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Pesquisa : G02.111.660.871.790.600.962 [Categoria DeCS]
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Texto completo SciELO Chile
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Id: biblio-1115779
Autor: Rivera-Krstulović, Catalina; Duran-Aniotz, Claudia.
Título: La respuesta a proteínas mal plegadas como blanco terapéutico en la enfermedad de Alzheimer / Unfolded protein response as a target in the treatment of Alzheimer's disease
Fonte: Rev. méd. Chile;148(2):216-223, feb. 2020. graf.
Idioma: es.
Projeto: FONDECYT; . CONICYT; . FONDEF.
Resumo: The clinical features of Alzheimer's disease (AD), for example the progressive memory loss, are produced by neuronal loss and synaptic dysfunction. These events have been associated with histopathological alterations in AD brain, including the presence of amyloid plaques and neurofibrillary tangles. Recent studies suggest that cellular stress produced by the aggregation of misfolded proteins leads to alterations in protein homeostasis, that is regulated for the most part by endoplasmic reticulum (ER). The ER is the main compartment involved in the folding and secretion of proteins and is drastically affected in AD neurons. Recent evidence implicates the participation of adaptive responses to stress within the ER in the disease process through a signaling pathway known as the Unfolded Protein Response (UPR) which alleviates the protein aggregation and ER stress. Based on the involvement of ER stress in several diseases, efforts are being done to identify small molecules that can inhibit or activate selective UPR components. Here, we review the findings suggesting a functional role of ER stress in the etiology of AD. Possible therapeutic strategies to mitigate ER stress in the context of AD are discussed.
Descritores: Doença de Alzheimer
-Transdução de Sinais
Retículo Endoplasmático
Resposta a Proteínas não Dobradas
Estresse do Retículo Endoplasmático
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Texto completo SciELO Brasil
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Id: lil-777091
Autor: Xie, Hong; Huang, Liu; Li, Yayun; Zhang, Han; Liu, Hao.
Título: Endoplasmic reticulum stress and renal lesion in mice with combination of high-fat diet and streptozotocin-induced diabetes
Fonte: Acta cir. bras;31(3):150-155, Mar. 2016. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Creative Scientific Research Project for Postgraduate of Bengbu Medical College.
Resumo: ABSTRACT PURPOSE : To investigate in the kidney the pathologic changes and expression of GRP78 and CHOP in the Kunming (KM) mice with combination of high-fat diet and streptozotocin-induced diabetes. METHODS : Sixty two male KM mice were randomly divided into a normal control (NC) group (n=20) and a high-fat diet (HFD) group (n=42). After a four-week dietary manipulation, the KM mice in the HFD group were injected intraperitoneally with streptozotocin to induce diabetes. After diabetic models were successfully established, the kidneys were excised and conserved for further test. RESULTS : No significant difference in the body weight was observed after the dietary manipulation (p=0.554). After the streptozotocin was injected, fasting blood glucose levels in the diabetes group (DM) were significantly higher than that in the NC group (p<0.0001). Glomerular atrophy observed under light microscope in the DM group was more serious compared with the NC group. The expression of GRP78 and CHOP in the kidneys of the mice in the DM group were higher compared with the NC group. CONCLUSION : Renal lesion occurs in the diabetic Kunming mice induced by combination of high-fat diet and low-dose streptozotocin, and endoplasmic reticulum stress and CHOP may contribute to the injury process.
Descritores: Diabetes Mellitus Experimental/metabolismo
Nefropatias Diabéticas/metabolismo
Nefropatias Diabéticas/patologia
Estresse do Retículo Endoplasmático/fisiologia
Dieta Hiperlipídica
-Glicemia/análise
Peso Corporal/fisiologia
Distribuição Aleatória
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/patologia
Modelos Animais de Doenças
Fator de Transcrição CHOP/metabolismo
Resposta a Proteínas não Dobradas/fisiologia
Proteínas de Choque Térmico/metabolismo
Rim/metabolismo
Rim/patologia
Limites: Animais
Masculino
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-748273
Autor: Santos, Maria Mercês; Tannuri, Ana Cristina Aoun; Coelho, Maria Cecilia Mendonça; Gonçalves, Josiane de Oliveira; Serafini, Suellen; Silva, Luiz Fernando Ferraz da; Tannuri, Uenis.
Título: Immediate expression of c-fos and c-jun mRNA in a model of intestinal autotransplantation and ischemia-reperfusion in situ
Fonte: Clinics;70(5):373-379, 05/2015. tab, graf.
Idioma: en.
Resumo: OBJECTIVE: Intestinal ischemia-reperfusion injury occurs in several clinical conditions and after intestinal transplantation. The aim of the present study was to investigate the phenomena of apoptosis and cell proliferation in a previously described intestinal ischemia-reperfusion injury autograft model using immunohistochemical markers. The molecular mechanisms involved in ischemia-reperfusion injury repair were also investigated by measuring the expression of the early activation genes c-fos and c-jun, which induce apoptosis and cell proliferation. MATERIALS AND METHODS: Thirty adult male Wistar rats were subjected to surgery for a previously described ischemia-reperfusion model that preserved the small intestine, the cecum and the ascending colon. Following reperfusion, the cecum was harvested at different time points as a representative segment of the intestine. The rats were allocated to the following four subgroups according to the reperfusion time: subgroup 1: 5 min; subgroup 2: 15 min; subgroup 3: 30 min; and subgroup 4: 60 min. A control group of cecum samples was also collected. The expression of c-fos, c-jun and immunohistochemical markers of cell proliferation and apoptosis (Ki67 and TUNEL, respectively) was studied. RESULTS: The expression of both c-fos and c-jun in the cecum was increased beginning at 5 min after ischemia-reperfusion compared with the control. The expression of c-fos began to increase at 5 min, peaked at 30 min, and exhibited a declining tendency at 60 min after reperfusion. A progressive increase in c-jun expression was observed. Immunohistochemical analyses confirmed these observations. CONCLUSION: The early activation of the c-fos and c-jun genes occurred after intestinal ischemia-reperfusion injury, and these genes can act together to trigger cell proliferation and apoptosis. .
Descritores: Estresse do Retículo Endoplasmático
Ácidos Graxos/metabolismo
Hepatócitos/fisiologia
Resposta a Proteínas não Dobradas
-Acetilcisteína/metabolismo
Linhagem Celular Tumoral
Células Cultivadas
Glutationa/metabolismo
Hepatócitos/metabolismo
MICE, INBRED CABDOMENABDOMINAL INJURIESBL
Oxirredução
Dobramento de Proteína
Limites: Animais
Camundongos
Ratos
Tipo de Publ: Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-730780
Autor: Saito, Renata de Freitas.
Título: Indução de estresse de retículo endoplasmático como estratégia de quimiossensibilização de melanoma / Endoplasmic reticulum stress induction as a melanoma cell chemosensitization strategy.
Fonte: São Paulo; s.n; 2014. [174] p. ilus, graf.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Faculdade de Medicina para obtenção do grau de Doutor.
Resumo: Embora muitos estudos tenham contribuído para o esclarecimento do processo de tumorigênese em melanomas, ainda não há tratamento eficaz para melanomas metastáticos. Esta ineficácia terapêutica pode estar relacionada com a adaptação e seleção de células de melanoma à indução de estresse de RE. Ultrapassar os níveis sustentados de estresse de RE, interferindo nas vias de adaptação a este estresse, foi o alvo deste estudo na tentativa de propor uma nova estratégia terapêutica para sensibilizar células de melanoma a morte induzida por cisplatina. Mostramos que GADD153, um dos componentes da via de UPR (Unfolded Protein Response) responsável por induzir apoptose em reposta ao estresse de RE, está excluída do núcleo em melanomas primários, metástases ganglionares e viscerais. Este dado sugere que a localização citoplasmática do fator de transcrição GADD153 possa estar envolvida na resposta adaptativa de melanomas ao estresse de RE, uma vez que se sabe que GADD153 se acumula no núcleo em resposta a este estresse. Investigamos se a indução de estresse de RE seria capaz de induzir a translocação de GADD153 para o núcleo e resultar na sensibilização de células de melanoma a morte induzida por cisplatina (CDDP). Realizamos o tratamento de células de melanoma (SbCl2, Mel85, SK-MEL- 29, SK-MEL-28 e SK-MEL-147) com tunicamicina (Tuni), indutor clássico de estresse de RE, previamente ao tratamento com CDDP. Demonstramos que em todas as linhagens exceto em SK-MEL-29, houve um aumento na porcentagem de células hipodiploides (>50%) no tratamento combinado (Tuni>CDDP) comparado ao tratamento com CDDP. As células SK-MEL-147 se mostraram mais sensíveis à indução de estresse de RE e as células SK-MEL-29 mais resistentes. Algumas diferenças entre estas linhagens como a expressão de GRP78 de superfície e presença de oligossacarídeos ?1-6 ligados de superfície podem estar relacionadas com esta resposta diferencial ao estresse de RE. Em todas as linhagens...

Melanoma is among the most aggressive malignancies with increasing worldwide incidence and there is no effective treatment for the metastatic disease. The absence of an effective therapy may be due to adaptation and selection of melanoma cells to endoplasmic reticulum (ER) stress. We showed that GADD153, one of the components of the ER stress-mediated apoptosis pathway, was mostly excluded from the nucleus of primary and metastatic melanoma cells compared to nevus cells. These data suggest that the unexpected GADD153 cellular localization could be involved in melanoma cell adaption to ER stress, since GADD153 accumulates in the nucleus during ER stress. Unfolded protein response (UPR) signaling induced in response to ER stress, is a dual process that induces a protective response to restore ER homeostasis or cell death if ER stress is severe or persistent. We investigated if induction of ER stress was a potential strategy to chemosensitize melanoma cells to a second insult by surpassing the adaptive levels to ER stress. We first treated human melanoma cells (SbCl2, SK-MEL-28, Mel85, SK-MEL-29 and SK-MEL-147) with tunicamycin (Tuni), an ER stress inducer, before cisplatin (CDDP) treatment. CDDP is a low cost chemotherapeutic drug currently used in Brazil as a second line for melanoma treatment, especially in youngsters. All cell lines, except SK-MEL-29, demonstrated an >50% increase in the percentage of hypodiploid cells with Tuni>CDDP treatment when compared to CDDP only. The same results were obtained with temozolomide (TMZ), equivalent drug to the active form of dacarbazine, the first line of cytotoxic treatment of melanomas. UPR markers, GRP78 and nuclear translocation of GADD153 were induced by Tuni. Differences between SK-MEL-29 and SK-MEL-147 as cell surface GRP78 and ?1-6 oligossacharides can be related with the differential ER stress sensitization observed in these cells. One of the cellular mechanisms that are regulated by ER stress is autophagy....
Descritores: Autofagia
Cisplatino
Melanoma
Fator de Transcrição CHOP
Resposta a Proteínas não Dobradas
Responsável: BR66.1 - Divisão de Biblioteca e Documentação
BR66.1


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Id: lil-591867
Autor: Moreno, Adrian A; Orellana, Ariel.
Título: The physiological role of the unfolded protein response in plants
Fonte: Biol. Res;44(1):75-80, 2011. ilus.
Idioma: en.
Projeto: Fondecyt.
Resumo: Unfolded protein response (UPR) is a signaling mechanism activated by misfolded protein accumulation in the endoplasmic reticulum. It is a widespread process that has been described in organisms ranging from yeasts to mammals. In recent years, our understanding of UPR signaling pathway in plants has advanced. Two transcription factors from Arabidopsis thaliana have been reported to function as the sensor/ transducer of this response (AtbZIP60 and AtbZIP28). They seem to be involved in both heat and biotic stress. Furthermore, overexpression of one of them (AtbZIP60) produces plants with a higher tolerance for salt stress, suggesting that this transcription factor may play a role in abiotic stress. Furthermore, some data suggest that crosstalk between genes involved in abiotic stress and UPR may also exist in plants. On the other hand, UPR is related to programmed cell death (PCD) in plants given that that triggering UPR results in induction of PCD-related genes. This article reviews the latest progress in understanding UPR signaling in plants and analyzes its relationship to key processes in plant physiology.
Descritores: Arabidopsis/fisiologia
Retículo Endoplasmático/fisiologia
Transdução de Sinais/fisiologia
Fatores de Transcrição/fisiologia
Resposta a Proteínas não Dobradas/fisiologia
-Estresse Fisiológico/fisiologia
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME



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