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[PMID]:29408405
[Au] Autor:Wang H; Park BS; Lim WA; Ki JS
[Ad] Endereço:Department of Biotechnology, Sangmyung University, Seoul 03016, South Korea.
[Ti] Título:CpMCA, a novel metacaspase gene from the harmful dinoflagellate Cochlodinium polykrikoides and its expression during cell death.
[So] Source:Gene;651:70-78, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Metacaspases (MCAs) are cysteine proteases that share sequence homology with caspases, and may play roles in programmed cell death (PCD). In the present study, we identified a novel MCA gene (CpMCA) from the red tide dinoflagellate Cochlodinium polykrikoides, and examined its molecular characteristics and gene expression in response to algicide-induced cell death. CpMCA cDNA is 1164 bp in length, containing a dinoflagellate spliced leader sequence (dinoSL), an 879-bp open reading frame (ORF), which codes for a 293-aa protein, and a poly (A) tail. Multi-sequence comparison indicated that CpMCA belongs to type I MCA, but it has a different structure at the N-terminal. Phylogenetic analysis showed that C. polykrikoides may have acquired the MCA gene from bacteria by means of horizontal gene transfer (HGT). In addition, expressions of CpMCA significantly increased following exposure to the common algicides copper sulfate and oxidizing chlorine, which trigger cell death in dinoflagellates, suggesting that CpMCA may be involved in cell death.
[Mh] Termos MeSH primário: Caspases/genética
Dinoflagelados/genética
[Mh] Termos MeSH secundário: Morte Celular/efeitos dos fármacos
Morte Celular/genética
DNA Complementar
DNA de Protozoário
Dinoflagelados/efeitos dos fármacos
Dinoflagelados/enzimologia
Expressão Gênica
Transferência Genética Horizontal
Genes Bacterianos
Genes de Protozoários
Herbicidas/farmacologia
Filogenia
Análise de Sequência de DNA
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (DNA, Protozoan); 0 (Herbicides); EC 3.4.22.- (Caspases)
[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:180207
[St] Status:MEDLINE


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[PMID]:28461165
[Au] Autor:Ahmed FRS; Amin R; Hasan I; Asaduzzaman AKM; Kabir SR
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Faculty of Science, University of Rajshahi, Rajshahi 6205, Bangladesh.
[Ti] Título:Antitumor properties of a methyl-ß-d-galactopyranoside specific lectin from Kaempferia rotunda against Ehrlich ascites carcinoma cells.
[So] Source:Int J Biol Macromol;102:952-959, 2017 Sep.
[Is] ISSN:1879-0003
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A lectin was isolated from the tuberous rhizome of Keampferia rotunda by using different chromatographic methods with the molecular weight of 21±1kDa. The lectin contained highest percentage of leucine and lowest percentage of tryptophan residues as determined by LC-MS. The lectin agglutinated mice and human erythrocytes and the hemagglutination activity was inhibited by Methyl-ß-d-galactopyranoside. The lectin did not lose its activity in the presence of urea but the activity abolished completely when treated with EDTA. The lectin exhibited its activity at the pH ranging from 6.0 to 9.0 and in a temperature range of 30-80°C. Antiproliferative activity was studied against Ehrlich ascites carcinoma (EAC) and U87 cell lines. No inhibitory effect was observed against U87 cell line whereas 43.7% cell growth inhibition was observed in vitro against EAC cells at 160µg/ml. The lectin was injected (i.p.) in EAC bearing Swiss albino mice at the doses of 3.0 and 6.0mg/kg/day for five consecutive days and 41 and 59% of EAC cell growth inhibition was observed, respectively. The cell growth inhibition was due to the induction of apoptosis in the EAC cells which was confirmed by cell morphological study, caspase-3 inhibitor and apoptosis-related gene expression.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Carcinoma de Ehrlich/patologia
Galactose/metabolismo
Lectinas de Plantas/farmacologia
Zingiberaceae/química
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Antineoplásicos/isolamento & purificação
Antineoplásicos/metabolismo
Apoptose/efeitos dos fármacos
Apoptose/genética
Caspases/metabolismo
Bovinos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Hemaglutinação/efeitos dos fármacos
Seres Humanos
Concentração de Íons de Hidrogênio
Camundongos
Peso Molecular
Lectinas de Plantas/química
Lectinas de Plantas/isolamento & purificação
Lectinas de Plantas/metabolismo
Especificidade por Substrato
Temperatura Ambiente
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Plant Lectins); EC 3.4.22.- (Caspases); X2RN3Q8DNE (Galactose)
[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:170503
[St] Status:MEDLINE


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[PMID]:29378549
[Au] Autor:Li S; Pasquin S; Eid HM; Gauchat JF; Saleem A; Haddad PS
[Ad] Endereço:Department of Pharmacology and Physiology, Université de Montréal, P.O. Box 6128, Downtown Postal Station, Montreal, (Quebec), H3C 3J7, Canada.
[Ti] Título:Anti-apoptotic potential of several antidiabetic medicinal plants of the eastern James Bay Cree pharmacopeia in cultured kidney cells.
[So] Source:BMC Complement Altern Med;18(1):37, 2018 Jan 30.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Our team has identified 17 Boreal forest species from the traditional pharmacopeia of the Eastern James Bay Cree that presented promising in vitro and in vivo biological activities in the context of type 2 diabetes (T2D). We now screened the 17 plants extracts for potential anti-apoptotic activity in cultured kidney cells and investigated the underlying mechanisms. METHODS: MDCK (Madin-Darnby Canine Kidney) cell damage was induced by hypertonic medium (700 mOsm/L) in the presence or absence of maximal nontoxic concentrations of each of the 17 plant extracts. After 18 h' treatment, cells were stained with Annexin V (AnnV) and Propidium iodide (PI) and subjected to flow cytometry to assess the cytoprotective (AnnV /PI ) and anti-apoptotic (AnnV /PI ) potential of the 17 plant extracts. We then selected a representative subset of species (most cytoprotective, moderately so or neutral) to measure the activity of caspases 3, 8 and 9. RESULTS: Gaultheria hispidula and Abies balsamea are amongst the most powerful cytoprotective and anti-apoptotic plants and appear to exert their modulatory effect primarily by inhibiting caspase 9 in the mitochondrial apoptotic signaling pathway. CONCLUSION: We conclude that several Cree antidiabetic plants exert anti-apoptotic activity that may be relevant in the context of diabetic nephropathy (DN) that affects a significant proportion of Cree diabetics.
[Mh] Termos MeSH primário: Hipoglicemiantes/farmacologia
Medicina Tradicional
Extratos Vegetais/farmacologia
Plantas Medicinais/química
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Anexina A5/química
Apoptose/efeitos dos fármacos
Canadá
Caspases/metabolismo
Nefropatias Diabéticas/metabolismo
Cães
Hipoglicemiantes/química
Células Madin Darby de Rim Canino
Extratos Vegetais/química
Propídio/química
Substâncias Protetoras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Hypoglycemic Agents); 0 (Plant Extracts); 0 (Protective Agents); 36015-30-2 (Propidium); EC 3.4.22.- (Caspases)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2104-1


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[PMID]:29339744
[Au] Autor:Lagrange B; Benaoudia S; Wallet P; Magnotti F; Provost A; Michal F; Martin A; Di Lorenzo F; Py BF; Molinaro A; Henry T
[Ad] Endereço:CIRI, Centre International de Recherche en Infectiologie, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, École Normale Supérieure de Lyon, Univ Lyon, F-69007, Lyon, France.
[Ti] Título:Human caspase-4 detects tetra-acylated LPS and cytosolic Francisella and functions differently from murine caspase-11.
[So] Source:Nat Commun;9(1):242, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Caspase-4/5 in humans and caspase-11 in mice bind hexa-acylated lipid A, the lipid moeity of lipopolysaccharide (LPS), to induce the activation of non-canonical inflammasome. Pathogens such as Francisella novicida express an under-acylated lipid A and escape caspase-11 recognition in mice. Here, we show that caspase-4 drives inflammasome responses to F. novicida infection in human macrophages. Caspase-4 triggers F. novicida-mediated, gasdermin D-dependent pyroptosis and activates the NLRP3 inflammasome. Inflammasome activation could be recapitulated by transfection of under-acylated LPS from different bacterial species or synthetic tetra-acylated lipid A into cytosol of human macrophage. Our results indicate functional differences between human caspase-4 and murine caspase-11. We further establish that human Guanylate-binding proteins promote inflammasome responses to under-acylated LPS. Altogether, our data demonstrate a broader reactivity of caspase-4 to under-acylated LPS than caspase-11, which may have important clinical implications for management of sepsis.
[Mh] Termos MeSH primário: Caspases Iniciadoras/metabolismo
Caspases/metabolismo
Francisella/metabolismo
Lipopolissacarídeos/metabolismo
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Acilação
Animais
Caspases/genética
Caspases Iniciadoras/genética
Células Cultivadas
Citosol/microbiologia
Francisella/fisiologia
Seres Humanos
Inflamassomos/genética
Inflamassomos/metabolismo
Macrófagos/microbiologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Interferência de RNA
Especificidade da Espécie
Células U937
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Lipopolysaccharides); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); EC 3.4.22.- (CASP4 protein, human); EC 3.4.22.- (Casp11 protein, mouse); EC 3.4.22.- (Caspases); EC 3.4.22.- (Caspases, Initiator)
[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:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02682-y


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[PMID]:29223571
[Au] Autor:Perdigão GMC; Lopes MS; Marques LB; Prazeres PHDM; Gomes KS; de Oliveira RB; Pinto MCX; de Souza-Fagundes EM
[Ad] Endereço:Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Título:Novel nitroaromatic compound activates autophagy and apoptosis pathways in HL60 cells.
[So] Source:Chem Biol Interact;283:107-115, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:N-(2-butanoyloxyethyl)-4-(chloromethyl)-3-nitrobenzamide (NBCN) is a nitroaromatic bioreducible compound with cytotoxic effects in cancer cell lines. The aim of this work was to investigate the molecular mechanisms involved in cell death promoted by NBCN in HL60 cells. We observed that NBCN treatment increased intracellular ROS and reduced mitochondria membrane potential (ΔΨm). NBCN treatment also induced morphological changes, phosphatidylserine exposure, cell cycle arrest in G2/M-phase, DNA condensation and fragmentation, but it did not show cytotoxic effects on normal human peripheral blood mononuclear cells (PBMCs). NBCN-induced caspase 3- and 9-dependent DNA fragmentation, which was blocked by pretreatment with the broad-spectrum caspase inhibitor, z-VAD-fmk. Flow cytometry analysis demonstrated that NBCN also increased of the number of autophagic vesicles in HL60 cells, which was not observed when cells were pre-treated with bafilomycin A1. Taken together, these results indicate that NBCN triggered the mitochondrial apoptotic pathway and led to the onset of autophagic cell death, which contributed to its cytotoxic effects.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Benzamidinas/toxicidade
[Mh] Termos MeSH secundário: Clorometilcetonas de Aminoácidos/farmacologia
Benzamidinas/química
Inibidores de Caspase/farmacologia
Caspases/metabolismo
Células Cultivadas
Fragmentação do DNA/efeitos dos fármacos
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Células HL-60
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/metabolismo
Pontos de Checagem da Fase M do Ciclo Celular/efeitos dos fármacos
Macrolídeos/farmacologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (Benzamidines); 0 (Caspase Inhibitors); 0 (Macrolides); 0 (Reactive Oxygen Species); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 3459-99-2 (3-nitrobenzamidine); 88899-55-2 (bafilomycin A1); EC 3.4.22.- (Caspases)
[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:171211
[St] Status:MEDLINE


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[PMID]:28460485
[Au] Autor:Lv LX; Zhou ZX; Zhou Z; Zhang LJ; Yan R; Zhao Z; Yang LY; Bian XY; Jiang HY; Li YD; Sun YS; Xu QQ; Hu GL; Guan WJ; Li YQ
[Ad] Endereço:Institute of Pharmaceutical Biotechnology and College of Pharmaceutical Sciences, Zhejiang University, 310058 Hangzhou, China.
[Ti] Título:Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization.
[So] Source:Oncotarget;8(16):26992-27006, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hispidin and its derivatives are widely distributed in edible mushrooms. Hispidin is more cytotoxic to A549, SCL-1, Bel7402 and Capan-1 cancer cells than to MRC5 normal cells; by contrast, hispidin protects H9c2 cardiomyoblast cells from hydrogen peroxide-induced or doxorubicin-induced apoptosis. Consequently, further research on how hispidin affects normal and cancer cells may help treat cancer and reduce chemotherapy-induced side effects. This study showed that hispidin caused caspase-independent death in SGC-7901 cancer cells but not in GES-1 normal cells. Hispidin-induced increases in LC3-II occurred in SGC-7901 cells in a time independent manner. Cell death can be partially inhibited by treatment with ATG5 siRNA but not by autophagy or necroptosis inhibitors. Ultrastructural evidence indicated that hispidin-induced necrotic cell death involved autophagy. Hispidin-induced lysosomal membrane permeabilization (LMP) related to complex cell death occurred more drastically in SGC-7901 cells than in GES-1 cells. Ca2+ rather than cathepsins from LMP contributed more to cell death. Hispidin induced microtubule depolymerization, which can cause LMP, more drastically in SGC-7901 cells than in GES-1 cells. At 4.1 µM, hispidin promoted cell-free tubulin polymerization but at concentrations higher than 41 µM, hispidin inhibited polymerization. Hispidin did not bind to tubulin. Alterations in microtubule regulatory proteins, such as stathmin phosphorylation at Ser16, contributed to hispidin-induced SGC-7901 cell death. In conclusion, hispidin at concentrations higher than 41 µM may inhibit tubulin polymerization by modulating microtubule regulatory proteins, such as stathmin, causing LMP and complex SGC-7901 cell death. This mechanism suggests a promising novel treatment for human cancer.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Membranas Intracelulares/efeitos dos fármacos
Lisossomos/metabolismo
Multimerização Proteica/efeitos dos fármacos
Pironas/farmacologia
Tubulina (Proteína)/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspases/metabolismo
Morte Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Microtúbulos/química
Microtúbulos/metabolismo
Óxido Nítrico/biossíntese
Permeabilidade
Fosforilação
Estatmina/metabolismo
Tubulina (Proteína)/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyrones); 0 (STMN1 protein, human); 0 (Stathmin); 0 (Tubulin); 31C4KY9ESH (Nitric Oxide); EC 3.4.22.- (Caspases); SSJ18CG55E (hispidin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15935


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[PMID]:29441925
[Au] Autor:Cai QY; Liu XL; Zhang XQ; Liu YX; Li M; Zhao CZ; Zhang XM; Meng QH
[Ti] Título:Anti-neuroinflammation activity of acetylpuerarin mediated by a PKC-δ-dependent caspase signaling pathway: and studies.
[So] Source:Pharmazie;71(10):575-582, 2016 Oct 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study was performed to evaluate the regulating effects of acetylpuerarin on inflammation in an Alzheimer's disease (AD) rat model and an inflammatory cell model. METHODS: Healthy female Wistar rats and mouse BV2 microglia cells were selected. AD rat models were established with the method of bilateral intrahippocampal amyloid-ß(Aß)1-42 injections and the inflammatory cell models were established using Aß25-35-induced mouse BV2 microglia cells. The cytotoxicity of acetylpuerarin on BV2 microglial cells was detected by MTT assay and the morphological changes of BV2 microglia cells were observed under inverted phase contrast microscope. As inflammatory parameters, the expressions of IL-1ß, iNOS, IL-6 and TNF-α were examined by Elisa, Immunohistochemistry, Quantitative real-time PCR (qRT-PCR), Western blot and Immunofluorescence analyses. We also examined the acetylpuerarin's effect on the activity of PKC-δ, IKKß and caspase-8/caspase-3 pathway. RESULTS: Acetylpuerarin exerted no significant cytotoxicity on BV2 microglia cells and was applied in all subsequent experiments. Acetylpuerarin treatment mitigated Aß25-35-induced morphological changes associated with microglia activation. Moreover, the expressions of caspase-8, cleaved caspase-3, PKC-δ, IKKß, iNOS, IL-1ß and TNF-α in Aß25-35-stimulated BV2 microglia cells were significantly suppressed by acetylpuerarin and in a dose-dependent manner. Additionally, the expression of IL-1ß in hippocampus and the level of IL-6 in serum of Aß1-42 treated rat were reduced by acetylpuerarin and in a concentration-dependent manner. CONCLUSION: Our results suggest that acetylpuerarin's anti-inflammation mechanism on AD may be mediated through the PKC-δ-dependent caspase signalling pathway.
[Mh] Termos MeSH primário: Caspases/efeitos dos fármacos
Encefalite/tratamento farmacológico
Isoflavonas/farmacologia
Proteína Quinase C-delta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Doença de Alzheimer/induzido quimicamente
Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/patologia
Peptídeos beta-Amiloides
Animais
Sobrevivência Celular/efeitos dos fármacos
Citocinas/metabolismo
Encefalite/induzido quimicamente
Feminino
Ativação de Macrófagos/efeitos dos fármacos
Camundongos
Microglia/efeitos dos fármacos
Fragmentos de Peptídeos
Ratos
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Cytokines); 0 (Isoflavones); 0 (Peptide Fragments); 0 (acetylpuerarin); 0 (amyloid beta-protein (1-42)); 0 (amyloid beta-protein (25-35)); EC 2.7.1.- (Prkcd protein, rat); EC 2.7.11.13 (Protein Kinase C-delta); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6660


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[PMID]:28462526
[Au] Autor:Man SM; Karki R; Kanneganti TD
[Ad] Endereço:Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
[Ti] Título:Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases.
[So] Source:Immunol Rev;277(1):61-75, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cell death is a fundamental biological phenomenon that is essential for the survival and development of an organism. Emerging evidence also indicates that cell death contributes to immune defense against infectious diseases. Pyroptosis is a form of inflammatory programmed cell death pathway activated by human and mouse caspase-1, human caspase-4 and caspase-5, or mouse caspase-11. These inflammatory caspases are used by the host to control bacterial, viral, fungal, or protozoan pathogens. Pyroptosis requires cleavage and activation of the pore-forming effector protein gasdermin D by inflammatory caspases. Physical rupture of the cell causes release of the pro-inflammatory cytokines IL-1ß and IL-18, alarmins and endogenous danger-associated molecular patterns, signifying the inflammatory potential of pyroptosis. Here, we describe the central role of inflammatory caspases and pyroptosis in mediating immunity to infection and clearance of pathogens.
[Mh] Termos MeSH primário: Caspases/metabolismo
Infecção/imunologia
Inflamassomos/metabolismo
Mediadores da Inflamação/metabolismo
Piroptose
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Imunidade
Interleucina-18/metabolismo
Interleucina-1beta/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 (Inflammasomes); 0 (Inflammation Mediators); 0 (Interleukin-18); 0 (Interleukin-1beta); EC 3.4.22.- (Caspases)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12534


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[PMID]:29338725
[Au] Autor:Hu B; Zhang T; An HM; Zheng JL; Yan X; Huang XW
[Ad] Endereço:Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, People's Republic of China. beearhu@hotmail.com.
[Ti] Título:Herbal formula YGJDSJ inhibits anchorage-independent growth and induces anoikis in hepatocellular carcinoma Bel-7402 cells.
[So] Source:BMC Complement Altern Med;18(1):17, 2018 Jan 16.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Based on clinical medications and related studies, we established a Yang-Gan Jie-Du Sang-Jie (YGJDSJ) herbal formula for hepatocarcinoma treatment. In present study, we evaluated the anti-cancer potential of YGJDSJ on suspension-grown human hepatocellular carcinoma Bel-7402 cells. METHODS: Bel-7402 cells were cultured in poly(2-hydroxyethyl methacrylate) (poly-HEMA) coated plates and treated with YGJDSJ. Anchorage-independent cell growth was detected by cell Counting Kit-8 (CCK-8) assay and soft agar colony formation assay. Anoikis was detected by ethdium homodimer-1 (EthD-1) staining and flow cytometry analysis. Caspases activities were detected by the cleavage of chromogenic substrate. Reactive oxygen species (ROS) was detected by 2',7'-dichlorofluorescin diacetate (DCFH-DA) staining. Protein expression and phosphorylation was identified by western blot. Protein expression was knocked-down by siRNA. RESULTS: YGJDSJ inhibited the proliferation of Bel-7402 cells in poly-HEMA coated plates and anchorage-independent growth of Bel-7402 cells in soft agar. YGJDSJ also induced anoikis in Bel-7402 cells as indicated by EthD-1 staining and flow cytometry analysis. YGJDSJ activated caspase-3, - 8, and - 9 in suspension-grown Bel-7402 cells. The pan-caspase inhibitor Z-VAD-FMK significantly abrogated the effects of YGJDSJ on anoikis in suspension-grown Bel-7402 cells. In addition, YGJDSJ increased ROS in suspension-grown Bel-7402 cells. The ROS scavenger N-acetyl-L-cysteine (NAC) partially attenuated YGJDSJ-induced activation of caspase-3, - 8 and - 9 and anoikis in suspension-grown Bel-7402 cells. Furthermore, YGJDSJ inhibited expression and phosphorylation of protein tyrosine kinase 2 (PTK2) in suspension-grown Bel-7402 cells. Over-expression of PTK2 significantly abrogated YGJDSJ induced anoikis. CONCLUSIONS: YGJDSJ inhibits anchorage-independent growth and induce caspase-mediated anoikis in Bel-7402 cells, and may relate to ROS generation and PTK2 downregulation.
[Mh] Termos MeSH primário: Anoikis/efeitos dos fármacos
Carcinoma Hepatocelular/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Neoplasias Hepáticas/metabolismo
[Mh] Termos MeSH secundário: Caspases/metabolismo
Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Quinase 1 de Adesão Focal/metabolismo
Seres Humanos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Reactive Oxygen Species); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-018-2083-2


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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



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