Downregulation of the klotho gene in the kidney under sustained circulatory stress in rats

Hiroki Aizawa, Yuichiro Saito, Tetsuya Nakamura, Masahiro Inoue, Tetsuro Imanari, Yoshio Ohyama, Yutaka Matsumura, Hiroaki Masuda, Shigenori Oba, Naobumi Mise, Kenjiro Kimura, Akira Hasegawa, Masahiko Kurabayashi, Makoto Kuro-O, Yo Ichi Nabeshima, Ryozo Nagai

Research output: Contribution to journalArticlepeer-review

112 Scopus citations


We recently reported the isolation of the klotho gene, which is predominantly expressed in the kidney and involved in human aging phenotypes. In our previous studies, we demonstrated that the Klotho protein or its metabolites may possibly function as humoral factor(s) and protect against endothelial dysfunction because acetylcholine-mediated NO production in arteries was impaired in heterozygous klotho deficient mice (kl/+). However, the pathophysiological significance of the Klotho protein has not been clarified yet. In the present study, we examined expression of the klotho gene in the kidney of the following rat models for human diseases: (1) spontaneously hypertensive rat, (2) deoxycorticosterone acetate-salt hypertensive rat, (3) 5/6 nephrectomized rat, (4) non-insulin-dependent diabetes mellitus rat (the Otsuka Long-Evans Tokushima Fatty rat), and (5) rat with acute myocardial infarction. The expression levels of klotho mRNA in the kidney in these models were significantly lower than controls except for MI rats. This is the first report showing that expression of the klotho gene in the kidney is regulated under sustained circulatory stress such as long-term hypertension, diabetes mellitus, and chronic renal failure.

Original languageEnglish (US)
Pages (from-to)865-871
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - Aug 28 1998

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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