Sikora E, Radziszewska E, Kmieć T, Maślińska D
Department of Cellular Biochemistry, M. Nencki Institute of Experimental Biology, Warsaw, Poland.
Acta Biochim Pol. 1993;40(2):269-72.
The study of human disorders known as premature aging syndromes may provide insight into the mechanisms of cellular senescence. The main feature of cellular senescence in vitro is cessation of cell proliferation. Down syndrome (DS) and neuronal ceroid-lypofuscinosis (NCL) are clinically characterized by the premature onset of numerous features normally associated with human aging. Phytohemagglutinin stimulated lymphocytes derived from DS subjects showed a statistically significant diminished proliferation capacity in comparison with lymphocytes derived from NCL and healthy individuals. We demonstrated, by applying the electrophoretic mobility shift assay, slightly impaired AP-1 DNA binding activity in NCL lymphocytes and strong in DS ones. Our results showed that the same molecular mechanisms of proliferation cessation could exist in fibroblasts characterized by replicative senescence and in lymphocytes derived from individuals with premature aging syndromes (Down).
对被称为早衰综合征的人类疾病的研究可能会为细胞衰老机制提供见解。体外细胞衰老的主要特征是细胞增殖停止。唐氏综合征（DS）和神经元蜡样脂褐质沉积症（NCL）的临床特征是过早出现许多通常与人类衰老相关的特征。与来自NCL患者和健康个体的淋巴细胞相比，来自DS患者的植物血凝素刺激的淋巴细胞显示出增殖能力在统计学上显著降低。通过应用电泳迁移率变动分析，我们证明NCL淋巴细胞中的AP-1 DNA结合活性略有受损，而DS淋巴细胞中的则很强。我们的结果表明，在以复制性衰老为特征的成纤维细胞和来自早衰综合征（唐氏）个体的淋巴细胞中可能存在相同的增殖停止分子机制。
