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Decreased miR-26a Expression Correlates with the Progression of Podocyte Injury in Autoimmune Glomerulonephritis

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Title: Decreased miR-26a Expression Correlates with the Progression of Podocyte Injury in Autoimmune Glomerulonephritis
Authors: Ichii, Osamu Browse this author →KAKEN DB
Otsuka-Kanazawa, Saori Browse this author →KAKEN DB
Horino, Taro Browse this author
Kimura, Junpei Browse this author
Nakamura, Teppei Browse this author
Matsumoto, Manabu Browse this author
Toi, Makoto Browse this author
Kon, Yasuhiro Browse this author →KAKEN DB
Issue Date: 17-Oct-2014
Publisher: The Public Library of Science
Journal Title: PLOS one
Volume: 9
Issue: 10
Start Page: e110383
Publisher DOI: 10.1371/journal.pone.0110383
Abstract: MicroRNAs contribute to the pathogenesis of certain diseases and may serve as biomarkers. We analyzed glomerular microRNA expression in B6.MRLc1, which serve as a mouse model of autoimmune glomerulonephritis. We found that miR-26a was the most abundantly expressed microRNA in the glomerulus of normal C57BL/6 and that its glomerular expression in B6.MRLc1 was significantly lower than that in C57BL/6. In mouse kidneys, podocytes mainly expressed miR-26a, and glomerular miR-26a expression in B6.MRLc1 mice correlated negatively with the urinary albumin levels and podocytespecific gene expression. Puromycin-induced injury of immortalized mouse podocytes decreased miR-26a expression, perturbed the actin cytoskeleton, and increased the release of exosomes containing miR-26a. Although miR-26a expression increased with differentiation of immortalized mouse podocytes, silencing miR-26a decreased the expression of genes associated with the podocyte differentiation and formation of the cytoskeleton. In particular, the levels of vimentin and actin significantly decreased. In patients with lupus nephritis and IgA nephropathy, glomerular miR-26a levels were significantly lower than those of healthy controls. In B6.MRLc1 and patients with lupus nephritis, miR-26a levels in urinary exosomes were significantly higher compared with those for the respective healthy control. These data indicate that miR-26a regulates podocyte differentiation and cytoskeletal integrity, and its altered levels in glomerulus and urine may serve as a marker of injured podocytes in autoimmune glomerulonephritis.
Type: article
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 市居 修

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