Ishii T
J Am Geriatr Soc. 1977 May;25(5):206-17. doi: 10.1111/j.1532-5415.1977.tb00301.x.
Aortic medial calcification was investigated in rats in which the progeria-like syndrome (PLS) was evoked by administering dihydrotachysterol. In 35 experimental rats and 15 controls, calcification was studied morphologically by light and electron microscopy, and by enzyme histochemistry. Body weight, food intake and serum calcium levels were also determined. Calcification occurred along and on the elastic lamellae in association with the accumulation of ground substance. In the smooth-muscle cells surrounding the calcified foci, the activities of various lysosomal enzymes increased concomitantly with a tendency toward transformation of smooth-muscle cells to a modified form. From these observations, the role of ground-substance formation by smooth-muscle cells is postulated, and participation in the catabolism of ground substance by the lysosomal enzymes of these cells is suggested. It appears the increased activity of adenosine monophosphatase should be linked to the calcification. The etiology of weight loss, skin manifestations and aortic calcification in PLS rats seems to be different from that in human progeric diseases. Therefore, the PLS rat should not be readily accepted as an animal model for the study of progeric diseases.
在通过给予二氢速甾醇诱发早衰样综合征（PLS）的大鼠中研究了主动脉中层钙化。在35只实验大鼠和15只对照大鼠中，通过光学显微镜、电子显微镜以及酶组织化学对钙化进行了形态学研究。还测定了体重、食物摄入量和血清钙水平。钙化沿着弹性板并在弹性板上发生，与基质的积聚相关。在钙化灶周围的平滑肌细胞中，各种溶酶体酶的活性增加，同时平滑肌细胞有向改良形式转化的趋势。根据这些观察结果，推测了平滑肌细胞形成基质的作用，并提示这些细胞的溶酶体酶参与了基质的分解代谢。看来腺苷单磷酸酶活性的增加应与钙化有关。PLS大鼠体重减轻、皮肤表现和主动脉钙化的病因似乎与人类早衰疾病不同。因此，PLS大鼠不应轻易被接受为早衰疾病研究的动物模型。
