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Abstract: SA-PO453

All-Trans Retinoic Acid Directly Acts on Podocytes by Regulating CD80 Expression

Session Information

  • Pediatric Nephrology - II
    October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Pediatric Nephrology

  • 1600 Pediatric Nephrology

Authors

  • Akagawa, Yuko, Kansai Medical University, Osaka, Japan
  • Tsuji, Shoji, Kansai Medical University, Osaka, Japan
  • Akagawa, Shohei, Kansai Medical University, Osaka, Japan
  • Yamanouchi, Sohsaku, Kansai Medical University, Osaka, Japan
  • Kimata, Takahisa, Kansai Medical University, Osaka, Japan
  • Kaneko, Kazunari, Kansai Medical University, Osaka, Japan
Background

Pathogenesis of minimal change nephrotic syndrome (MCNS) remains unclear, though recent studies suggest a role for malfunction of regulatory T cells (Tregs) and abnormal expression of several podocyte-related molecules, such as CD80 (Garin E, et al. Pediatric Nephrology, 2016). All-trans retinoic acid (ATRA) has the potential to regulate the immune system, including induction and differentiation of Tregs, in addition to its vitamin function. Therefore, we aimed to investigate the potential of ATRA as a protective therapy for MCNS through suppression of CD80 in vitro.

Methods

Human-derived immortalized podocytes were treated with puromycin aminonucleoside (PAN) as an in vitro model of MCNS. Cells were treated with ATRA (10 µM) or DMSO in starvation medium on day 1 followed by PAN (50 µg/ml), or PBS on day 0. Samples were collected after 72 h for analysis. Protein expression levels of CD80 and retinoic acid receptor (RAR) were measured by western blotting.

Results

PAN induced increased protein expression of CD80 and RAR both of which were restored by ATRA treatment (Figure1). These results suggested that the overexpression of CD80 after PAN stimulation can be restored by ATRA through RAR.

Conclusion

ATRA suppresses CD80 overexpression caused by PAN stimulation through RAR in podocytes. ATRA might have an antiproteinuric effect on MCNS through its direct effect on podocytes.