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[PMID]:29429180
[Au] Autor:Hu J; Chen ZC; Zhang YZ; Han P; Ma WJ; Zhang Q; Xu M
[Ad] Endereço:Department of Otorhinolaryngology Head and Neck Surgery, Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an 710004, China.
[Ti] Título:[The experimental study on endoplasmic reticulum stress-participated outer hair cell apoptosis in cadherin 23 gene mutant mice].
[So] Source:Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi;53(2):110-117, 2018 Feb 07.
[Is] ISSN:1673-0860
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To test the mechanism and upstream pathway of outer hair cell apoptosis in Cadherin 23 (Cdh23) gene mutant mice. The mutant 23 ( ) 57 /6 ( 6) . 70 . - ( ) . ( ) ( ) . - - ( ) / ( ) . . . 23 . The ABR thresholds in mice were significantly higher than those in B6 mice at the age of 1 and 3 months (both <0.05). The surface preparation with TUNEL staining confirmed OHC apoptosis in mouse cochleae which showed a higher TUNEL positive cell ratio than B6 mouse( =11.291, <0.01). The ER stress marker and mRNA were upregulated in the mouse inner ear, when compared with those in the B6 mouse(both <0.05). The BiP protein extracted from the mouse cochleae was significantly higher than that of B6 mouse measured by Western blot ( =3.66, =0.02). Immunostaining showed that BiP and CHOP were highly detected in the OHC in mouse cochleae, and was mainly detected in the perinuclear region of OHC. However, a bare BiP and CHOP signal were shown in B6 mouse cochleae. The CDH23 protein was specifically localized at the top of the OHC in B6 mice, indicating the localization of the tip links in hair bundle stereocilia. On the contrary, the CDH23 protein was found to be localized from the top to the nuclei of the OHC in mice. Portions of the CDH23 proteins failed to reach the top of the hair bundles and remained in the OHC cytoplasm. As the downstream response of the Cdh23 gene mutation, portions of the mutant CDH23 protein was accumulated in ER lumen resulting in the increase of ER loading and ultimately triggered ER stress and hair cell apoptosis in mouse cochleae.
[Mh] Termos MeSH primário: Apoptose/genética
Caderinas/genética
Estresse do Retículo Endoplasmático/genética
Células Ciliadas Auditivas Externas/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Cóclea/patologia
Estresse do Retículo Endoplasmático/fisiologia
Potenciais Evocados Auditivos do Tronco Encefálico
Células Ciliadas Vestibulares
Marcação In Situ das Extremidades Cortadas
Linfocinas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mutação
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Cdh23 protein, mouse); 0 (Lymphokines); 0 (RNA, Messenger); 0 (immunoglobulin-binding factors); 147336-12-7 (Transcription Factor CHOP)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1673-0860.2018.02.006


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[PMID]:29482510
[Au] Autor:Zhao MH; Hu J; Li S; Wu Q; Lu P
[Ad] Endereço:Department of Ophthalmology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
[Ti] Título:P66Shc expression in diabetic rat retina.
[So] Source:BMC Ophthalmol;18(1):58, 2018 Feb 27.
[Is] ISSN:1471-2415
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: P66Shc is partially localised within the mitochondrial fraction. It is primarily related to the generation of mitochondrial reactive oxygen species and apoptosis. Based on previous studies, we hypothesize that in the retina, p66Shc may exist and affect the development of diabetic retinopathy. The purpose of this study was to investigate p66Shc expression in retinal in streptozotocin-induced diabetic (SD) rats, which may provide a pathway to study the pathogenesis of diabetic retinopathy. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and western blot were used to detect retinal p66Shc mRNA and protein expression in SD rats, respectively. Immunohistochemical staining was applied to detect the location of rat retinal p66Shc expression. TUNEL assay was applied to detect the number of apoptotic cells. RESULTS: P66Shc expression was found in the retina of normal and diabetic rats, and the level of mRNA and protein expression increased with the progression of diabetes mellitus (DM). P66Shc expression was mainly located in the retinal ganglion cell layer and inner nuclear layer. Compared with the normal group, retinal cell tissue apoptosis rate in the D12w group was significantly increased. CONCLUSION: Rat retinal p66Shc expression was mainly in the ganglion cell layer and inner nuclear layer. As the degree of DM progressed, p66Shc expression gradually increased, and the number of apoptotic cells also increased.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/metabolismo
Retinopatia Diabética/metabolismo
Retina/metabolismo
Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Masculino
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Células Ganglionares da Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Shc1 protein, rat); 0 (Src Homology 2 Domain-Containing, Transforming Protein 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180228
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-018-0724-3


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[PMID]:27776507
[Au] Autor:Konstantinidou C; Taraviras S; Pachnis V
[Ad] Endereço:The Francis Crick Institute, Mill Hill Laboratory, The Ridgeway, Mill Hill, London, NW7 1AA, UK.
[Ti] Título:Geminin prevents DNA damage in vagal neural crest cells to ensure normal enteric neurogenesis.
[So] Source:BMC Biol;14(1):94, 2016 10 24.
[Is] ISSN:1741-7007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In vertebrate organisms, the neural crest (NC) gives rise to multipotential and highly migratory progenitors which are distributed throughout the embryo and generate, among other structures, the peripheral nervous system, including the intrinsic neuroglial networks of the gut, i.e. the enteric nervous system (ENS). The majority of enteric neurons and glia originate from vagal NC-derived progenitors which invade the foregut mesenchyme and migrate rostro-caudally to colonise the entire length of the gut. Although the migratory behaviour of NC cells has been studied extensively, it remains unclear how their properties and response to microenvironment change as they navigate through complex cellular terrains to reach their target embryonic sites. RESULTS: Using conditional gene inactivation in mice we demonstrate here that the cell cycle-dependent protein Geminin (Gem) is critical for the survival of ENS progenitors in a stage-dependent manner. Gem deletion in early ENS progenitors (prior to foregut invasion) resulted in cell-autonomous activation of DNA damage response and p53-dependent apoptosis, leading to severe intestinal aganglionosis. In contrast, ablation of Gem shortly after ENS progenitors had invaded the embryonic gut did not result in discernible survival or migratory deficits. In contrast to other developmental systems, we obtained no evidence for a role of Gem in commitment or differentiation of ENS lineages. The stage-dependent resistance of ENS progenitors to mutation-induced genotoxic stress was further supported by the enhanced survival of post gut invasion ENS lineages to γ-irradiation relative to their predecessors. CONCLUSIONS: Our experiments demonstrate that, in mammals, NC-derived ENS lineages are sensitive to genotoxic stress in a stage-specific manner. Following gut invasion, ENS progenitors are distinctly resistant to Gem ablation and irradiation in comparison to their pre-enteric counterparts. These studies suggest that the microenvironment of the embryonic gut protects ENS progenitors and their progeny from genotoxic stress.
[Mh] Termos MeSH primário: Dano ao DNA/efeitos dos fármacos
Sistema Nervoso Entérico/citologia
Geminina/farmacologia
Crista Neural/citologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Células Cultivadas
Sistema Nervoso Entérico/efeitos dos fármacos
Feminino
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Camundongos
Neurogênese/efeitos dos fármacos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Geminin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29324796
[Au] Autor:Li XM; Liu J; Pan FF; Shi DD; Wen ZG; Yang PL
[Ad] Endereço:Key Laboratory for Feed Biotechnology of the Ministry of Agriculture, Feed Research Institute, Chinese Academy of Agricultural Sciences, Beijing, China.
[Ti] Título:Quercetin and aconitine synergistically induces the human cervical carcinoma HeLa cell apoptosis via endoplasmic reticulum (ER) stress pathway.
[So] Source:PLoS One;13(1):e0191062, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Up till now, studies have not been conducted on how the combination of Quercetin (Q), Aconitine (A) and apoptosis induction affects human cervical carcinoma HeLa cells. The result of our findings shows that the combination of Q and A (QA) is capable of synergistically inhibiting the proliferation of HeLa cells in a number of concentrations. QA synergistically inhibits the proliferation of MDR1 gene in the HeLa cells. It is concluded based on our result that QA induces apoptosis and ER stress just as QA-induced ER stress pathway may mediate apoptosis by upregulating mRNA expression levels of eIF2α, ATF4, IRE1, XBP1, ATF6, PERK and CHOP in the HeLa cells. The up-regulating of mRNA expression level of GRP78 and activation of UPR are a molecular basis of QA-induced ER stress.
[Mh] Termos MeSH primário: Aconitina/farmacologia
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Quercetina/farmacologia
Neoplasias do Colo do Útero/patologia
[Mh] Termos MeSH secundário: Subfamília B de Transportador de Cassetes de Ligação de ATP/genética
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Feminino
Células HeLa
Seres Humanos
Marcação In Situ das Extremidades Cortadas
Espécies Reativas de Oxigênio/metabolismo
Resposta a Proteínas não Dobradas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ABCB1 protein, human); 0 (ATP Binding Cassette Transporter, Sub-Family B); 0 (Reactive Oxygen Species); 9IKM0I5T1E (Quercetin); X8YN71D5WC (Aconitine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191062


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[PMID]:29227512
[Au] Autor:Anumanthan G; Sharma A; Waggoner M; Hamm CW; Gupta S; Hesemann NP; Mohan RR
[Ti] Título:Efficacy and Safety Comparison Between Suberoylanilide Hydroxamic Acid and Mitomycin C in Reducing the Risk of Corneal Haze After PRK Treatment In Vivo.
[So] Source:J Refract Surg;33(12):834-839, 2017 Dec 01.
[Is] ISSN:1081-597X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: This study compared the efficacy and safety of suberoylanilide hydroxamic acid (SAHA) and mitomycin C (MMC) up to 4 months in the prevention of corneal haze induced by photorefractive keratectomy (PRK) in rabbits in vivo. METHODS: Corneal haze in rabbits was produced with -9.00 diopter PRK. A single application of SAHA (25 µM) or MMC (0.02%) was applied topically immediately after PRK. Effects of the two drugs were analyzed by slit-lamp microscope, specular microscope, TUNEL assay, and immunofluorescence. RESULTS: Single topical adjunct use of SAHA (25 µM) or MMC (0.02%) after PRK attenuated more than 95% corneal haze and myofibroblast formation (P < .001). SAHA did not reduce keratocyte density, cause keratocyte apoptosis, or increase immune cell infiltration compared to MMC (P < .01 or .001). Furthermore, SAHA dosing did not compromise corneal endothelial phenotype, density, or function in rabbit eyes, whereas MMC application did (P < .01 or .001). CONCLUSIONS: SAHA and MMC significantly decreased corneal haze after PRK in rabbits in vivo. SAHA exhibited significantly reduced short- and long-term damage to the corneal endothelium compared to MMC in rabbits. SAHA is an effective and potentially safer alternative to MMC for the prevention of corneal haze after PRK. Clinical trials are warranted. [J Refract Surg. 2017;33(12):834-839.].
[Mh] Termos MeSH primário: Alquilantes/uso terapêutico
Opacidade da Córnea/prevenção & controle
Modelos Animais de Doenças
Inibidores de Histona Desacetilases/uso terapêutico
Ácidos Hidroxâmicos/uso terapêutico
Mitomicina/uso terapêutico
Ceratectomia Fotorrefrativa/efeitos adversos
[Mh] Termos MeSH secundário: Alquilantes/efeitos adversos
Animais
Apoptose
Córnea/cirurgia
Opacidade da Córnea/etiologia
Técnica Indireta de Fluorescência para Anticorpo
Inibidores de Histona Desacetilases/efeitos adversos
Ácidos Hidroxâmicos/efeitos adversos
Marcação In Situ das Extremidades Cortadas
Mitomicina/efeitos adversos
Coelhos
Lâmpada de Fenda
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 50SG953SK6 (Mitomycin); 58IFB293JI (vorinostat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.3928/1081597X-20170921-02


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[PMID]:29248134
[Au] Autor:Monti D; Sotgia F; Whitaker-Menezes D; Tuluc M; Birbe R; Berger A; Lazar M; Cotzia P; Draganova-Tacheva R; Lin Z; Domingo-Vidal M; Newberg A; Lisanti MP; Martinez-Outschoorn U
[Ad] Endereço:Marcus Institute of Integrative Health at Thomas Jefferson University, Philadelphia, PA.
[Ti] Título:Pilot study demonstrating metabolic and anti-proliferative effects of in vivo anti-oxidant supplementation with N-Acetylcysteine in Breast Cancer.
[So] Source:Semin Oncol;44(3):226-232, 2017 06.
[Is] ISSN:1532-8708
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: High oxidative stress as defined by hydroxyl and peroxyl activity is often found in the stroma of human breast cancers. Oxidative stress induces stromal catabolism, which promotes cancer aggressiveness. Stromal cells exposed to oxidative stress release catabolites such as lactate, which are up-taken by cancer cells to support mitochondrial oxidative phosphorylation. The transfer of catabolites between stromal and cancer cells leads to metabolic heterogeneity between these cells and increased cancer cell proliferation and reduced apoptosis in preclinical models. N-Acetylcysteine (NAC) is an antioxidant that reduces oxidative stress and reverses stromal catabolism and stromal-carcinoma cell metabolic heterogeneity, resulting in reduced proliferation and increased apoptosis of cancer cells in experimental models of breast cancer. The purpose of this clinical trial was to determine if NAC could reduce markers of stromal-cancer metabolic heterogeneity and markers of cancer cell aggressiveness in human breast cancer. METHODS: Subjects with newly diagnosed stage 0 and I breast cancer who were not going to receive neoadjuvant therapy prior to surgical resection were treated with NAC before definitive surgery to assess intra-tumoral metabolic markers. NAC was administered once a week intravenously at a dose of 150 mg/kg and 600 mg twice daily orally on the days not receiving intravenous NAC. Histochemistry for the stromal metabolic markers monocarboxylate transporter 4 (MCT4) and caveolin-1 (CAV1) and the Ki67 proliferation assay and TUNEL apoptosis assay in carcinoma cells were performed in pre- and post-NAC specimens. RESULTS: The range of days on NAC was 14-27 and the mean was 19 days. Post-treatment biopsies showed significant decrease in stromal MCT4 and reduced Ki67 in carcinoma cells. NAC did not significantly change stromal CAV1 and carcinoma TUNEL staining. NAC was well tolerated. CONCLUSIONS: NAC as a single agent reduces MCT4 stromal expression, which is a marker of glycolysis in breast cancer with reduced carcinoma cell proliferation. This study suggests that modulating metabolism in the tumor microenvironment has the potential to impact breast cancer proliferation.
[Mh] Termos MeSH primário: Acetilcisteína/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Carcinoma Ductal de Mama/tratamento farmacológico
Carcinoma Intraductal não Infiltrante/tratamento farmacológico
Depuradores de Radicais Livres/uso terapêutico
Mastectomia
[Mh] Termos MeSH secundário: Adulto
Apoptose
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/metabolismo
Carcinoma Ductal de Mama/patologia
Carcinoma Intraductal não Infiltrante/metabolismo
Carcinoma Intraductal não Infiltrante/patologia
Carcinoma Papilar/tratamento farmacológico
Carcinoma Papilar/metabolismo
Carcinoma Papilar/patologia
Caveolina 1/metabolismo
Proliferação Celular
Feminino
Seres Humanos
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Antígeno Ki-67/metabolismo
Meia-Idade
Transportadores de Ácidos Monocarboxílicos/metabolismo
Proteínas Musculares/metabolismo
Terapia Neoadjuvante
Estadiamento de Neoplasias
Projetos Piloto
Células Estromais/metabolismo
Resultado do Tratamento
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CAV1 protein, human); 0 (Caveolin 1); 0 (Free Radical Scavengers); 0 (Ki-67 Antigen); 0 (Monocarboxylic Acid Transporters); 0 (Muscle Proteins); 0 (SLC16A4 protein, human); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:27775705
[Au] Autor:Horiuchi D; Camarda R; Zhou AY; Yau C; Momcilovic O; Balakrishnan S; Corella AN; Eyob H; Kessenbrock K; Lawson DA; Marsh LA; Anderton BN; Rohrberg J; Kunder R; Bazarov AV; Yaswen P; McManus MT; Rugo HS; Werb Z; Goga A
[Ad] Endereço:Department of Cell and Tissue Biology, University of California, San Francisco (UCSF), San Francisco, California, USA.
[Ti] Título:PIM1 kinase inhibition as a targeted therapy against triple-negative breast tumors with elevated MYC expression.
[So] Source:Nat Med;22(11):1321-1329, 2016 11.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triple-negative breast cancer (TNBC), in which cells lack expression of the estrogen receptor (ER), the progesterone receptor (PR) and the ERBB2 (also known as HER2) receptor, is the breast cancer subtype with the poorest outcome. No targeted therapy is available against this subtype of cancer owing to a lack of validated molecular targets. We previously reported that signaling involving MYC-an essential, pleiotropic transcription factor that regulates the expression of hundreds of genes-is disproportionally higher in triple-negative (TN) tumors than in receptor-positive (RP) tumors. Direct inhibition of the oncogenic transcriptional activity of MYC has been challenging to achieve. Here, by conducting a shRNA screen targeting the kinome, we identified PIM1, a non-essential serine-threonine kinase, in a synthetic lethal interaction with MYC. PIM1 expression was higher in TN tumors than in RP tumors and was associated with poor prognosis in patients with hormone- and HER2-negative tumors. Small-molecule PIM kinase inhibitors halted the growth of human TN tumors with elevated MYC expression in patient-derived tumor xenograft (PDX) and MYC-driven transgenic mouse models of breast cancer by inhibiting the oncogenic transcriptional activity of MYC and restoring the function of the endogenous cell cycle inhibitor, p27. Our findings warrant clinical evaluation of PIM kinase inhibitors in patients with TN tumors that have elevated MYC expression.
[Mh] Termos MeSH primário: Carcinoma Ductal de Mama/metabolismo
Neoplasias Mamárias Experimentais/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
Proteínas Proto-Oncogênicas c-pim-1/antagonistas & inibidores
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Feminino
Seres Humanos
Marcação In Situ das Extremidades Cortadas
Neoplasias Mamárias Experimentais/tratamento farmacológico
Neoplasias Mamárias Experimentais/genética
Camundongos Transgênicos
Microscopia de Fluorescência
Prognóstico
Proteínas Proto-Oncogênicas c-myc/genética
Proteínas Proto-Oncogênicas c-pim-1/metabolismo
RNA Interferente Pequeno
Reação em Cadeia da Polimerase em Tempo Real
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdkn1b protein, mouse); 0 (MYC protein, human); 0 (Myc protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Small Interfering); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.7.11.1 (PIM1 protein, human); EC 2.7.11.1 (Pim1 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-pim-1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4213


  8 / 17459 MEDLINE  
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[PMID]:29289695
[Au] Autor:Han X; Liu C; Zhang K; Guo M; Shen Z; Liu Y; Zuo Z; Cao M; Li Y
[Ad] Endereço:Department of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, PR China; Laboratory of RNA and Major Diseases of Brain and Heart, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, PR China.
[Ti] Título:Calpain and JNK pathways participate in isoflurane - induced nucleus translocation of apoptosis-inducing factor in the brain of neonatal rats.
[So] Source:Toxicol Lett;285:60-73, 2018 Mar 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent studies have demonstrated that volatile anesthetic causes caspase-dependent neuroapoptosis and persistent cognitive deficits in young animals. Apoptosis-inducing factor (AIF) can trigger apoptosis by caspase-independent pathway. Whether isoflurane induces neuroapoptosis by activation of AIF and its possible mechanism are underdetermined. Rats at postnatal day 7 were exposed to 1.1% isoflurane for 4 h and the expression of AIF, cytochrome c, caspase-3, µ-calpain, m-calpain, Bcl-2 and Bax in the mitochondrial, cytosolic, and nuclear fraction, as well as the number of both AIF and TUNEL positive neurons in the cortices of rats were measured. Moreover, the effects of calpain inhibitor MDL-28170 or JNK inhibitor SP600125 on isoflurane-induced AIF release, caspase activation and cognitive deficits were assessed. We found isoflurane activated CytC-caspase-3 dependent apoptosis pathway mainly in the early phase (0-6 h after exposure). Moreover, isoflurane activated mitochondrial µ-calpain, induced AIF truncation during early phase and activated m-calpain, induced AIF release from the mitochondria to cytosol and translocation into the nucleus in the late phase (6-24 h after exposure). MDL-28170 attenuated the isoflurane-induced mitochondrial AIF truncation, release and nuclear translocation, but did not change the expression of cleaved-caspase-3 and mitochondrial Bax and Bcl-2 proteins. SP600125 attenuated isoflurane-induced neuroapoptosis by inhibiting both AIF and caspase-3 pathways and reduced cognitive impairment in neonatal rats. This is the first study to provide the evidence that isoflurane induced AIF-dependent neuroapoptosis by activation of mitochondrial µ-calpain and m-calpain in neonatal rats. JNK inhibition reversed isoflurane-induced neuroapoptosis and subsequent long-term neurocognitive impairment, acting via inhibiting activation of both AIF and caspase-3 pathways.
[Mh] Termos MeSH primário: Anestésicos Inalatórios/toxicidade
Fator de Indução de Apoptose/metabolismo
Encéfalo/efeitos dos fármacos
Calpaína/metabolismo
Núcleo Celular/efeitos dos fármacos
Isoflurano/toxicidade
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Apoptose/efeitos dos fármacos
Encéfalo/metabolismo
Encéfalo/patologia
Calpaína/antagonistas & inibidores
Núcleo Celular/metabolismo
Marcação In Situ das Extremidades Cortadas
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurônios/patologia
Transporte Proteico
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anesthetics, Inhalation); 0 (Apoptosis Inducing Factor); CYS9AKD70P (Isoflurane); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.4.22.- (Calpain)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


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[PMID]:29322247
[Au] Autor:Han JW; Choi J; Kim YS; Kim J; Brinkmann R; Lyu J; Park TK
[Ad] Endereço:Department of Ophthalmology, College of Medicine, Soonchunhyang University, Bucheon, South Korea.
[Ti] Título:Comparison of the neuroinflammatory responses to selective retina therapy and continuous-wave laser photocoagulation in mouse eyes.
[So] Source:Graefes Arch Clin Exp Ophthalmol;256(2):341-353, 2018 Feb.
[Is] ISSN:1435-702X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: This study investigated microglia and inflammatory cell responses after selective retina therapy (SRT) with microsecond-pulsed laser in comparison to continuous-wave laser photocoagulation (cwPC). METHODS: Healthy C57BL/6 J mice were treated with either a train of short pulses (SRT; 527-nm, Q-switched, 1.7-µs pulse) or a conventional thermal continuous-wave (532-nm, 100-ms pulse duration) laser. The mice were sacrificed and their eyes were enucleated 1, 3, 7, and 14 days after both laser treatments. Pattern of cell death on retinal section was evaluated by TUNEL assay, and the distribution of activated inflammatory cells and glial cells were observed under immunohistochemistry. Consecutive changes for the expression of cytokines such as IL-1ß, TNF-α, and TGF-ß were also examined using immunohistochemistry, and compared among each period after quantification by Western blotting. RESULTS: The numbers of TUNEL-positive cells in the retinal pigment epithelium (RPE) layer did not differ in SRT and cwPC lesions, but TUNEL-positive cells in neural retinas were significantly less on SRT. Vague glial cell activation was observed in SRT-treated lesions. The population of inflammatory cells was also significantly decreased after SRT, and the cells were located in the RPE layer and subretinal space. Proinflammatory cytokines, including IL-1ß and TNF-α, showed significantly lower levels after SRT; conversely, the level of TGF-ß was similar to the cwPC-treated lesion. CONCLUSIONS: SRT resulted in selective RPE damage without collateral thermal injury to the neural retina, and apparently produced negligible glial activation. In addition, SRT showed a markedly less inflammatory response than cwPC, which may have important therapeutic implications for several macular diseases.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Fotocoagulação a Laser/métodos
Lasers de Estado Sólido/uso terapêutico
Neuroglia/patologia
Doenças Retinianas/cirurgia
Epitélio Pigmentado da Retina/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Western Blotting
Contagem de Células
Modelos Animais de Doenças
Angiofluoresceinografia/métodos
Fundo de Olho
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Camundongos
Camundongos Endogâmicos C57BL
Neuroglia/metabolismo
Doenças Retinianas/diagnóstico
Doenças Retinianas/metabolismo
Epitélio Pigmentado da Retina/metabolismo
Tomografia de Coerência Óptica/métodos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1007/s00417-017-3883-7


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[PMID]:29293568
[Au] Autor:Do K; Laing BT; Landry T; Bunner W; Mersaud N; Matsubara T; Li P; Yuan Y; Lu Q; Huang H
[Ad] Endereço:Department of Kinesiology, East Carolina University, Greenville, North Carolina, United States of America.
[Ti] Título:The effects of exercise on hypothalamic neurodegeneration of Alzheimer's disease mouse model.
[So] Source:PLoS One;13(1):e0190205, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alzheimer's disease is a neurodegenerative disorder that affects the central nervous system. In this study, we characterized and examined the early metabolic changes in the triple transgenic mouse AD model (3xtg-AD), and their relationship with the hypothalamus, a key regulator of metabolism in the central nervous system. We observed that the 3xtg-AD model exhibited significantly higher oxygen consumption as well as food intake before reported amyloid plaque formation, indicating that metabolic abnormalities occurred at early onset in the 3xtg-AD model compared with their counterparts. Analysis of gene expression in the hypothalamus indicated increased mRNA expression of inflammation- and apoptosis-related genes, as well as decreased gene expression of Agouti-related protein (AgRP) and Melanocortin 4 receptor (MC4R) at 12 weeks of age. Immunofluorescence analysis revealed that pro-opiomelanocortin (POMC) and NPY-expressing neurons decreased at 24 weeks in the 3xtg-AD model. Four weeks of voluntary exercise were sufficient to reverse the gene expression of inflammation and apoptotic markers in the hypothalamus, six weeks of exercise improved glucose metabolism, moreover, 8 weeks of voluntary exercise training attenuated apoptosis and augmented POMC and NPY-expressing neuronal populations in the hypothalamus compared to the control group. Our results indicated that early onset of metabolic abnormalities may contribute to the pathology of AD, which is associated with increased inflammation as well as decreased neuronal population and key neuropeptides in the hypothalamus. Furthermore, early intervention by voluntary exercise normalized hypothalamic inflammation and neurodegeneration as well as glucose metabolism in the 3xtg-AD model. The data, taken as a whole, suggests a hypothalamic-mediated mechanism where exercise prevents the progression of dementia and of Alzheimer's disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/patologia
Modelos Animais de Doenças
Hipotálamo/patologia
Condicionamento Físico Animal
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Regulação da Expressão Gênica
Glucose/metabolismo
Hipotálamo/metabolismo
Marcação In Situ das Extremidades Cortadas
Camundongos
Camundongos Transgênicos
Mitocôndrias/metabolismo
Pró-Opiomelanocortina/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 66796-54-1 (Pro-Opiomelanocortin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190205



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