Senescence marker protein 30 is up-regulated in kainate-induced hippocampal damage through ERK-mediated astrocytosis
Senescence marker protein 30 is up-regulated in kainate-induced hippocampal damage through ERK-mediated astrocytosis
复制标题
通过 ERK 介导的星形细胞增多，红藻氨酸诱导的海马损伤中衰老标记蛋白 30 上调
DOI：
10.1002/jnr.22122
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
J
中科院分区：
文献类型：
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作者：
Son;T. G.;Park;H. R.;Kim;S. J.;Kim;K.;Kim;MS.;Ishigami;A.;Handa;S.;Maruyama;N. Chung;H. Y. and Lee;J
肾脏和肝脏中的衰老标记蛋白30（SMP 30）随年龄增长以雄激素非依赖性方式降低。然而，SMP 30在大脑中的表达的调节尚未在衰老和神经退行性疾病中进行检查。为了研究SMP 30在脑中的表达，我们利用了衰老和红藻氨酸（KA）诱导的神经退行性疾病模型。有趣的是，SMP 30的表达在老年脑中不太可能减少，但在KA损伤后4周，SMP 30蛋白的总水平增加。KA后同时观察到胶质细胞酸性蛋白（GFAP）增加和SMP 30表达升高，表明脑中SMP 30表达的调节可能与星形胶质细胞增多相关。我们证实KA诱导大鼠星形胶质细胞GFAP表达，并增加SMP 30。此外，我们发现ERK 1/2激活参与了星形胶质细胞中SMP 30的上调。我们的研究结果表明，在激活的星形胶质细胞中升高的SMP 30在脑损伤后起着重要的支持作用。© 2009 Wiley利斯公司
Senescence maker protein 30 (SMP30) is decreased in an androgen‐independent manner in kidney and liver with age. However, regulation of SMP30 expression in the brain has not been examined in aging and neurodegenerative diseases. To investigate SMP30 expression in the brain, we utilized aging and kainate (KA)‐induced neurodegenerative disease models. Interestingly, expression of SMP30 was unlikely to decrease in the aged brain, but total levels of SMP30 protein were increased at 4 weeks after KA injury. Increased glial fibrillary acidic protein (GFAP) with elevated SMP30 expression was observed at the same time post‐KA, indicating that regulation of SMP30 expression in the brain may be associated with astrocytosis. We confirmed that KA induced GFAP expression with increased SMP30 in rat astrocyte cells. Moreover, we found that ERK1/2 activation was involved in the up‐regulation of SMP30 in astrocytes. Our results suggest that elevated SMP30 in activated astrocytes plays an important supportive role after brain damage. © 2009 Wiley‐Liss, Inc.