Biochemical and biophysical research communications · 2024
SETD2 regulates SLC family transporter-mediated sodium and glucose reabsorptions in renal tubule.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Mitome Taku, Wakui Hiromichi, Azushima Kengo, Uehara Tatsuki, Jikuya Ryosuke, Ohtake Shinji, Noguchi Go, Kawaura Sachi, Iribe Yasuhiro, Aomori Kota, Tatenuma Tomoyuki, Ito Hiroki, Kawahara Takashi, Komeya Mitsuru, Ito Yusuke, Muraoka Kentaro, Furuya Mitsuko, Kato Ikuma, Fujii Satoshi, Nagahama Kiyotaka, Nishiyama Akira, Tamura Tomohiko, Kimura Yayoi, Kawagoe Tatsukata, Mizuki Nobuhisa, Huang Gang, Uemura Hiroji, Yao Masahiro, Makiyama Kazuhide, Tamura Kouichi, Hasumi Hisashi
Аннотация
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.