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Kidney Week

Abstract: PO1995

OASIS in Podocytes Promoted Tubular Injury by Suppressing PRKCI Expression

Session Information

  • Podocyte Biology
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

  • 1204 Podocyte Biology


  • Miyake, Yoshiaki, Osaka University, Suita, Osaka, Japan
  • Obana, Masanori, Osaka University, Suita, Osaka, Japan
  • Yamamoto, Ayaha, Osaka University, Suita, Osaka, Japan
  • Harada, Takeo, Osaka University, Suita, Osaka, Japan
  • Nakae, Takafumi, Osaka University, Suita, Osaka, Japan
  • Noda, Shunsuke, Osaka University, Suita, Osaka, Japan
  • Mitsuoka, Sayuri, Osaka University, Suita, Osaka, Japan
  • Tanaka, Koki, Osaka University, Suita, Osaka, Japan
  • Tanaka, Shota, Osaka University, Suita, Osaka, Japan
  • Maeda, Makiko, Osaka University, Suita, Osaka, Japan
  • Imaizumi, Kazunori, Hiroshima Daigaku, Higashihiroshima, Hiroshima, Japan
  • Asanuma, Katsuhiko, Chiba Daigaku Daigakuin Igaku Kenkyuin Igakubu, Chiba, Chiba, Japan
  • Fujio, Yasushi, Osaka University, Suita, Osaka, Japan

Old astrocyte specifically induced substance (OASIS), a transcription factor, plays important roles in physiological and pathophysiological processes, such as bone formation. Previously, we found that OASIS is expressed in podocytes in murine kidney. However, the pathophysiological roles of OASIS in podocytes remains unknown. The aim of this study is to investigate the functional roles of OASIS in podocytes in the development of kidney diseases.


The expression of OASIS protein was investigated in glomeruli of murine kidney and cultured mouse podocytes cell line after lipopolysaccharide (LPS) treatment. To examine the roles of OASIS in podocytes on kidney injury, podocyte-specific OASIS knockout (OASIS CKO) mice were established and subjected to LPS. Twenty-four hours after LPS treatment, serum creatinine and urinary albumin ratio were measured. Podocytes injury was assessed by electron microscope analysis and tubular injury was analyzed by PAS staining and by measuring LCN2 mRNA expression. To explore the secretory molecules downstream of OASIS, DNA microarray analysis was performed using podocytes with lentiviral overexpression of OASIS. In order to examine the effects of the downstream molecule of OASIS on proximal tubule cells, HK-2 cells were cultured.


LPS treatment increased OASIS expression in glomeruli of murine kidney and in cultured podocytes. Podocyte-specific OASIS deletion suppressed LPS-increased serum creatinine (sCr) level (sCr (mg/dL): control-LPS; 1.01±0.27, OASIS CKO-LPS; 0.76±0.16, n=8-10, p<0.05), but did not influence albuminuria and podocyte injury. Surprisingly, on the other hand, OASIS CKO mice were protected from LPS-mediated tubular injury. DNA microarray analysis using OASIS-overexpressed podocytes revealed that PRKCI was negatively regulated by OASIS in podocytes. Finally, we found that recombinant PRKCI suppressed LPS-induced LCN2 mRNA expression in HK-2 cells in a dose-dependent manner.


Suppression of OASIS in podocytes attenuated LPS-induced tubular injury in part by increased PRKCI secretion. Targeting OASIS-PRKCI signaling in podocytes could be of therapeutic value in kidney diseases.