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microRNA-20b contributes to high glucose-induced podocyte apoptosis by targeting SIRT7

Xiaojing Wang1, Bo Lin2, Lin Nie3

  • 1Department of Endocrinology, Yuncheng Central Hospital, Yuncheng, Shanxi 044000, P.R. China.

Molecular Medicine Reports
|August 30, 2017
PubMed

Insights

MicroRNA-20b (miR-20b) promotes high glucose-induced podocyte apoptosis in diabetic nephropathy by targeting Sirtuin 7 (SIRT7). Inhibiting miR-20b offers a potential therapeutic strategy for diabetic kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • Diabetic nephropathy (DN) pathogenesis involves microRNAs (miRNAs) and podocyte apoptosis.
  • High glucose (HG) induces podocyte apoptosis, a hallmark of DN.
  • The specific role of miRNAs in HG-induced podocyte apoptosis requires further elucidation.

Purpose of the Study:

  • To investigate the role of miRNA-20b (miR-20b) in HG-induced podocyte apoptosis.
  • To elucidate the underlying molecular mechanism of miR-20b in this process.

Main Methods:

  • Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to measure miR-20b levels.
  • Caspase-3 activity assays and TUNEL assays to assess apoptosis.
  • Dual-Luciferase reporter assay, RT-qPCR, and western blot to identify miR-20b targets.
  • In vitro experiments involving miR-20b inhibitors, SIRT7 silencing, and SIRT7 overexpression.

Main Results:

  • miR-20b was significantly upregulated in HG-treated podocytes.
  • Inhibiting miR-20b suppressed HG-induced podocyte apoptosis.
  • Sirtuin 7 (SIRT7) was identified as a direct target of miR-20b.
  • SIRT7 silencing exacerbated HG-induced podocyte apoptosis, while SIRT7 overexpression attenuated it.
  • SIRT7 silencing blocked the protective effect of miR-20b suppression against HG-induced apoptosis.

Conclusions:

  • miR-20b contributes to HG-induced podocyte apoptosis by targeting SIRT7.
  • The miR-20b/SIRT7 axis represents a potential therapeutic target for diabetic nephropathy.

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