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Interleukin-36α as a potential biomarker for renal tubular damage induced by dietary phosphate load.
Hirano, Yoshitaka; Kurosu, Hiroshi; Shiizaki, Kazuhiro; Iwazu, Yoshitaka; Tsuruoka, Shuichi; Kuro-O, Makoto.
Afiliação
  • Hirano Y; Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
  • Kurosu H; Department of Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
  • Shiizaki K; Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
  • Iwazu Y; Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
  • Tsuruoka S; Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
  • Kuro-O M; Department of Clinical Laboratory Medicine, Jichi Medical University, Shimotsuke, Japan.
FEBS Open Bio ; 10(5): 894-903, 2020 05.
Article em En | MEDLINE | ID: mdl-32191399
ABSTRACT
Excessive intake of phosphate has been known to induce renal tubular damage and interstitial inflammation, leading to acute kidney injury or chronic kidney disease in rodents and humans. However, sensitive and early biomarkers for phosphate-induced kidney damage remain to be identified. Our previous RNA sequencing analysis of renal gene expression identified interleukin-36α (IL-36α) as a gene significantly upregulated by dietary phosphate load in mice. To determine the time course and dose dependency of renal IL-36α expression induced by dietary phosphate load, we placed mice with or without uninephrectomy on a diet containing either 0.35%, 1.0%, 1.5%, or 2.0% inorganic phosphate for 10 days, 4 weeks, or 8 weeks and evaluated renal expression of IL-36α and other markers of tubular damage and inflammation by quantitative RT-PCR, immunoblot analysis, and immunohistochemistry. We found that IL-36α expression was induced in distal convoluted tubules and correlated with phosphate excretion per nephron. The increase in IL-36α expression was simultaneous with but more robust in amplitude than the increase in tubular damage markers such as Osteopontin and neutrophil gelatinase-associated lipocalin, preceding the increase in expression of other inflammatory cytokines, including transforming growth factor-α, interleukin-1ß, and transforming growth factor-ß1. We conclude that IL-36α serves as a marker that reflects the degree of phosphate load excreted per nephron and of associated kidney damage.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fosfatos / Interleucina-1alfa / Túbulos Renais Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fosfatos / Interleucina-1alfa / Túbulos Renais Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Ano de publicação: 2020 Tipo de documento: Article