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Guided Differentiation of Mature Kidney Podocytes from Human Induced Pluripotent Stem Cells Under Chemically Defined Conditions
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Published on: July 2, 2020

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LncRNA SOX2OT alleviates the high glucose-induced podocytes injury through autophagy induction by the miR-9/SIRT1

Yan Zhang1, Baochao Chang1, Jiqiang Zhang1

  • 1Departments of Nephrology, The First Affiliated Hospital of Bengbu Medical College, No. 287 Changhuai Road, Bengbu, Anhui 233000, PR China.

Experimental and Molecular Pathology
|July 14, 2019
PubMed
Abstract

Insights

Long non-coding RNA SOX2OT protects against high glucose-induced podocyte injury in diabetic nephropathy by promoting autophagy via the miR-9/SIRT1 pathway.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Nephrology

Background:

  • Podocyte injury is a key factor in diabetic nephropathy (DN) progression.
  • Understanding the molecular mechanisms underlying podocyte damage is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of long non-coding RNA SOX2OT in high glucose (HG)-induced human podocyte cells (HPCs) injury.
  • To elucidate the underlying molecular mechanism involving SOX2OT in DN.

Main Methods:

  • Cell proliferation and apoptosis assays (MTT, flow cytometry) were used to assess HPCs viability.
  • Western blot analysis quantified protein levels of SIRT1 and autophagy markers (Beclin-1, LC3-II, Atg7, p62).
  • Luciferase activity assays determined the interactions between SOX2OT, miR-9, and SIRT1.

Main Results:

  • SOX2OT overexpression significantly reduced HG-induced HPCs injury and promoted autophagy.
  • Autophagy induction was blocked by an autophagy inhibitor (3-MA) and SIRT1 knockdown.
  • SOX2OT functions as a competing endogenous RNA (ceRNA), sponging miR-9 to upregulate SIRT1 and induce autophagy.

Conclusions:

  • SOX2OT overexpression alleviates podocyte injury in DN by inducing autophagy.
  • The miR-9/SIRT1 axis is a critical mediator of SOX2OT's protective effects in HG-induced podocyte injury.
Keywords:
AutophagyDiabetic nephropathySIRT1SOX2OTmiR-9

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