ABSTRACT
BACKGROUND: To evaluate the macrophage migration inhibitory factor and E-selectin levels in patients with acute coronary syndrome. MATERIALS/METHODS: We examined the plasma migration inhibitory factor and E-selectin levels in 87 patients who presented with chest pain at our hospital. The patients were classified into two groups according to their cardiac status. Sixty-five patients had acute myocardial infarction, and 22 patients had non-cardiac chest pain (non-coronary disease). We designated the latter group of patients as the control group. The patients who presented with acute myocardial infarction were further divided into two subgroups: ST-elevated myocardial infarction (n = 30) and non-ST elevated myocardial infarction (n = 35). RESULTS: We found higher plasma migration inhibitory factor levels in both acute myocardial infarction subgroups than in the control group. However, the E-selectin levels were similar between the acute myocardial infarction and control patients. In addition, we did not find a significant difference in the plasma migration inhibitory factor levels between the ST elevated myocardial infarction and NST-elevated myocardial infarction subgroups. DISCUSSION: The circulating concentrations of migration inhibitory factor were significantly increased in acute myocardial infarction patients, whereas the soluble E-selectin levels were similar between acute myocardial infarction patients and control subjects. Our results suggest that migration inhibitory factor may play a role in the atherosclerotic process. .
Subject(s)
Animals , Female , Mice , /metabolism , Interferon-gamma/metabolism , Mammary Neoplasms, Animal/immunology , Spheroids, Cellular/immunology , T-Lymphocytes, Cytotoxic/metabolism , T-Lymphocytes, Helper-Inducer/metabolism , Alginates , Antigens, Neoplasm/immunology , Antigens, Neoplasm/metabolism , Cell Line, Tumor , Cell Movement , Chitosan , /genetics , /immunology , Glucuronic Acid , Granzymes/metabolism , Hexuronic Acids , Immunity, Cellular , Interferon-gamma/genetics , Interferon-gamma/immunology , Mammary Neoplasms, Animal/genetics , Mammary Neoplasms, Animal/metabolism , Mammary Neoplasms, Animal/pathology , Spheroids, Cellular/metabolism , Spheroids, Cellular/pathology , T-Lymphocytes, Cytotoxic/immunology , T-Lymphocytes, Helper-Inducer/immunology , Tumor MicroenvironmentABSTRACT
Malignant transformation is accompanied by changes in cell-matrix interations. Upon transfection with EJ-ras oncogene, transformed fibroblasts, acquired a migratory phenotype towards laminin-1. The increase in integrin expression was responsible for the migratory activity of transformed fibroblasts. In addition alpha(6)beta(1) integrins, both galectin-3 and an unidentified laminin-binding polypeptide had their expression pattern altered upon transformation. Here, we review these two classes of laminin-binding proteins and their possible roles in cell-laminin interactions.
Subject(s)
Humans , Fibroblasts/immunology , Genes, ras/genetics , Laminin/immunology , Lectins/immunology , Mammary Neoplasms, Animal/immunology , Blotting, Western , Ink Blot Tests , Oncogenes/immunologyABSTRACT
Durante el crecimiento de los tumores el papel del sistema inmune es controvertido, y a pesar de las grandes expectativas en poder estimularlo para que fuera eficiente en el rechazo de los mismos, este objetivo aún no se ha cumplido. En este revisión se resumen y se analizan los estudios inmunológicos realizados con modelos de tumores murinos en nuestro laboratorio. Nosotros hemos trabajado con tumores de mama murinos, y en nuestros primeros estudios hemos determinado que el sistema inmune de los portadores de tumor durante las primeras etapas de su evolución reconoce en forma específica los antígenos tumorales, y que sus linfocitos están activados para respuestas de hipersensibilidad retardada in vivo e in vitro y angiogénesis linfocitaria. Sin embargo, esta funcionalidad no se correlaciona con los mecanismos efectores de rechazo tumoral. El reconocimiento y activación linfocitarias desaparecem a medida que tumor crece. Las células tumorales y linfocitos del portador de tumor secretan factores solubles que exacerban el crecimiento tumoral y metastásico. Las poblaciones de neutrófilos y mastocitos también se encuentran alteradas durante el crecimiento del tumor. Postulamos que las células tumorales secretan factores que inducen poblaciones celulares a producir inmunosupresores que favorecem el desarrollo del mismo tumor.