Nuclear paraspeckle assembly transcript 1 promotes the podocyte injury via targeting miR-23b-3p/B-cell lymphoma-2

Jing Wang1, Junpeng Luo2, Li Du3

  • 1Department of Emergency, The First Medical Center to Chinese People's Liberation Army General Hospital, Beijing, China.

Renal Failure
|November 9, 2022
PubMed
Abstract

Insights

Nuclear paraspeckle assembly transcript 1 (NEAT1) promotes kidney podocyte injury by targeting the miR-23b-3p/BNIP3L pathway. This study elucidates NEAT1

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Nephrology

Background:

  • Nuclear paraspeckle assembly transcript 1 (NEAT1) has known effects on kidney injury.
  • The specific role of NEAT1 in podocyte function and injury remains unclear.

Purpose of the Study:

  • To investigate the impact of NEAT1 on podocyte injury.
  • To elucidate the molecular mechanisms by which NEAT1 influences podocyte damage.

Main Methods:

  • Established an adriamycin (ADR)-induced mouse podocyte injury model (MPC5 cells).
  • Utilized NEAT1 overexpression (oe-NEAT1) and knockdown (shNEAT1) constructs.
  • Verified target relationships using dual-luciferase reporter and RNA immunoprecipitation assays.
  • Assessed cell viability (CCK-8) and apoptosis (flow cytometry).
  • Quantified gene and protein expression via qRT-PCR and Western blot.

Main Results:

  • NEAT1 expression was elevated in ADR-induced podocyte injury.
  • NEAT1 overexpression exacerbated podocyte injury markers (Desmin) and apoptosis while reducing viability markers (WT1, Nephrin).
  • NEAT1 knockdown demonstrated opposite effects.
  • NEAT1 negatively regulated miR-23b-3p, which in turn targeted BNIP3L.
  • Modulation of the NEAT1/miR-23b-3p/BNIP3L axis affected key proteins involved in apoptosis and epithelial-mesenchymal transition.

Conclusions:

  • NEAT1 promotes podocyte injury through the miR-23b-3p/BNIP3L axis.
  • Targeting this pathway may offer therapeutic strategies for kidney injury.

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