic proteins.
[So] Source:Biofabrication;9(2):025028, 2017 Jun 01.
[Is] ISSN:1758-5090
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bone regeneration is a complicated process and includes a number of distinct and sequential stages of coordinated cellular actions under the regulation of multiple growth factors. Therefore, bone grafting materials in which growth factors can be incorporated and released in a programmed order in line with the bone tissue healing process may lead to desirable clinical outcomes. In the present study, a double-layered chitosan/gelatin/genipin (d-CSG/G) nanosphere coating is developed by using layer-by-layer electrophoretic deposition and genipin crosslinking. The surface morphology, physicochemical and mechanical properties of the coatings are explored. Cytochrome C is used as a therapeutic model protein and is successfully loaded on the inner and outer layers of the coating. The protein release can be controlled by the loading position, genipin concentration and thickness of the outer layer. Furthermore, the cell response to the coatings was evaluated. Real-time polymerase chain reactions, immunofluorescence staining and extracellular matrix mineralization assay confirmed that the functions of the loaded growth factor are fully preserved after fabrication. Overall, the d-CSG/G nanosphere coating could be a promising growth factor delivery system to promote bone tissue regeneration.
[Mh] Termos MeSH primário: Biomimética/métodos
Quitosana/química
Materiais Revestidos Biocompatíveis/química
Citocromos c/uso terapêutico
Gelatina/química
Iridoides/química
Nanosferas/química
[Mh] Termos MeSH secundário: Animais
Proteína Morfogenética Óssea 2/química
Calcificação Fisiológica
Bovinos
Reagentes para Ligações Cruzadas/química
Preparações de Ação Retardada
Matriz Extracelular/metabolismo
Imunofluorescência
Células Mesenquimais Estromais/citologia
Nanosferas/ultraestrutura
Osteocalcina/metabolismo
Ratos
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Recombinantes/química
Soluções
Espectroscopia de Infravermelho com Transformada de Fourier
Propriedades de Superfície
Fator de Crescimento Transformador beta/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 2); 0 (Coated Materials, Biocompatible); 0 (Cross-Linking Reagents); 0 (Delayed-Action Preparations); 0 (Iridoids); 0 (Recombinant Proteins); 0 (Solutions); 0 (Transforming Growth Factor beta); 0 (recombinant human bone morphogenetic protein-2); 104982-03-8 (Osteocalcin); 9000-70-8 (Gelatin); 9007-43-6 (Cytochromes c); 9012-76-4 (Chitosan); A3V2NE52YG (genipin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1088/1758-5090/aa70c3


  2 / 9614 MEDLINE  
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[PMID]:29299551
[Au] Autor:Qi H; Jiang Y; Yin Z; Jiang K; Li L; Shuai J
[Ad] Endereço:Complex Systems Research Center, Shanxi University, Taiyuan 030006, China.
[Ti] Título:Optimal pathways for the assembly of the Apaf-1·cytochrome c complex into apoptosome.
[So] Source:Phys Chem Chem Phys;20(3):1964-1973, 2018 Jan 17.
[Is] ISSN:1463-9084
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The formation of a heptameric apoptosome is a crucial event in the intrinsic cell death pathway. Considerable progress has been made towards unraveling the constituents and the structure of the apoptosome as well as the mechanism of apoptosome-mediated caspase-9 activation. However, a significant gap remains in the understanding of this process, i.e., how seven Apaf-1·cytochrome c complexes stepwisely assemble into an apoptosome. Here, we construct a biophysical model that incorporates current biochemical knowledge about the formation of apoptosome. We propose 11 elementary routes and enumerate all 2047 possible assembly pathways from the Apaf-1·cytochrome c complex to the heptameric apoptosome. By combining mathematical analysis and numerical simulation, we find that two elementary routes are the most favorable biochemical reaction routes and there are 52 optimal assembly pathways which are economical and relatively fast. Our study yields the first comprehensive analysis of apoptosome assembly and provides insights into complex assembly pathways.
[Mh] Termos MeSH primário: Apoptossomas/metabolismo
Fator Apoptótico 1 Ativador de Proteases/metabolismo
Caspase 9/metabolismo
[Mh] Termos MeSH secundário: Apoptossomas/química
Fator Apoptótico 1 Ativador de Proteases/química
Citocromos c/metabolismo
Seres Humanos
Cinética
Modelos Moleculares
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APAF1 protein, human); 0 (Apoptosomes); 0 (Apoptotic Protease-Activating Factor 1); 9007-43-6 (Cytochromes c); EC 3.4.22.- (Caspase 9)
[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:180105
[St] Status:MEDLINE
[do] DOI:10.1039/c7cp06726g


  3 / 9614 MEDLINE  
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[PMID]:29232945
[Au] Autor:Su L; Yang JF; Fu X; Dong L; Zhou DY; Sun LM; Gong Z
[Ad] Endereço:School of Food Science and Technology, Dalian Polytechnic University, National Engineering Research Center of Seafood , Number 1 Qinggongyuan, Ganjingzi District, Dalian 116034, P. R. China.
[Ti] Título:Ultraviolet-Ray-Induced Sea Cucumber (Stichopus japonicus) Melting Is Mediated by the Caspase-Dependent Mitochondrial Apoptotic Pathway.
[So] Source:J Agric Food Chem;66(1):45-52, 2018 Jan 10.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sea cucumber body-wall melting occurs under certain circumstances. We have shown that apoptosis but not autolysis plays a critical role in the initial stage. However, it is still unclear how apoptosis is triggered in this process. In this study, we examined the levels of reactive oxygen species (ROS), the levels of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax) proteins, the depolarization of mitochondrial transmembrane potentials, and cytochrome c (Cyt c) release during sea cucumber melting induced by ultraviolet (UV) exposure. We also investigated the contribution of caspase in this process by injecting a pan-caspase inhibitor. Our data showed that UV exposure stimulates ROS production, dysfunction of mitochondria, and the release of Cyt c in sea cucumber coelomic fluid cells and body walls. We found a decrease of Bcl-2 and increase of Bax in the mitochondria after UV exposure. We also demonstrated that these changes are associated with elevated caspase-9 and -3 activity. Finally, our data showed that the inhibition of caspases-9 and -3 using an inhibitor suppresses UV-induced sea cucumber melting. These results suggest that apoptosis during sea cucumber melting is mediated by mitochondrial dysfunction and follows the activation of the caspase-signaling pathway. This study presents a novel insight into the mechanism of sea cucumber melting.
[Mh] Termos MeSH primário: Caspases/metabolismo
Pepinos-do-Mar/fisiologia
Pepinos-do-Mar/efeitos da radiação
[Mh] Termos MeSH secundário: Clorometilcetonas de Aminoácidos/farmacologia
Animais
Apoptose/efeitos da radiação
Inibidores de Caspase/farmacologia
Citocromos c/metabolismo
Potencial da Membrana Mitocondrial/efeitos da radiação
Mitocôndrias/metabolismo
Transporte Proteico/efeitos da radiação
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Pepinos-do-Mar/efeitos dos fármacos
Raios Ultravioleta
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (Caspase Inhibitors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Reactive Oxygen Species); 0 (bcl-2-Associated X Protein); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 9007-43-6 (Cytochromes c); EC 3.4.22.- (Caspases)
[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:171214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b03888


  4 / 9614 MEDLINE  
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[PMID]:27779444
[Au] Autor:Salimi A; Roudkenar MH; Sadeghi L; Mohseni A; Seydi E; Pirahmadi N; Pourahmad J
[Ad] Endereço:a Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences , Tehran , Iran ; Department of Pharmacology and Toxicology , School of Pharmacy, Ardabil University of Medical Science , Ardabil , Iran ; Students Research Committee, School of Pharmacy, Shahid Beheshti University of Medical Scie
[Ti] Título:Selective Anticancer Activity of Acacetin Against Chronic Lymphocytic Leukemia Using Both In Vivo and In Vitro Methods: Key Role of Oxidative Stress and Cancerous Mitochondria.
[So] Source:Nutr Cancer;68(8):1404-1416, 2016 Nov-Dec.
[Is] ISSN:1532-7914
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The present study investigates the in vitro and in vivo effect of acacetin (4'-methoxy-5,7-dihydroxyflavone) on chronic lymphocytic leukemia (CLL) B-lymphocytes and mitochondria. CLL B-lymphocytes and healthy B-lymphocytes were obtained from CLL patients and healthy donors, respectively. Mitochondria were isolated from B-lymphocytes of both groups. Xenografts in severe combined immune deficient mice were used to examine the toxicity and anti CLL activity of acacetin. We evaluated and compared the mechanism of action of acacetin on CLL and healthy B-lymphocytes and their mitochondria. We have found that acacetin (10 µM) can selectively induce apoptosis on CLL B-lymphocyte (25% at 24 h) by directly targeting mitochondria, through increased reactive oxygen species (ROS) formation, MMP collapse, MPT, release of cytochrome c, caspase 3 activation, and finally apoptosis, while sparing normal healthy B-lymphocytes unaffected at similar concentrations. Besides, oral administration of acacetin showed a potent in vivo anticancer activity in CLL xenograft mouse models. Our in vivo findings indicate that acacetin accumulates and kills CLL B-lymphocyte in a rather selective way through targeting cancerous mitochondria and ROS formation, which ends in CLL therapy. Finally, we can recommend acacetin as a promising compound for further drug development assays for the CLL treatment.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Flavonas/farmacologia
Leucemia Linfocítica Crônica de Células B/tratamento farmacológico
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
[Mh] Termos MeSH secundário: Idoso
Animais
Antineoplásicos/farmacologia
Linfócitos B/efeitos dos fármacos
Linfócitos B/patologia
Citocromos c/metabolismo
Seres Humanos
Leucemia Linfocítica Crônica de Células B/patologia
Metaloproteinases da Matriz/metabolismo
Camundongos SCID
Meia-Idade
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Flavones); 0 (Reactive Oxygen Species); 9007-43-6 (Cytochromes c); EC 3.4.24.- (Matrix Metalloproteinases); KWI7J0A2CC (acacetin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE


  5 / 9614 MEDLINE  
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[PMID]:27770269
[Au] Autor:Arany I; Carter A; Hall S; Fulop T; Dixit M
[Ad] Endereço:Department of Pediatrics, Division of Pediatric Nephrology, University of Mississippi Medical Center, Research Wing Room R116/B, 2500 N. State St., Jackson, MS, 39216, USA. iarany@umc.edu.
[Ti] Título:Coenzyme Q10 protects renal proximal tubule cells against nicotine-induced apoptosis through induction of p66 -dependent antioxidant responses.
[So] Source:Apoptosis;22(2):220-228, 2017 Feb.
[Is] ISSN:1573-675X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic nicotine exposure (via smoking, E-cigarettes) increases oxidative stress in the kidney that sensitizes it to additional injury in experimental models and in the renal patient. The pro-apoptotic p66 protein-via serine36 phosphorylation that facilitates its mitochondrial translocation and therein cytochrome c binding-generates oxidative stress that leads to injury of renal proximal tubule cells during chronic nicotine exposure. Coenzyme Q10-a clinically safe antioxidant-has been used against nicotine/smoke extract-associated oxidative stress in various non-renal cells. This study explored the anti-oxidant/anti-apoptotic effect of Coenzyme Q10 on nicotine-induced oxidative stress and its impact on p66shc in cultured rat renal proximal tubule cells (NRK52E). We studied the anti-oxidant effect of 10 µM Coenzyme Q10 using various mutants of the p66shc gene and also determined the induction of selected anti-oxidant entities (antioxidant response element, promoter of the manganese superoxide dismutase gene) in reporter luciferase assay during oxidative stress induced by 200 µM nicotine. Our studies revealed that Coenzyme Q10 strongly inhibits nicotine-mediated production of reactive oxygen species and consequent apoptosis that requires serine36 phosphorylation but not mitochondrial translocation/cytochrome c binding of p66 . While both nicotine and Coenzyme Q10 stimulates the p66shc promoter, only nicotine exposure results in mitochondrial translocation of p66 . In contrast, the Coenzyme Q10-stimulated and non-mitochondrial p66 activates the anti-oxidant manganese superoxide dismutase promoter via the antioxidant response elements and hence, rescues cells from nicotine-induced oxidative stress and consequent apoptosis.
[Mh] Termos MeSH primário: Apoptose/genética
Túbulos Renais Proximais/metabolismo
Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/genética
Ubiquinona/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Apoptose/efeitos dos fármacos
Citocromos c/metabolismo
Sistemas Eletrônicos de Liberação de Nicotina
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Nicotina/toxicidade
Estresse Oxidativo/efeitos dos fármacos
Fosforilação
Ratos
Espécies Reativas de Oxigênio
Fumar/efeitos adversos
Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/metabolismo
Ubiquinona/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Reactive Oxygen Species); 0 (Shc1 protein, rat); 0 (Src Homology 2 Domain-Containing, Transforming Protein 1); 1339-63-5 (Ubiquinone); 6M3C89ZY6R (Nicotine); 9007-43-6 (Cytochromes c); EJ27X76M46 (coenzyme Q10)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s10495-016-1309-3


  6 / 9614 MEDLINE  
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[PMID]:29287084
[Au] Autor:Ong L; McDonald KO; Ledgerwood EC
[Ad] Endereço:Department of Biochemistry, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
[Ti] Título:Differentiation and cell density upregulate cytochrome c levels in megakaryoblastic cell lines: Implications for analysis of CYCS-associated thrombocytopenia.
[So] Source:PLoS One;12(12):e0190433, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in the cytochrome c gene (CYCS) cause autosomal dominant thrombocytopenia by an unknown mechanism. While attempting to generate megakaryoblastic cell lines exogenously expressing cytochrome c variants, we discovered that endogenous cytochrome c expression increased both upon induction of differentiation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), and as cell density increased. A concomitant increase in cytochrome c oxidase subunit II in response to PMA, but not cell higher cell density, suggests upregulation of the mitochondrial respiratory chain may be a specific feature of differentiation. These results highlight the likely importance of cytochrome c in both differentiating and proliferating cells, and illustrate the unsuitability of megakaryoblastic lines for modeling CYCS-associated thrombocytopenia.
[Mh] Termos MeSH primário: Diferenciação Celular
Citocromos c/metabolismo
Células Progenitoras de Megacariócitos/enzimologia
Regulação para Cima
[Mh] Termos MeSH secundário: Diferenciação Celular/efeitos dos fármacos
Células HeLa
Seres Humanos
Acetato de Tetradecanoilforbol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9007-43-6 (Cytochromes c); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190433


  7 / 9614 MEDLINE  
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[PMID]:29254330
[Au] Autor:Shi H; Zou J; Zhang T; Che H; Gao X; Wang C; Wang Y; Xue C
[Ad] Endereço:College of Food Science and Engineering, Ocean University of China , No. 5 Yushan Road, Qingdao, Shandong Province 266003, PR China.
[Ti] Título:Protective Effects of DHA-PC against Vancomycin-Induced Nephrotoxicity through the Inhibition of Oxidative Stress and Apoptosis in BALB/c Mice.
[So] Source:J Agric Food Chem;66(2):475-484, 2018 Jan 17.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The clinical use of glycopeptide antibiotic vancomycin is usually accompanied by nephrotoxicity, limiting its application and therapeutic efficiency. The aim of this study was to investigate the protection of DHA-enriched phosphatidylcholine (DHA-PC) against nephrotoxicity using a model of vancomycin-induced male BALB/c mice with renal injury by measuring death curves, histological changes, and renal function indexes. The addition of DHA in DHA and DHA-PC groups were 300 mg/kg per day on the basis of human intake level in our study. Results indicated that DHA-PC could dramatically extend the survival time of mice, while traditional DHA and PC had no significant effects. Moreover, oral administration of DHA-PC exhibited better effects on reducing vancomycin-induced increases of blood urea nitrogen, creatinine, cystatin C, and kidney injury molecule-1 levels than traditional DHA and PC. DHA-PC significantly delayed the development of vancomycin-induced renal injury, including tubular necrosis, hyaline casts, and tubular degeneration. A further mechanistic study revealed that the protective effect of DHA-PC on vancomycin-mediated toxicity might be attributed to its ability to inhibit oxidative stress and inactivate mitogen-activated protein kinase (MAPK) signaling pathways, which was associated with upregulation of Bcl-2 and downregulation of caspase-9, caspase-3, cytochrome-c, p38, and JNK. These findings suggest that DHA-PC may be acted as the dietary supplements or functional foods against vancomycin-induced nephrotoxicity.
[Mh] Termos MeSH primário: Antibacterianos/toxicidade
Apoptose/efeitos dos fármacos
Ácidos Docosa-Hexaenoicos/administração & dosagem
Nefropatias/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Fosfatidilcolinas/administração & dosagem
Substâncias Protetoras/administração & dosagem
Vancomicina/toxicidade
[Mh] Termos MeSH secundário: Animais
Caspase 3/genética
Caspase 3/metabolismo
Caspase 9/genética
Caspase 9/metabolismo
Citocromos c/metabolismo
Ácidos Docosa-Hexaenoicos/química
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/fisiopatologia
Nefropatias/etiologia
Nefropatias/genética
Nefropatias/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Proteínas Quinases Ativadas por Mitógeno/genética
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fosfatidilcolinas/química
Substâncias Protetoras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Phosphatidylcholines); 0 (Protective Agents); 25167-62-8 (Docosahexaenoic Acids); 6Q205EH1VU (Vancomycin); 9007-43-6 (Cytochromes c); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b04565


  8 / 9614 MEDLINE  
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[PMID]:28471452
[Au] Autor:Chowdhury SR; Ray U; Chatterjee BP; Roy SS
[Ad] Endereço:Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Council of Scientific and Industrial Research, Kolkata, India.
[Ti] Título:Targeted apoptosis in ovarian cancer cells through mitochondrial dysfunction in response to Sambucus nigra agglutinin.
[So] Source:Cell Death Dis;8(5):e2762, 2017 May 04.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ovarian carcinoma (OC) patients encounter the severe challenge of clinical management owing to lack of screening measures, chemoresistance and finally dearth of non-toxic therapeutics. Cancer cells deploy various defense strategies to sustain the tumor microenvironment, among which deregulated apoptosis remains a versatile promoter of cancer progression. Although recent research has focused on identifying agents capable of inducing apoptosis in cancer cells, yet molecules efficiently breaching their survival advantage are yet to be classified. Here we identify lectin, Sambucus nigra agglutinin (SNA) to exhibit selectivity towards identifying OC by virtue of its specific recognition of α-2, 6-linked sialic acids. Superficial binding of SNA to the OC cells confirm the hyper-sialylated status of the disease. Further, SNA activates the signaling pathways of AKT and ERK1/2, which eventually promotes de-phosphorylation of dynamin-related protein-1 (Drp-1). Upon its translocation to the mitochondrial fission loci Drp-1 mediates the central role of switch in the mitochondrial phenotype to attain fragmented morphology. We confirmed mitochondrial outer membrane permeabilization resulting in ROS generation and cytochrome-c release into the cytosol. SNA response resulted in an allied shift of the bioenergetics profile from Warburg phenotype to elevated mitochondrial oxidative phosphorylation, altogether highlighting the involvement of mitochondrial dysfunction in restraining cancer progression. Inability to replenish the SNA-induced energy crunch of the proliferating cancer cells on the event of perturbed respiratory outcome resulted in cell cycle arrest before G2/M phase. Our findings position SNA at a crucial juncture where it proves to be a promising candidate for impeding progression of OC. Altogether we unveil the novel aspect of identifying natural molecules harboring the inherent capability of targeting mitochondrial structural dynamics, to hold the future for developing non-toxic therapeutics for treating OC.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Mitocôndrias/metabolismo
Dinâmica Mitocondrial/efeitos dos fármacos
Lectinas de Plantas/farmacologia
Proteínas Inativadoras de Ribossomos/farmacologia
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Citocromos c/metabolismo
Citosol/metabolismo
Feminino
GTP Fosfo-Hidrolases/metabolismo
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Microscopia Confocal
Proteínas Associadas aos Microtúbulos/metabolismo
Proteínas Mitocondriais/metabolismo
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Pontos de Checagem da Fase S do Ciclo Celular/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins); 0 (Mitochondrial Proteins); 0 (Plant Lectins); 0 (Reactive Oxygen Species); 0 (Sambucus nigra lectins); 9007-43-6 (Cytochromes c); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 3.2.2.22 (Ribosome Inactivating Proteins); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.5.5 (DNM1L protein, human)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.77


  9 / 9614 MEDLINE  
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[PMID]:29227073
[Au] Autor:Uspenska KR; Gergalova GL; Lykhmus OY; Skok MV
[Ti] Título:The effect of amixin and agmatine on cytochrome C release from isolated mitochondria
[So] Source:Ukr Biochem J;88(1):5-10, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Mitochondrial nicotinic acetylcholine receptors (nAChRs) control permeability transition pore formation and cytochrome c release in the presence of apoptogenic factors. This study demonstrates that pharmacological agents amixin and agmatine affect mitochondrial nAChR functioning: they slightly suppress cytochrome c release from mouse brain and liver mitochondria stimulated with apoptogenic dose of Са2+ and prevent the effect of α7 nAChR agonist PNU282987. We conclude that mitochondria may be one of therapeutic targets of amixin and agmatine.
[Mh] Termos MeSH primário: Agmatina/farmacologia
Indutores de Interferon/farmacologia
Mitocôndrias/efeitos dos fármacos
Tilorona/farmacologia
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzamidas/antagonistas & inibidores
Benzamidas/farmacologia
Encéfalo/efeitos dos fármacos
Compostos Bicíclicos com Pontes/antagonistas & inibidores
Compostos Bicíclicos com Pontes/farmacologia
Cálcio/farmacologia
Fracionamento Celular
Citocromos c/antagonistas & inibidores
Citocromos c/secreção
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mitocôndrias/metabolismo
Agonistas Nicotínicos/farmacologia
Especificidade de Órgãos
Receptor Nicotínico de Acetilcolina alfa7/agonistas
Receptor Nicotínico de Acetilcolina alfa7/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (Bridged Bicyclo Compounds); 0 (Interferon Inducers); 0 (Nicotinic Agonists); 0 (PNU-282987); 0 (alpha7 Nicotinic Acetylcholine Receptor); 70J407ZL5Q (Agmatine); 9007-43-6 (Cytochromes c); O6W7VEW6KS (Tilorone); SY7Q814VUP (Calcium)
[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/ubj88.01.005


  10 / 9614 MEDLINE  
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[PMID]:27770420
[Au] Autor:Harper-Leatherman AS; Wallace JM; Rolison DR
[Ad] Endereço:Chemistry and Biochemistry Department, Fairfield University, 1073 North Benson Road, Fairfield, CT, 06824, USA. aharper@fairfield.edu.
[Ti] Título:Cytochrome c Stabilization and Immobilization in Aerogels.
[So] Source:Methods Mol Biol;1504:149-163, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sol-gel-derived aerogels are three-dimensional, nanoscale materials that combine large surface area with high porosity. These traits make them useful for any rate-critical chemical process, particularly sensing or electrochemical applications, once physical or chemical moieties are incorporated into the gels to add their functionality to the ultraporous scaffold. Incorporating biomolecules into aerogels, other than such rugged species as lipases or cellulose, has been challenging due to the inability of most biomolecules to remain structurally intact within the gels during the necessary supercritical fluid (SCF) processing. However, the heme protein cytochrome c (cyt.c) forms self-organized superstructures around gold (or silver) nanoparticles in buffer that can be encapsulated into wet gels as the sol undergoes gelation. The guest-host wet gel can then be processed to form composite aerogels in which cyt.c retains its characteristic visible absorption. The gold (or silver) nanoparticle-nucleated superstructures protect the majority of the protein from the harsh physicochemical conditions necessary to form an aerogel. The Au~cyt.c superstructures exhibit rapid gas-phase recognition of nitric oxide (NO) within the bioaerogel matrix, as facilitated by the high-quality pore structure of the aerogel, while remaining viable for weeks at room temperature. More recently, careful control of synthetic parameters (e.g., buffer concentration, protein concentration, SCF extraction rate) have allowed for the preparation of cyt.c-silica aerogels, sans nucleating nanoparticles; these bioaerogels also exhibit rapid gas-phase sensing while retaining protein structural stability.
[Mh] Termos MeSH primário: Citocromos c/química
Enzimas Imobilizadas/química
Géis/química
Dióxido de Silício/química
[Mh] Termos MeSH secundário: Animais
Estabilidade Enzimática
Ouro/química
Cavalos
Nanopartículas Metálicas/química
Nanopartículas Metálicas/ultraestrutura
Óxido Nítrico/análise
Transição de Fase
Prata/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzymes, Immobilized); 0 (Gels); 31C4KY9ESH (Nitric Oxide); 3M4G523W1G (Silver); 7440-57-5 (Gold); 7631-86-9 (Silicon Dioxide); 9007-43-6 (Cytochromes c)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180115
[Lr] Data última revisão:
180115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE



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