SETD2 regulates SLC family transporter-mediated sodium and glucose reabsorptions in renal tubule

Biochem Biophys Res Commun. 2024 Nov 19:734:150730. doi: 10.1016/j.bbrc.2024.150730. Epub 2024 Sep 28.

Abstract

A regulatory mechanism for SLC family transporters, critical transporters for sodium and glucose reabsorptions in renal tubule, is incompletely understood. Here, we report an important regulation of SLC family transporter by SETD2, a chromatin remodeling gene whose alterations have been found in a subset of kidney cancers. Kidney-specific inactivation of Setd2 resulted in hypovolemia with excessive urine excretion in mouse and interestingly, RNA-sequencing analysis of Setd2-deficient murine kidney exhibited decreased expressions of SLC family transporters, critical transporters for sodium and glucose reabsorptions in renal tubule. Importantly, inactivation of Setd2 in murine kidney displayed attenuated dapagliflozin-induced diuresis and glucose excretion, further supporting that SETD2 might regulate SLCfamily transporter-mediated sodium and glucose reabsorptions in renal tubule. These data uncover an important regulation of SLC family transporter by SETD2, which may illuminate a crosstalk between metabolism and epigenome in renal tubule.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Glucose* / metabolism
  • Histone-Lysine N-Methyltransferase* / genetics
  • Histone-Lysine N-Methyltransferase* / metabolism
  • Kidney Tubules* / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Renal Reabsorption
  • Sodium* / metabolism
  • Sodium* / urine
  • Solute Carrier Proteins / genetics
  • Solute Carrier Proteins / metabolism

Substances

  • Histone-Lysine N-Methyltransferase
  • Glucose
  • Sodium
  • SETD2 protein, mouse
  • Solute Carrier Proteins