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

Author:

Mitome Taku1,Wakui Hiromichi1,Azushima Kengo1,Uehara Tatsuki1,Jikuya Ryosuke1,Ohtake Shinji1,Noguchi Go1,Kawaura Sachi1,Iribe Yasuhiro1,Aomori Kota1,Tatenuma Tomoyuki1,Ito Hiroki1,Kawahara Takashi1,Komeya Mitsuru1,Ito Yusuke1,Muraoka Kentaro1,Furuya Mitsuko2,Kato Ikuma1,Fujii Satoshi1,Nagahama Kiyotaka3,Nishiyama Akira1,Tamura Tomohiko1,Kimura Yayoi1,Kawagoe Tatsukata1,Mizuki Nobuhisa1,Huang Gang4,Uemura Hiroji1,Yao Masahiro1,Makiyama Kazuhide1,Tamura Kouichi1,Hasumi Hisashi1

Affiliation:

1. Yokohama City University Graduate School of Medicine

2. Eurofins Genetic Lab Co., Ltd

3. Kyorin University

4. Cincinnati Children's Hospital Medical Center

Abstract

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 SLC family 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.

Publisher

Springer Science and Business Media LLC

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