Altered Ca2+ homeostasis in lymphoblasts from patients with late-onset Alzheimer disease.
Altered Ca2+ homeostasis in lymphoblasts from patients with late-onset Alzheimer disease.
复制标题
晚发性阿尔茨海默病患者淋巴母细胞中 Ca2 稳态的改变。
DOI：
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发表时间：
1997
影响因子：
2.1
通讯作者：
M. Ayuso
中科院分区：
文献类型：
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作者：
D. Ibarreta;R. Parrilla;M. Ayuso
作者报道了来自晚发性阿尔茨海默病患者和年龄匹配的健康对照组的转化淋巴细胞的钙(Ca~(2+))稳态特征。阿尔茨海默病淋巴母细胞的基础胞浆游离[Ca~(2+)]高于对照组。抗免疫球蛋白M抗体或β-淀粉样多肽片段25-35诱导的阿尔茨海默病淋巴母细胞胞浆游离[Ca~(2+)]升高高于对照细胞。然而，钙耗竭细胞的钙补充动力学显示，阿尔茨海默病患者细胞内钙的积聚高于对照组，当钙外流受到抑制时，这一点得到了更好的认识。因此，作者得出结论，阿尔茨海默病淋巴母细胞的钙缓冲能力低于正常细胞，可能是由于细胞内钙结合结构的可用性或内在功能特性的变化。衰老改变了淋巴母细胞中钙离子补充的动力学，其方式类似于阿尔茨海默病。然而，与阿尔茨海默病不同的是，衰老不会改变细胞内最大游离[Ca~(2+)]，这表明衰老和晚发性阿尔茨海默病中钙稳态改变的机制不同。
The authors report calcium (Ca2+) homeostasis features of transformed lymphocytes from patients with late-onset Alzheimer disease and healthy age-matched controls. Alzheimer lymphoblasts show higher basal cytosolic-free [Ca2+] than controls. The antibodies anti-immunoglobulin M or the beta-amyloid (beta-amyloid) peptide fragment 25-35-induced elevation of cytosolic-free [Ca2+] was higher in Alzheimer disease lymphoblasts than in control cells. However, the kinetics of Ca2+ replenishment of Ca(2+)-depleted cells shows a higher accumulation of cytosolic Ca2+ in Alzheimer disease than in control lymphoblasts, which is better appreciated when the Ca2+ efflux is inhibited. Thus, the authors concluded that Alzheimer disease lymphoblasts have a lower Ca2+ buffering capacity than normal cells, probably because of changes in availability or intrinsic functional properties of the intracellular Ca(2+)-binding structures. Aging alters the kinetics of the Ca2+ replenishment in lymphoblasts in a manner that resembles Alzheimer disease. However, unlike Alzheimer disease, aging does not change the maximum cytosolic-free [Ca2+], suggesting that the mechanisms underlying the altered Ca2+ homeostasis in aging and late-onset Alzheimer disease are different.