RESUMO
The physiological performance of an organ depends on an interplay between changes in cellular function and organ size, determined by cell growth, proliferation and death. Nowhere is this more evident than in the endocrine pancreas, where disturbances in function or mass result in severe disease. Recently, the insulin signal-transduction pathway has been implicated in both the regulation of hormone secretion from beta cells in mammals as well as the determination of cell and organ size in Drosophila melanogaster. A prominent mediator of the actions of insulin and insulin-like growth factor 1 (IGF-1) is the 3'-phosphoinositide-dependent protein kinase Akt, also known as protein kinase B (PKB). Here we report that overexpression of active Akt1 in the mouse beta cell substantially affects compartment size and function. There was a significant increase in both beta-cell size and total islet mass, accompanied by improved glucose tolerance and complete resistance to experimental diabetes.
Assuntos
Ilhotas Pancreáticas/citologia , Proteínas Serina-Treonina Quinases/metabolismo , Proteínas Proto-Oncogênicas , Animais , Divisão Celular , Tamanho Celular , Sobrevivência Celular , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/prevenção & controle , Ativação Enzimática , Feminino , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Proteínas Serina-Treonina Quinases/genética , Proteínas Proto-Oncogênicas c-akt , RatosRESUMO
Mast cells are stimulatory factors in prognosis of various immunogenic and allergic diseases in human body. These cells play an important role in various immunological and metabolic diseases. The aim of present article is to explore the molecular targets to suppress the over expression of mast cells in obesity. The last 20 years literature were searched by various bibliographic data bases like Pubmed, google Scholar, Scopus and web of Science. The data were collected by keywords like "Mast Cell" "obesity" and "role of mast cell or role in obesity". Articles and their abstract were reviewed with a counting of 827 publications, in which 87 publications were considered for study and remaining was excluded because of its specificity to the subject. This review explains the characteristics, molecular targets and role of mast cells in obesity and existing research with mast cells to the area of metabolic diseases.
Assuntos
Mastócitos/fisiologia , Obesidade/etiologia , Animais , Quimases/fisiologia , Citocinas/fisiologia , Humanos , Mastócitos/efeitos dos fármacos , Obesidade/tratamento farmacológico , Proteínas Proto-Oncogênicas c-kit/fisiologia , Receptores de IgE/químicaRESUMO
We have investigated the effects of the growth of A431 human squamous carcinoma cells as three-dimensional aggregates (multicellular tumor spheroids) on the expression and enzyme activity of heme oxygenase (HO). We demonstrate that A431 squamous carcinoma cells grown as day 4 spheroids selectively increase the expression of heme oxygenase 1 (HO-1), caused, directly or indirectly, by three-dimensional cell-cell contact effects. Steady-state levels of both mRNA and protein are significantly enhanced in spheroids compared with day 4 monolayers (approximately 13-fold). Because of the similarity of apparent half-lives between monolayers (2.7 h) and spheroids (2.1 h), it appears that the increases are caused at least partly by altered transcriptional rates. Total HO enzyme activity, measured by carbon monoxide production, is also up-regulated (2.6-fold) in spheroids, compared to that in monolayers. This increase indicates that the up-regulation in HO-1 protein expression corresponds to an increase in functional enzyme levels. We propose that HO may play a more complex role in cellular metabolism than would be evident from studies using two-dimensional monolayer cultures.
Assuntos
Carcinoma de Células Escamosas/enzimologia , Comunicação Celular/fisiologia , Heme Oxigenase (Desciclizante)/metabolismo , RNA Mensageiro/metabolismo , Northern Blotting , Western Blotting , Carcinoma de Células Escamosas/patologia , Heme Oxigenase (Desciclizante)/análise , Humanos , RNA Mensageiro/análise , Células Tumorais CultivadasRESUMO
Complement-Dependent Cytotoxicity (CDC) is a common technique used for isolating and characterizing cell populations. However, the molecular events resulting from CDC-mediated cell injury remain obscure. In order to use CDC as a selection procedure for studies at the RNA level, we examined if CDC is associated with rapid degradation of RNAs from target cells without affecting the stability and viability of RNAs of non-target cells. Using a model of anti-CD3-mediated CDC, we show that T cell-specific RNAs were absent immediately after CDC. However, ribosomal RNAs and mRNAs from non-targeted cells (non-T cells) were not affected by CDC. Our results indicate that CDC is associated with rapid degradation of only target cell RNAs, validating CDC as a method for cell isolation without interfering with further studies at the RNA level.
Assuntos
Proteínas do Sistema Complemento/imunologia , Citotoxicidade Imunológica/imunologia , RNA Mensageiro/imunologia , Receptores de Antígenos de Linfócitos T alfa-beta/imunologia , Anticorpos Monoclonais , Northern Blotting , Complexo CD3/imunologia , Contagem de Células , Antígenos de Histocompatibilidade Classe I/imunologia , Humanos , RNA Ribossômico 18S/imunologia , RNA Ribossômico 28S/imunologiaRESUMO
OBJECTIVE: The purpose of our study was to report the radiographic findings of biopsy-proven lymphoid hyperplasia of the stomach in five adult patients. CONCLUSION: Lymphoid hyperplasia of the stomach is characterized by distinctive findings on double-contrast upper gastrointestinal tract barium examinations; all five patients had innumerable tiny (1--3 mm in diameter) round frequently umbilicated nodules that carpeted the mucosa of the gastric antrum or antrum and body. Three of these five patients had associated Helicobacter pylori gastritis. The diagnosis of gastric lymphoid hyperplasia, therefore, can be suggested on the basis of the radiographic findings.