下调和上调
转录因子
生物
缺血
细胞生物学
分子生物学
医学
基因
内科学
生物化学
作者
Ming Fei Lang,Armin Schneider,Carola Krüger,Roland M. Schmid,Roman Dziarski,Markus Schwaninger
标识
DOI:10.1016/j.neulet.2007.10.027
摘要
Cerebral ischemia triggers inflammation and apoptosis, and the transcription factor NF-kappaB is a key regulator of both events. Here, we report on the induction of the peptidoglycan recognition protein-S (PGRP-S) in a mouse model of cerebral ischemia. Upregulation was reduced if the NF-kappaB subunit RelA was conditionally deleted in the brain. Regulation of PGRP-S transcription by RelA was confirmed in vitro. Cotransfection of a RelA expression plasmid stimulated the expression of a PGRP-S luciferase fusion gene. Mutation of two NF-kappaB response elements in the PGRP-S promoter disrupted stimulation by RelA. To investigate the function of PGRP-S in cerebral ischemia, we subjected PGRP-S(-/-) mice to cerebral ischemia. However, there was no difference in the infarct size in PGRP-S-deficient mice compared to controls. In summary, the data show that PGRP-S is induced in cerebral ischemia by RelA, but its role in ischemia is unclear.
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