Abstract
So far, we have identified a macrophage molecule, M‐mod (macrophage‐modulator), whose expression level was affected during differentiation. To explore biological roles of M‐mod, we established M‐mod knockdown (KD) cells using short hairpin RNA. Since M‐mod KD cells did not affect expression of CD11b and CD11c, M‐mod is dispensable for M1 macrophage differentiation. On the other hand, M‐mod KD potentiated expression of type2 diabetes‐associated genes such as adipocyte protein 2 (aP2), plasminogen activator inhibitor (PAI)‐1, and monocyte chemoattractant protein (MCP)‐1. In agreement, supernatant from M‐mod KD cells decreased insulin sensitivity of 3T3‐L1 adipocytes. M‐mod KD did not influenced phosphorylation of protein kinases (such as JNK, ERK, p38 and Akt) and their downstream transcriptional regulators (such as AP‐1, PPARs and NF‐κB). By contrast, M‐mod KD promoted methylation of histone H3 Lys4 at aP2 locus. Collectively, M‐mod might be an epigenetic suppressor of type2 diabetes‐associated genes in M1 macrophages. This study was supported by AstraZeneca, Ono Medical Research Foundation, and Suzuken Memorial Foundation.
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