Figure 2.
qRT-PCR of genes specific for the classical, the alternative activated type of macrophages and deactivating targets 5 days after myocardial infarction. All fold changes (FC) are expressed relative to mRNA abundance in myocardial infarction (MI), which was set to 1. Tumour necrosis factor α (TNFα) (A), interleukin 6 (IL6) (B) and interleukin 1β (IL1β) (C) are all strongly up-regulated in macrophages compared with myocardial infarction, BZ, MonoB and LV. This indicates a myocardial-specific regulation predominantly in macrophages. Arginase 1 (ARG1) (D), arginase 2 (ARG2) (E) and chitinase3 like 3 (CHI3L3, also designated YM1) (F) are mainly transcribed by macrophages compared with MI, BZ and LV. In connection with ARG2 as well as CHI3L3, a moderate transcription was also detected in monocytes isolated from blood compared with MI, BZ and LV, which indicates an incomplete cardiac-specific expression. Suppressor of cytokine signalling 3 (SOCS3) (G), interleukin 1 receptor antagonist (IL1rn) (H) and interleukin 10 (IL10) (I), which are all known to suppress the inflammatory response, are predominantly transcribed by macrophages. Note that especially IL10 shows a very strong up-regulation in macrophages compared with controls. (FC, fold change; LV, left ventricle; MonoB, monocytes isolated from blood; BZ, border zone of infarcted area; MI, entire infarcted area; MAC, macrophages isolated from infarcted area; each n= 6).