MiR-93 regulates Msk2-mediated chromatin remodelling in diabetic nephropathy

Shawn S. Badal, Yin Wang, Jianyin Long, David L. Corcoran, Benny H. Chang, Luan Truong, Yashpal S. Kanwar, Paul A. Overbeek, Farhad R. Danesh

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


How the kidney responds to the metabolic cues from the environment remains a central question in kidney research. This question is particularly relevant to the pathogenesis of diabetic nephropathy (DN) in which evidence suggests that metabolic events in podocytes regulate chromatin structure. Here, we show that miR-93 is a critical metabolic/epigenetic switch in the diabetic milieu linking the metabolic state to chromatin remodelling. Mice with inducible overexpression of a miR-93 transgene exclusively in podocytes exhibit significant improvements in key features of DN. We identify miR-93 as a regulator of nucleosomal dynamics in podocytes. miR-93 has a critical role in chromatin reorganization and progression of DN by modulating its target Msk2, a histone kinase, and its substrate H3S10. These findings implicate a central role for miR-93 in high glucose-induced chromatin remodelling in the kidney, and provide evidence for a previously unrecognized role for Msk2 as a target for DN therapy.

Original languageEnglish (US)
Article number12076
JournalNature Communications
StatePublished - Jun 28 2016

ASJC Scopus subject areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)


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