Michalovicz Lindsay T, Lally Brent, Konat Gregory W
Department of Neurobiology and Anatomy, West Virginia University School of Medicine, 1 Medical Center Dr., Morgantown, WV 26506-9128, USA.
Department of Neurobiology and Anatomy, West Virginia University School of Medicine, 1 Medical Center Dr., Morgantown, WV 26506-9128, USA.
J Neuroimmunol. 2015 Aug 15;285:137-42. doi: 10.1016/j.jneuroim.2015.06.003. Epub 2015 Jun 12.
Peripheral challenge with a viral mimetic, polyinosinic-polycytidylic acid (PIC) induces hippocampal hyperexcitability in mice. Here, we characterized this hippocampal response through a whole genome transcriptome analysis. Intraperitoneal injection of PIC resulted in temporal dysregulation of 625 genes in the hippocampus, indicating an extensive genetic reprogramming. The bioinformatics analysis of these genes revealed the complement pathway to be the most significantly activated. The gene encoding complement factor B (CfB) exhibited the highest response, and its upregulation was commensurate with the development of hyperexcitability. Collectively, these results suggest that the induction of hippocampal hyperexcitability may be mediated by the alternative complement cascades.
用病毒模拟物聚肌苷酸-聚胞苷酸(PIC)对外周进行刺激会诱导小鼠海马体兴奋性过高。在此,我们通过全基因组转录组分析对这种海马体反应进行了表征。腹腔注射PIC导致海马体中625个基因出现时间性失调,表明发生了广泛的基因重编程。对这些基因的生物信息学分析显示补体途径是激活最显著的途径。编码补体因子B(CfB)的基因表现出最高的反应,其上调与兴奋性过高的发展程度相当。总体而言,这些结果表明海马体兴奋性过高的诱导可能由替代补体级联反应介导。