Colburn P, Kobayashi E, Buonassisi V
Departamento de Bioquímica, Escola Paulista de Medicina, São Paulo, Brazil.
J Cell Physiol. 1994 Apr;159(1):121-30. doi: 10.1002/jcp.1041590116.
Exposure of cultured endothelial cells to endotoxin causes an increase in the amount of cellular heparan sulfate proteoglycan and a depletion of this molecule in the extracellular matrix. Concomitant with the decrease in the extracellular matrix is the appearance of a fraction of proteoglycan bearing altered carbohydrate moieties in the culture medium. beta-mercaptoethanol, mannitol, and dimethyl sulfoxide bring back to normal the structural properties of the proteoglycan in the medium and restore the matrix content in proteoglycan to a level comparable to that of control cells but do not affect the increase in the amount of proteoglycan on the cell. This "uncoupling" suggests that two independent chains of events underlie the synthetic and structural changes of the proteoglycan triggered by endotoxin in the endothelial cell.
将培养的内皮细胞暴露于内毒素会导致细胞硫酸乙酰肝素蛋白聚糖的量增加,同时细胞外基质中该分子减少。伴随着细胞外基质的减少,培养基中出现了一部分带有改变的碳水化合物部分的蛋白聚糖。β-巯基乙醇、甘露醇和二甲亚砜使培养基中蛋白聚糖的结构特性恢复正常,并使蛋白聚糖的基质含量恢复到与对照细胞相当的水平,但不影响细胞上蛋白聚糖量的增加。这种“解偶联”表明,内毒素触发的内皮细胞中蛋白聚糖的合成和结构变化是由两个独立的事件链引起的。