Inhibition of OASIS in podocytes suppressed diabetes-induced kidney dysfunction

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  • Miyake Yoshiaki
    Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University
  • Obana Masanori
    Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University
  • Yamamoto Ayaha
    Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University
  • Noda Shunsuke
    Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University
  • Kanemoto Soshi
    Laboratory of Functional Anatomy and Neuroscience, Asahikawa Medical University
  • Maeda Makiko
    Project Laboratory of Clinical Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Asanuma Katsuhiko
    Department of Nephrology, Graduate School of Medicine, Chiba University
  • Imaizumi Kazunori
    Department of Biochemistry, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • Nakayama Hiroyuki
    Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University
  • Fujio Yasushi
    Laboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University Project Laboratory of Clinical Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University

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Other Title
  • ポドサイトにおけるOASISの発現抑制は糖尿病による腎機能の悪化を抑制する

Abstract

<p>[Background] Diabetes is a major risk factor for chronic kidney disease (CKD). However, the mechanisms of diabetes-induced kidney injury remain to be fully elucidated. Here, we focused on old astrocyte specifically induced substance (OASIS), a transcriptional factor, because OASIS mRNA is increased in kidneys of CKD patients in the Nephroseq database. The aim is to determine the pathological roles of OASIS in diabetes-induced kidney injury.</p><p>[Methods/Results] C57BL/6J mice were injected with STZ to induce diabetes. Laser microdissection and immunoblotting revealed that OASIS was upregulated in glomeruli of STZ-treated mice. OASIS was detected in podocytes by immunohistochemical staining. To examine the roles of OASIS in podocytes, we generated podocyte-specific OASIS knockout mice (CKO). Mice were subjected to unilateral nephrectomy (UNx) before STZ injection to accelerate kidney injury. After UNx-STZ treatment, the level of serum creatinine (sCr) and the rate of kidney weight to body weight (Kw/Bw) got lower in CKO, compared with control (sCr (mg/dL): control; 0.85±0.11, CKO; 0.59±0.14, Kw/Bw (mg/g): control; 15.0±1.5, CKO;12.4±1.2, P&lt;0.05, N=3-5).</p><p>[Conclusion] Podocyte OASIS could be a therapeutic target for the treatment of diabetic kidney disease.</p><p></p>

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