Fig. 1

The methyltransferase G9a in cooperation with its homologue G9a-like protein (GLP) is responsible for the majority of dimethylation of H3K9me2. Cells that lack G9a (or GLP) display a drastic reduction in this modification [26]. H3K9me2 acts as a major repressive histone methylation mark in euchromatin, that affects also the interleukin 17 gene locus, resulting in inhibition of IL-17 expression [27]. Harrison et al. demonstrated that mice lacking IL-17 do not develop sustained hypertension after treatment with angiotensin II. In contrast to wild-type mice, IL-17−/− mice do not exhibit an increase in superoxide production and there is no reduction in endothelial-dependent vasodilatation. Furthermore, there was a reduction in vascular accumulation of leukocytes in IL-17−/− mice, probably due to a reduction of chemotaxis normally induced by IL-17 [35]