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Id: biblio-829110
Autor: Frasson, Murilo Zomer; Kock, Kaiser S; Monteiro, Letícia F; Romagna, Jonas V.
Título: Number of lymph nodes dissected in colorectal cancer and probability of positive nodes, angiolymphatic/perineural invasion, and intracellular mucin in a referral service / Número de Linfonodos Dissecados no Câncer Colorretal e Probabilidade de Nodos Positivos, Invasão Angiolinfática, Perineural e Mucina Intracelular em Serviço de Referência
Fonte: J. coloproctol. (Rio J., Impr.);36(4):220-226, Oct.-Dec. 2016. tab, graf.
Idioma: en.
Resumo: Among the malignancies, colorectal cancer ranks fourth in incidence in Brazil. The main prognostic measure is related to the amount of affected lymph nodes. Thus, many studies try to correlate the number of extracted lymph nodes, with the probability of obtaining positive nodes. Study objectives: Determine whether dissection ≥12 lymph nodes increases probability of finding neoplastic involvement in relation to resection of fewer. Assess the presence of angiolymphatic invasion; perineural and intracelluar mucin and correlate it with tumor differentiation and TNM classification. Correlate the average of positive nodes with angiolymphatic and perineural involvement. Methods: Pathological reports of patients operated for CRC from 1997 to 2013 were analyzed. A probability (p) less than 0.05 was considered to indicate statistical significance. Results: Median of lymph nodes sent to analysis was 12 nodes. Average number of lymph nodes affected was higher when a number ≥12 lymph nodes were dissected (p = 0.001) (Kruskal-Wallis). There was positive association between average of affected lymph nodes and presence of angiolymphatic (p < 0.0001) or perineural invasion (p = 0.024). Angiolymphatic and intracellular mucin are less present in well-differentiated adenocarcinomas. Perineural and angiolymphatic were more present in T4 stages. Conclusions: Dissection ≥ 12 lymph nodes increases chances of finding positive nodes. There is relation between angiolymphatic invasion; perineural and intracellular mucin and type of tumor differentiation, as well as TNM classification. Average number of lymph nodes affected was higher in presence of perineural or angiolymphatic invasion.

Dentre as neoplasias malignas, o câncer colorretal ocupa o quarto lugar em incidência no Brasil. Uma das principais medidas de prognóstico está relacionada à quantidade de linfonodos acometidos. Sendo assim, muitos trabalhos estudam meios de correlacionar o número de linfonodos dissecados, com a probabilidade de se obterem linfonodos positivos. Objetivos do estudo: Determinar se a dissecção ≥ 12 linfonodos aumenta a probabilidade de se encontrar acometimento neoplásico nos mesmos em relação à menor ressecção. Avaliar a presença de invasão angiolinfática; perineural e mucina intracelular e correlacioná-la com diferenciação tumoral e classificação TNM. Correlacionar a média de nodos positivos com acometimento angiolinfático e perineural. Métodos: Foram analisados laudos anatomopatológicos de pacientes operados por câncer colorretal (CCR) de 1997 a 2013. A probabilidade (p) menor que 0,05 foi considerada para indicar significância estatística. Resultados: A média de linfonodos comprometidos foi maior quando um número ≥ 12 linfonodos foram dissecados (p = 0,001) (Kruskal-Wallis). Houve associação positiva entre a média de linfonodos afetados e a presença de invasão angiolinfática (p < 0,0001) ou perineural (p = 0,024). A invasão angiolinfática e a mucina intracelular estavam menos presentes em adenocarcinomas bem diferenciados. Invasão perineural e angiolinfática estiveram mais presentes nos estádios T4. Conclusões: A dissecção ≥ 12 linfonodos aumenta as chances de se encontrar nodo positivo. Existe relação entre invasão angiolinfática; perineural e mucina intracelular e o tipo de diferenciação tumoral, bem como a classificação TNM. A média de linfonodos comprometidos foi maior na presença de invasão perineural ou angiolinfática.
Descritores: Nervos Periféricos
Neoplasias Colorretais/diagnóstico
Membranas Intracelulares
Excisão de Linfonodo
Linfonodos
Mucinas
-Glicoproteínas de Membrana
Neoplasias Colorretais
Neoplasias Colorretais/cirurgia
Laparoscopia
Linfonodos/cirurgia
Limites: Humanos
Masculino
Feminino
Pessoa de Meia-Idade
Responsável: BR545.3 - Biblioteca ICBS


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Id: biblio-846821
Autor: Cerqueira, Fernanda Menezes.
Título: Efeitos da restrição calórica nas vias de sinalização por insulina e óxido nítrico: implicações para biogênese, morfologia e função mitocondriais / Calorie restriction restriction effects on insulin and nitric oxide signaling: implications to mitochondrial biogenesis, morphology and function.
Fonte: São Paulo; s.n; 2012. 129 p. tab, graf, ilus.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Instituto de Química para obtenção do grau de Doutor.
Resumo: A restrição calórica (RC) estende a expectativa de vida de muitos organismos por mecanismos ainda em estudo. Entre os vários efeitos fisiológicos da RC encontra-se o aumento na biogênese mitocondrial, dependente de óxido nítrico (NO•), sintetizado pela enzima óxido nítrico sintase endotelial (eNOS). Um dos indutores fisiológicos mais potentes da eNOS é a insulina, cujos níveis plasmáticos são consideravelmente reduzidos nos organismos em RC. O objetivo deste trabalho foi investigar os mecanismos associados ao aumento da sinalização por NO• durante a RC in vivo e in vitro, e as conseqüências celulares do aumento de massa mitocondrial no que diz respeito à longevidade e capacidade respiratória celulares. Submetemos camundongos Swiss fêmeas à RC de 40% e observamos um considerável aumento tecido-específico na fosforilação basal de Akt e eNOS em músculo esquelético, tecido adiposo visceral e cérebro, os quais também apresentaram maior massa mitocondrial. A associação entre a sinalização por insulina, NO• e biogênese mitocondrial foi adicionalmente confirmada em um grupo de camundongos tratados com o desacoplador mitocondrial dinitrofenol (DNP), que também reduz a insulinemia e aumenta a longevidade em camundongos. Para o estudo mecanístico deste fenômeno, usamos soros de ratos Sprague-Dawley submetidos à RC de 40% ou alimentados ad libitum (AL) em cultura celular de células vasculares da musculatura lisa (VSMC), reproduzindo um protocolo descrito para RC in vitro. O uso do soro RC aumentou a fosforilação do receptor de insulina e Akt, a expressão de eNOS e nNOS (forma neural da NOS) e a fosforilação de eNOS, o que se refletiu em maior liberação de nitrito (NO2) no meio de cultura. Inibindo-se a Akt, todos os efeitos promovidos pela RC na sinalização por NO• foram revertidos. Ao se imunoprecipitar do soro a adiponectina, citocina conhecida por aumentar a sensibilidade à insulina, aumentada durante a RC, os efeitos do soro RC na via de sinalização de insulina foram abolidos e, conseqüentemente, os efeitos na sinalização por •NO foram prevenidos. Neurônios de células granulosas de cerebelo, que não expressam eNOS, apenas nNOS, foram cultivados com os soros AL ou RC, e também apresentaram considerável aumento na sinalização por •NO. Estas alterações induziram a biogênese mitocondrial e capacidade respiratória, e foram associadas à maior longevidade celular. Os mesmos efeitos mitocondriais foram observados em células secretoras de insulina, INS1, entretanto a secreção de insulina em resposta à glicose tornou-se inibida, por um mecanismo desconhecido, porém associado a reduzidos níveis intracelulares de espécies oxidantes, moléculas-chave para a secreção de insulina; e à alteração da morfologia mitocondrial, provavelmente devido à maior expressão de mitofusina-2 (Mfn-2). Ao se nocautear a Mfn-2, houve um aumento na geração de EROs e as células em RC passaram a secretar insulina a níveis comparáveis aos das células controle. Concluímos que durante a RC a maior sensibilidade à insulina aumenta a atividade de eNOS, via Akt, associada à maior biogênese mitocondrial. A adiponectina é uma molécula-central nestes eventos. A expressão de nNOS também é afetada, por mecanismos desconhecidos. O aumento de biogênese mitocondrial eleva a capacidade respiratória celular e impacta positivamente a longevidade in vitro. A alteração da morfologia mitocondrial associa-se a alterações na produção de oxidantes intracelulares e mudanças na secreção de insulina

Calorie restriction (RC) is known to extend the lifespan in many organisms, and its mechanisms of action are still under investigation. Enhanced mitochondrial biogenesis driven by nitric oxide (•NO), synthesized by the endothelial nitric oxide synthase (eNOS), is proposed to be a CR central effect. Insulin is one of the most potent physiological activators of eNOS. However, plasmatic insulin levels are dramatically reduced in organisms under CR. The goal of this work was uncover the mechanisms associated with enhanced •NO signaling during CR, in vivo and in vitro, as well as the cellular consequences of increased mitochondrial mass, regarding lifespan and reserve respiratory capability. Female Swiss mice were submitted to 40% of CR. A tissue-specific (skeletal muscle, abdominal adipose tissue and brain) increment in basal Akt and eNOS phosphorylation, which was related to enhanced mitochondrial biogenesis, was observed. Indeed, this association was also verified in tissues from mice treated with low doses of a mitochondrial uncoupler, dinitrophenol (DNP). To unveil the mechanism behind the insulin signaling effects on •NO levels, serum from Sprague-Dawley rats submmited to 40% of CR was used to culture in VSMC cells, an in vitro CR protocol. CR sera enhanced insulin receptor (IR) and Akt phosphorylation, as well as nitrite (NO2-) accumulation in the culture media, the expression of eNOS and nNOS (neural NOS isoform) and eNOS phosphorylation. The effects of CR sera were reversed by Akt inhibition. The immunoprecipitation of serum adiponectin, a cytokine known to improve peripheral insulin sensitivity, also reversed the CR serum effects on insulin and •NO signaling. Cerebellar neurons, which do not express eNOS, just nNOS, were also cultured with CR or AL serum and also presented striking increments in •NO signaling, associated with mitochondrial biogenesis, increased reserve respiratory capability and lifespan extension. The mitochondrial effects promoted by CR were also observed in insulin secreting cells (INS1). However, under the CR condition, insulin secretion stimulated by glucose was impaired. The likely explanations are reduced mitochondrial reactive oxygen species (ROS) generation, or the alteration in mitochondrial morphology, associated, in our model, with enhanced mitofusin-2 expression (Mfn-2). In cells which the Mfn-2 was knocked down, insulin secretion in CR and AL groups was responsive to glucose at the same level, and the intracellular oxidants levels were much higher. Overall, CR improves •NO signaling due to enhanced insulin sensitivity, through Akt, and results in mitochondrial biogenesis. Adiponectin is a key molecule in this phenomenon. Increments in mitochondrial mass enhance the cellular reserve respiratory capability and lifespan. Mitochondrial morphology alterations are associated with possible decreases in ROS generation and impaired insulin release, maintained the low levels of plasmatic insulin
Descritores: Insulina/análise
Óxido Nítrico/análise
Biogênese de Organelas
-Adiponectina
Restrição Calórica/estatística & dados numéricos
Membranas Intracelulares
Síndrome Endotelial Iridocorneana
Limites: Animais
Feminino
Camundongos
Tipo de Publ: Técnicas In Vitro
Estudo de Avaliação
Responsável: BR40.1 - DBD - Divisão de Biblioteca e Documentacão do Conjunto das Químicas
BR40.1; T 574.192, C416e. 30100019894


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Id: lil-475566
Autor: Cortázar, Tania M; Hernández, Joselín; Echeverry, María Clara; Camacho, Marcela.
Título: Papel de la vacuola parasitófora de macrófagos de ratón infectados por Leishmania amazonensis en la adquisición de de moléculas / Role of the parasitophorous vacuole of murine macrophages infected with Leishmania amazonensis in molecule acquisition
Fonte: Biomédica (Bogotá);26(supl.1):26-37, oct. 2006.
Idioma: es.
Resumo: Introducción. Leishmania son parásitos intracelulares de macrófagos, confinados en compartimentos denominados vacuolas parasitóforas. La permeabilidad de este compartimento depende de su interacción con el tráfico vesicular y transportadores presentes en su membrana. Objetivo. En este trabajo se estudió la permeabilidad de la membrana de la vacuola parasitófora en la línea celular J774.A1 infectada con Leishmania amazonensis, in situ y en compartimentos aislados. Materiales y métodos. El aislamiento de vacuolas parasitóforas se hizo por gradiente de densidad. La permeabilidad de la membrana de estas se valoró por distribución de sondas fluorescentes y electrofisiología. Para establecer indirectamente el transporte de protones se usó naranja de acridina. La presencia de transportadores ABC sensibles a probenecid se estableció con amarillo lucifer y calceína. Por primera vez con la técnica de patch-clamp se registraron corrientes en la membrana de este compartimento aislado. Resultados. La vacuola parasitófora colorea de rojo con naranja de acridina indicando un pH ácido. Concentra amarillo lucifer a través de un transportador sensible a probenecid, pero excluye la sonda calceína. Vacuolas aisladas se marcan de rojo con naranja de acridina y concentran amarillo lucifer a través de un transportador sensible a probenecid. Estas vacuolas excluyeron calceína y presentaron en su membrana una corriente iónica que se activa a diferencias de potencial cercanas a 60 mV, con una conductancia de 46 ± 3 pS. Conclusiones. Se pueden aislar vacuolas parasitóforas con propiedades de permeabilidad que preservan mecanismos de transporte similares a los encontrados in situ. Se registra por primera vez la presencia de una corriente iónica poco selectiva en la membrana de este compartimiento.

Introduction. Leishmania are intracellular parasites of macrophages, confined into compartments known as parasitophorous vacuoles. The permeability of this compartment depends on its interaction with the endocytic pathway and transport proteins present on its membrane. Objective. The membrane permeability of the parasitophorous vacuole was studied in J774.A1- macrophage like cells infected with Leishmania amazonensis, in situ and on isolated compartments. Materials and methods. The parasitophorous vacuoles were isolated by density gradients. Fluorescent probe distribution and electrophysiological recordings were used to determine parasitophorous vacuole membrane permeability. Proton transport was evaluated indirectly by acridine orange staining. Probenecid sensitive ABC transporters were detected using the fluorescent probes lucifer yellow and calcein. For the first time ion currents were recorded on the membrane of isolated parasitophorous vacuoles using the patch clamp technique. Results. The parasitophorous vacuole stains red with acridine orange indicating an acidic compartment. It concentrates lucifer yellow by means of a probenecid sensitive transporter but excludes calcein. Isolated vacuoles stained red with acridine orange and concentrated lucifer yellow by means of a probenecid sensitive transporter. These vacuoles excluded calcein and showed an ion current in their membrane which is activated at potentials close to 60 mV with a mean conductance of 46 ± 3 pS. Conclusions. Isolated parasitophorous vacuoles with permeability properties preserving transport mechanisms similar to those found in situ can be purified. A poorly selective ion current on the parasitophorous vacuole membrane is reported for the first time.
Descritores: Proteínas de Transporte de Ânions
Membranas Intracelulares
Canais Iônicos
Transporte de Íons
Leishmania
-Permeabilidade
Vacúolos/parasitologia
Limites: Camundongos
Responsável: CO42.1 - Biblioteca Nacional de Salud José Celestino Mutis


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Id: lil-443669
Autor: Nuñez, M. T; Garate, M. A; Arredtondo, M; Tapia, V; Muñoz, P.
Título: The cellular mechanisms of body iron homeostasis
Fonte: Biol. Res;33(2):133-142, 2000. ilus, graf.
Idioma: en.
Projeto: Fondo Nacional de Ciencia y Tecnología.
Resumo: Cells tightly regulate iron levels through the activity of iron regulatory proteins (IRPs) that bind to RNA motifs called iron responsive elements (IREs). When cells become iron-depleted, IRPs bind to IREs present in the mRNAs of ferritin and the transferrin receptor, resulting in diminished translation of the ferritin mRNA and increased translation of the transferrin receptor mRNA. Similarly, body iron homeostasis is maintained through the control of intestinal iron absorption. Intestinal epithelia cells sense body iron through the basolateral endocytosis of plasma transferrin. Transferrin endocytosis results in enterocytes whose iron content will depend on the iron saturation of plasma transferrin. Cell iron levels, in turn, inversely correlate with intestinal iron absorption. In this study, we examined the relationship between the regulation of intestinal iron absorption and the regulation of intracellular iron levels by Caco-2 cells. We asserted that IRP activity closely correlates with apical iron uptake and transepithelial iron transport. Moreover, overexpression of IRE resulted in a very low labile or reactive iron pool and increased apical to basolateral iron flux. These results show that iron absorption is primarily regulated by the size of the labile iron pool, which in turn is regulated by the IRE/IRP system.
Descritores: Absorção Intestinal/fisiologia
Ferritinas
Ferro/metabolismo
Proteínas Reguladoras do Ferro/metabolismo
Receptores da Transferrina/metabolismo
-CELULAS CACO-TEMEFOS
Homeostase/fisiologia
Membranas Intracelulares/metabolismo
Mucosa Intestinal/citologia
Mucosa Intestinal/metabolismo
RNA Mensageiro/metabolismo
Transporte Biológico/fisiologia
Limites: Humanos
Responsável: BR1.1 - BIREME


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Id: lil-437528
Autor: Carrasco, María Angélica; Jaimovich, Enrique; Kemmerling, Ulrike; Hidalgo, Cecilia.
Título: Signal transduction and gene expression regulated by calcium release from internal stores in excitable cells
Fonte: Biol. Res;37(4):701-712, 2004. graf.
Idioma: en.
Resumo: Calcium regulation of several transcription factors involves different calcium-dependent signaling cascades and engages cytoplasmic as well as nuclear calcium signals. The study of the specific sources of calcium signals involved in regulation of gene expression in skeletal muscle has been addressed only recently. In this tissue, most cytoplasmic and nuclear calcium signals originate from calcium release from internal stores, mediated either by ryanodine receptor (RyR) or IP3 receptor (IP3R) channels. The latter are located both in the sarcoplasmic reticulum (SR) and in the nuclear membrane, and their activation results in long-lasting nuclear calcium increase. The calcium signals mediated by RyR and IP3R are very different in kinetics, amplitude and subcellular localization; an open question is whether these differences are differentially sensed by transcription factors. In neurons, it is well established that calcium entry through L-type calcium channels and NMDA receptors plays a role in the regulation of gene expression. Increasing evidence, however, points to a role for calcium release from intracellular stores in this process. In this article, we discuss how RyR-mediated calcium release contributes to the activation of the calcium-dependent transcription factor CREB and the subsequent LTP generation. We present novel results from our laboratory showing ERK-mediated CREB activation by hydrogen peroxide. This activation takes place in the absence of extracellular calcium and is blocked by inhibitory ryanodine concentrations, suggesting it is caused by redox activation of RyR-mediated calcium release.
Descritores: Agonistas dos Canais de Cálcio
Oxidação Química
Sinalização do Cálcio
Fatores Genéricos de Transcrição
Transdução de Sinais
Transdução de Sinais/fisiologia
-Membranas Intracelulares
Músculo Esquelético
Neurônios
Limites: Animais
Responsável: CL1.1 - Biblioteca Central


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Id: lil-437511
Autor: Kasri, Nael Nadif; Parys, Jan B; Callewaert, Geert; Missiaen, Ludwig; De Smedt, Humbert.
Título: Calmodulin and calcium-release channels
Fonte: Biol. Res;37(4):577-582, 2004. ilus.
Idioma: en.
Resumo: Calmodulin (CaM) is a ubiquitous cytosolic protein that plays a critical role in regulating cellular functions by altering the activity of a large number of ion channels. There are many examples for CaM directly mediating the feedback effects of Ca2+ on Ca2+ channels. Recently the molecular mechanisms by which CaM interacts with voltage-gated Ca2+ channels, Ca2+-activated K+ channels and ryanodine receptors have been clarified. CaM plays an important role in regulating these ion channels through lobe-specific Ca2+ detection. CaM seems to behave as a channel subunit. It binds at low [Ca2+] and undergoes conformational changes upon binding of Ca2+, leading to an interaction with another part of the channel to regulate its gating. Here we focus on the mechanism by which CaM regulates the inositol 1,4,5-trisphosphate receptor (IP3R). Although the IP3R is inhibited by CaM and by other CaM-like proteins in the presence of Ca2+, we conclude that CaM does not act as the Ca2+ sensor for IP3R function. Furthermore we discuss a novel Ca2+-induced Ca2+-release mechanism found in A7r5 (embryonic rat aorta) and 16HBE14o- (human bronchial mucosa) cells for which CaM acts as a Ca2+ sensor.
Descritores: Calmodulina/fisiologia
Canais de Cálcio/metabolismo
Membranas Intracelulares/metabolismo
Retículo Endoplasmático/metabolismo
-Técnicas de Cultura de Células
Receptores Citoplasmáticos e Nucleares/metabolismo
Transdução de Sinais
Limites: Humanos
Animais
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: lil-437502
Autor: Carafoli, Ernesto.
Título: Calcium signaling: a historical account
Fonte: Biol. Res;37(4):497-505, 2004. ilus.
Idioma: en.
Descritores: Canais de Cálcio/metabolismo
Mitocôndrias/metabolismo
Retículo Endoplasmático/metabolismo
Sinalização do Cálcio/fisiologia
-Transporte Biológico
Membranas Intracelulares/metabolismo
Limites: Animais
Responsável: CL1.1 - Biblioteca Central


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Id: lil-437382
Autor: Beltrán, Marianela; Barrientos, Genaro; Hidalgo, Cecilia.
Título: Fast kinetics of calcium dissociation from calsequestrin
Fonte: Biol. Res;39(3):493-503, 2006. ilus, graf.
Idioma: en.
Projeto: Fondo Nacional de Investigación Científica y Tecnológica. FONDAP Center for Molecular Studies of the Cell.
Resumo: We measured the kinetics of calcium dissociation from calsequestrin in solution or forming part of isolated junctional sarcoplasmic reticulum membranes by mixing calsequestrin equilibrated with calcium with calcium-free solutions in a stopped-flow system. In parallel, we measured the kinetics of the intrinsic fluorescence changes that take place following calcium dissociation from calsequestrin. We found that at 25°C calcium dissociation was 10-fold faster for calsequestrin attached to junctional membranes (k = 109 s-1) than in solution. These results imply that calcium dissociation from calsequestrin in vivo is not rate limiting during excitation-contraction coupling. In addition, we found that the intrinsic fluorescence decrease for calsequestrin in solution or forming part of junctional membranes was significantly slower than the rates of calcium dissociation. The kinetics of intrinsic fluorescence changes had two components for calsequestrin associated to junctional membranes and only one for calsequestrin in solution; the faster component was 8-fold faster (k = 54.1 s-1) than the slower component (k = 6.9 s-1), which had the same k value as for calsequestrin in solution. These combined results suggest that the presence of calsequestrin at high concentrations in a restricted space, such as when bound to the junctional membrane, accelerates calcium dissociation and the resulting structural changes, presumably as a result of cooperative molecular interactions.
Descritores: Cálcio/metabolismo
Calsequestrina/metabolismo
Retículo Sarcoplasmático/metabolismo
-Eletroforese em Gel de Poliacrilamida
Membranas Intracelulares/metabolismo
Limites: Animais
Coelhos
Responsável: BR1.1 - BIREME


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Zin, W. A
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Id: lil-428282
Autor: Garcia, C. S. N. B; Prota, L. F. M; Morales, M. M; Romero, P. V; Zin, W. A; Rocco, P. R. M.
Título: Understanding the mechanisms of lung mechanical stress
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;39(6):697-706, June 2006. ilus.
Idioma: en.
Resumo: Physical forces affect both the function and phenotype of cells in the lung. Bronchial, alveolar, and other parenchymal cells, as well as fibroblasts and macrophages, are normally subjected to a variety of passive and active mechanical forces associated with lung inflation and vascular perfusion as a result of the dynamic nature of lung function. These forces include changes in stress (force per unit area) or strain (any forced change in length in relation to the initial length) and shear stress (the stress component parallel to a given surface). The responses of cells to mechanical forces are the result of the cell's ability to sense and transduce these stimuli into intracellular signaling pathways able to communicate the information to its interior. This review will focus on the modulation of intracellular pathways by lung mechanical forces and the intercellular signaling. A better understanding of the mechanisms by which lung cells transduce physical forces into biochemical and biological signals is of key importance for identifying targets for the treatment and prevention of physical force-related disorders.
Descritores: Pulmão/fisiologia
Mecanorreceptores/fisiologia
Mecanotransdução Celular/fisiologia
-Matriz Extracelular/fisiologia
Junções Intercelulares/fisiologia
Membranas Intracelulares/fisiologia
Pulmão/citologia
Estresse Mecânico
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: lil-402174
Autor: Kamal, Ahmad M; Flower, Roderick J; Perretti, Mauro.
Título: An overview of the effects of annexin 1 on cells involved in the inflammatory process
Fonte: Mem. Inst. Oswaldo Cruz;100(supl.1):39-47, Mar. 2005. ilus.
Idioma: en.
Resumo: The concept of anti-inflammation is currently evolving with the definition of several endogenous inhibitory circuits that are important in the control of the host inflammatory response. Here we focus on one of these pathways, the annexin 1 (ANXA1) system. Originally identified as a 37 kDa glucocorticoid-inducible protein, ANXA1 has emerged over the last decade as an important endogenous modulator of inflammation. We review the pharmacological effects of ANXA1 on cell types involved in inflammation, from blood-borne leukocytes to resident cells. This review reveals that there is scope for more research, since most of the studies have so far focused on the effects of the protein and its peptido-mimetics on neutrophil recruitment and activation. However, many other cells central to inflammation, e.g. endothelial cells or mast cells, also express ANXA1: it is foreseen that a better definition of the role(s) of the endogenous protein in these cells will open the way to further pharmacological studies. We propose that a more systematic analysis of ANXA1 physio-pharmacology in cells involved in the host inflammatory reaction could aid in the design of novel anti-inflammatory therapeutics based on this endogenous mediator.
Descritores: Anexina A1/farmacologia
Mediadores da Inflamação/farmacologia
Inflamação/prevenção & controle
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
-Membranas Intracelulares/metabolismo
Linfócitos/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Monócitos/efeitos dos fármacos
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME



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