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Rapid, transient induction of ER stress in the liver and kidney after acute exposure to heavy metal: Evidence from transgenic sensor mice
Author(s) -
Hiramatsu Nobuhiko,
Kasai Ayumi,
Du Shuqi,
Takeda Masayuki,
Hayakawa Kunihiro,
Okamura Maro,
Yao Jian,
Kitamura Masanori
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.04.040
Subject(s) - endoplasmic reticulum , unfolded protein response , alkaline phosphatase , cadmium , endogeny , in vivo , chemistry , genetically modified mouse , kidney , transgene , phosphatase , medicine , endocrinology , trap (plumbing) , biochemistry , biology , enzyme , microbiology and biotechnology , organic chemistry , environmental engineering , gene , engineering
Endoplasmic reticulum (ER) stress‐responsive alkaline phosphatase (ES‐TRAP) serves as a sensitive indicator for ER stress. In response to heavy metals including cadmium, nickel and cobalt, hepatocytes and renal tubular cells expressing ES‐TRAP exhibited ER stress and decreased ES‐TRAP activity. In ES‐TRAP transgenic mice, acute exposure to cadmium showed rapid, transient decreases in the activity of serum ES‐TRAP. It was inversely correlated with the induction of endogenous ER stress markers in the liver and kidney. Our result provides first evidence for the acute, reversible induction of ER stress in vivo after exposure to heavy metal.