PRMT4 is involved in insulin secretion via the methylation of histone H3 in pancreatic β cells

Joong Kwan Kim, Yongchul Lim, Jung Ok Lee, Young Sun Lee, Nam Hee Won, Hyun Kim, Hyeon Soo Kim

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The relationship between protein arginine methyltransferases (PRMTs) and insulin synthesis in β cells is not yet well understood. In the present study, we showed that PRMT4 expression was increased in INS-1 and HIT-T15 pancreatic β cells under high-glucose conditions. In addition, asymmetric dimethylation of Arg17 in histone H3 was significantly increased in both cell lines in the presence of glucose. The inhibition or knockdown of PRMT4 suppressed glucose-induced insulin gene expression in INS-1 cells by 81.6 and 79% respectively. Additionally, the overexpression of mutant PRMT4 also significantly repressed insulin gene expression. Consistently, insulin secretion induced in response to high levels of glucose was decreased by both PRMT4 inhibition and knockdown. Moreover, the inhibition of PRMT4 blocked high-glucose-induced insulin gene expression and insulin secretion in primary pancreatic islets. These results indicate that PRMT4 might be a key regulator of high-glucose-induced insulin secretion from pancreatic β cells via H3R17 methylation.

Original languageEnglish
Pages (from-to)315-324
Number of pages10
JournalJournal of Molecular Endocrinology
Volume54
Issue number3
DOIs
Publication statusPublished - 2015 Apr 27

Keywords

  • Histone H3R17
  • Insulin secretion
  • Insulin synthesis
  • PRMT4

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology

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