RESUMEN
The progression of chronic renal diseases is characterized by the accumulation of extracellular matrix proteins in the glomerulus. The present experiments were designed to analyze the effect of hydrogen peroxide on the contractile and proliferative phenotypes of human mesangial cells grown on different culture substrates: plastic, collagen type I, and collagen type IV. Contraction was analyzed by measuring planar cell surface area and myosin light chain phosphorylation, whereas proliferation was studied by [(3)H]thymidine incorporation. No changes were detected in the proliferation rate of human mesangial cells grown on different culture substrates, neither under basal conditions nor in the presence of fetal calf serum or H(2)O(2). Cells grown on plastic or collagen did not contract in the presence of H(2)O(2), but cells grown on collagen I elicited a significant contraction with H(2)O(2). Platelet-activating factor induced contraction of human mesangial cells on the three culture substrates. The different contractile responses observed were not due to different degradation rates of H(2)O(2). The present experiments support the importance of extracellular matrix in the response to exogenous stimuli and point to the possibility that patients with changes in the mesangial matrix as a result of chronic renal diseases may have an increased susceptibility to the pathological actions of reactive oxygen species.
Asunto(s)
Matriz Extracelular/fisiología , Mesangio Glomerular/fisiología , Especies Reactivas de Oxígeno , Células Cultivadas , Colágeno , Medios de Cultivo , Sangre Fetal , Mesangio Glomerular/efectos de los fármacos , Humanos , Peróxido de Hidrógeno/farmacología , Fenotipo , Plásticos , Factor de Activación Plaquetaria/farmacologíaRESUMEN
We report in the present work that membrane fluidity in erythrocytes from rats under alimentary hyperlipidemia-hypercholesterolemia is slightly diminished despite the fact that in these cells the cholesterol/phospholipid molar ratio is nearly 45% higher than in erythrocytes from control animals. In addition, the erythrocyte count in the rats given the high-fat, high-cholesterol diet was normal. Only a slight reticulocytosis was observed in these animals although their erythrocytes showed a marked decrease in their ability to extrude sodium actively. A tentative explanation for these results is proposed on the basis of other findings suggesting cellular compensatory mechanisms.