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缺血诱导大鼠脑内2'-5'-寡腺苷酸合成酶mRNA水平的变化:与神经元细胞培养中内质网钙稳态紊乱所产生的变化相比较。

Ischemia-induced changes in 2'-5'-oligoadenylate synthethase mRNA levels in rat brain: comparison with changes produced by perturbations of endoplasmic reticulum calcium homeostasis in neuronal cell cultures.

作者信息

Paschen W, Althausen S, Doutheil J

机构信息

Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Cologne, Germany.

出版信息

Neurosci Lett. 1999 Mar 26;263(2-3):109-12. doi: 10.1016/s0304-3940(99)00119-6.

Abstract

2'-5' Oligoadenylate synthetase (OAS) expression is induced by interferon or viral infection of cells. To better understand ischemia-induced changes in gene expression and to elucidate the possible underlying mechanisms, changes in OAS mRNA levels were evaluated after 30 min four-vessel occlusion and 2, 4, 8 or 24 h recovery and compared to the temporal profile of changes in mRNA levels induced by a transient depletion of endoplasmic reticulum (ER) calcium stores in primary neuronal cell cultures. OAS mRNA levels dropped during early recovery both in vivo and in vitro. After 6 h recovery from ER calcium pool depletion, OAS mRNA levels increased to about 350% of controls and returned to control levels after 24 h of recovery. After 24 h recovery from ischemia, OAS mRNA levels rose to about 390% of controls in the hippocampus and striatum and to 210% of the control value in the cortex. It is concluded that transient ischemia place cells into an antiviral state, most pronounced in the hippocampus and striatum, and that disturbances of ER calcium homeostasis may contribute to this process.

摘要

2'-5'寡腺苷酸合成酶(OAS)的表达可由干扰素或细胞的病毒感染诱导。为了更好地理解缺血诱导的基因表达变化并阐明可能的潜在机制,在四动脉闭塞30分钟以及恢复2、4、8或24小时后,评估了OAS mRNA水平的变化,并将其与原代神经元细胞培养物中内质网(ER)钙储存短暂耗尽所诱导的mRNA水平变化的时间概况进行比较。在体内和体外,OAS mRNA水平在早期恢复过程中均下降。从ER钙池耗竭恢复6小时后,OAS mRNA水平增加至对照的约350%,并在恢复24小时后恢复至对照水平。从缺血恢复24小时后,海马和纹状体中的OAS mRNA水平升至对照的约390%,而皮质中的OAS mRNA水平升至对照值的210%。得出的结论是,短暂性缺血使细胞进入抗病毒状态,在海马和纹状体中最为明显,并且ER钙稳态的紊乱可能促成这一过程。

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