Expression data from P4H-TM deficient mouse cortexes after 24h of pMCAO. Expression data from P4H-TM deficient mouse cortexes after 24h of pMCAO

Genetic deletion of transmembrane prolyl-4-hydroxylase (P4H-TM) in mice leads to increased inflammatory microgliosis and neutrophil infiltration in the cortex after permanent midle cerebral artery occlusion (pMCAO) Overall design: Mice underwent pMCAO on a left side and 24h later cortexes from wild-type (WT) and P4H-TM deficient (KO) mice were collected for further mRNA extraction and microarray analysis. Corresponding contralateral cortex (c) was used as a control for inpsilateral injured (i) one. mRNA from 4 individual mice were pooled per experimental condition. Comparison was done between four experimental conditions: WTc, WTi, KOc, KOi.