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2022-12-14T03:46:32Z
461:462
Acute kidney injury induced by protein-overload nephropathy down-regulates gene expression of hepatic cerebroside sulfotransferase in mice, resulting in reduction of liver and serum sulfatides
Zhang, Xiaowei
Nakajima, Takero
Kamijo, Yuji
Li, Gang
Hu, Rui
Kannagi, Reiji
Kyogashima, Mamoru
Aoyama, Toshifumi
Hara, Atsushi
Copyright (c) 2009 Elsevier Inc.
Sulfatides
Sphingoglycolipids
Acute kidney injury
Protein-overload nephropathy
Peroxisome proliferator-activated receptor
alpha (Ppara)-null mice
Cerebroside sulfotransferase (CST)
Sulfatides, possible antithrombotic factors belonging to sphingoglycolipids, are widely distributed in mammalian tissues and serum. We recently found that the level of serum sulfatides was significantly lower in hemodialysis patients than that in normal subjects, and that the m serum level closely correlated to the incidence of cardiovascular disease. These findings suggest a relationship between the level of serum sulfatides and kidney function; however, the molecular mechanism underlying this relationship remains unclear. In the present study, the influence of kidney dysfunction on the metabolism of sulfatides was examined using an established murine model of acute kidney injury, protein-overload nephropathy in mice. Protein-overload treatment caused severe proximal tubular injuries within 4 days, and this treatment obviously decreased both serum and hepatic sulfatide levels. The sphingoid composition of serum sulfatides was very similar to that of hepatic ones at each time point, suggesting that the serum sulfatide level is dependent on the hepatic secretory ability of sulfatides. The treatment also decreased hepatic expression of cerebroside sulfotransferase (CST), a key enzyme in sulfatide metabolism, while it scarcely influenced the expression of the other sulfatide-metabolizing enzymes, including arylsulfatase A, ceramide galactosyltransferase, and galactosylceramidase. Pro-inflammatory responses were not detected in the liver of these mice: however, potential oxidative stress was increased. These results suggest that down-regulation of hepatic CST expression, probably affected by oxidative stress from kidney injury, causes reduction in liver and serum sulfatide levels. This novel mechanism, indicating the crosstalk between kidney injury and specific liver function, may prove useful for helping to understand the situation where human hemodialysis patients have low levels of serum sulfatides.
Article
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 390(4):1382-1388 (2009)
ACADEMIC PRESS INC ELSEVIER SCIENCE
2009-12-25
eng
journal article
AM
http://hdl.handle.net/10091/10814
https://soar-ir.repo.nii.ac.jp/records/3904
https://pubmed.ncbi.nlm.nih.gov/19895791
19895791
https://doi.org/10.1016/j.bbrc.2009.10.164
10.1016/j.bbrc.2009.10.164
0006-291X
AA00564395
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
390
4
1382
1388
https://soar-ir.repo.nii.ac.jp/record/3904/files/Acute_kidney_injury.pdf
application/pdf
721.2 kB
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