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大鼠脑缺血再灌注早期骨桥蛋白表达:右皮质表达增强被醋氨酚抑制。

Osteopontin expression during early cerebral ischemia-reperfusion in rats: enhanced expression in the right cortex is suppressed by acetaminophen.

机构信息

Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey, United States of America.

出版信息

PLoS One. 2011 Jan 21;6(1):e14568. doi: 10.1371/journal.pone.0014568.

DOI:10.1371/journal.pone.0014568
PMID:21283687
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3024983/
Abstract

Osteopontin (OPN) is a pleiotropic protein implicated in various inflammatory responses including ischemia-reperfusion (I-R) injury. Two distinct forms of the protein have been identified: an extensively studied secreted form (sOPN) and a less-well-known intracellular form (iOPN). Studies have shown that increased OPN expression parallels the time course of macrophage infiltration into injured tissue, a late event in the development of cerebral infarcts. sOPN has been suggested to promote remodeling of the extracellular matrix in the brain; the function of iOPN may be to facilitate certain signal transduction processes. Here, we studied OPN expression in adult male Sprague-Dawley rats subjected to global forebrain I-R injury. We found iOPN in the cytoplasm of both cortices and the hippocampus, but unexpectedly only the right cortex exhibited a marked increase in the iOPN level after 45 min of reperfusion. Acetaminophen, a drug recently shown to decrease apoptotic incidence, caspase-9 activation, and mitochondrial dysfunction during global I-R, significantly inhibited the increase in iOPN protein in the right cortex, suggesting a role for iOPN in the response to I-R injury in the right cortex.

摘要

骨桥蛋白 (OPN) 是一种多功能蛋白,参与多种炎症反应,包括缺血再灌注 (I-R) 损伤。该蛋白有两种不同的形式:一种是广泛研究的分泌型(sOPN),另一种是不太知名的胞内型(iOPN)。研究表明,OPN 表达的增加与巨噬细胞浸润损伤组织的时间进程相平行,这是脑梗死发展的晚期事件。sOPN 被认为可促进大脑细胞外基质的重塑;iOPN 的功能可能是促进某些信号转导过程。在这里,我们研究了成年雄性 Sprague-Dawley 大鼠在全脑 I-R 损伤后 OPN 的表达。我们发现,iOPN 存在于皮质和海马体的细胞质中,但令人意外的是,只有右侧皮质在再灌注 45 分钟后 iOPN 水平显著增加。醋氨酚是一种最近被发现可在全脑 I-R 期间降低细胞凋亡发生率、半胱天冬酶-9 激活和线粒体功能障碍的药物,它显著抑制了右侧皮质中 iOPN 蛋白的增加,这表明 iOPN 在右侧皮质对 I-R 损伤的反应中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/d549584d96df/pone.0014568.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/99dc1ef39b03/pone.0014568.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/fb19eaeafc11/pone.0014568.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/adde4f099a00/pone.0014568.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/2379faaac5be/pone.0014568.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/d549584d96df/pone.0014568.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/99dc1ef39b03/pone.0014568.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/fb19eaeafc11/pone.0014568.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/adde4f099a00/pone.0014568.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/2379faaac5be/pone.0014568.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/717c/3024983/d549584d96df/pone.0014568.g005.jpg

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