| First Author | Fujimoto S | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 404 |
| Issue | 1 | Pages | 223-7 |
| PubMed ID | 21110946 | Mgi Jnum | J:167452 |
| Mgi Id | MGI:4868306 | Doi | 10.1016/j.bbrc.2010.11.097 |
| Citation | Fujimoto S, et al. (2011) In vivo evidence of enhanced di-methylation of histone H3 K4 on upregulated genes in adipose tissue of diabetic db/db mice. Biochem Biophys Res Commun 404(1):223-7 |
| abstractText | Di-methylation of histone H3 lysine (K) 4, a component of the epigenetic memory, is associated with gene transactivation. In this study, we examined whether the development of diabetes induces di-methylation of histone H3 K4 on the upregulated genes. We searched for upregulated genes in mesenteric adipose tissue of insulin-resistant/diabetic db/db mice compared with non-diabetic db/m mice using microarray analysis. We also performed chromatin immunoprecipitation assays for di-methylation of histone H3 K4 in the upregulated genes in mesenteric adipose tissue of db/m and db/db mice. Di-methylation of histone H3 K4 was enhanced at the upstream and/or transcribed regions of upregulated genes including Atp6v0d2, Mmp12, Trem2 and Clec4d genes in mesenteric adipose tissue of db/db mice, as compared with db/m mice. These results suggest that di-methylation of histone H3 K4 is involved in the induction of Atp6v0d2, Mmp12, Trem2 and Clec4d in mesenteric adipose tissue in db/db mice. |
