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LincRNA-p21 sponges miR-18b to promote the progression of diabetic nephropathy

Jingjing Zhang1, Xinling Cao1, Shun Wang1

  • 1Department of Nephropathy, The First Affiliated Hospital of Xinjiang Medical University Urumqi 830054, Xinjiang Uygur Autonomous Region, China.

American Journal of Translational Research
|June 12, 2018
PubMed

Insights

Down-regulating long non-coding RNA p21 (lincRNA-p21) alleviates diabetic nephropathy progression. LincRNA-p21 promotes kidney cell proliferation and extracellular matrix accumulation via interaction with miR-18b.

Area of Science:

  • Molecular Biology
  • Nephrology
  • Genetics

Background:

  • Diabetic nephropathy (DN) is a major complication of diabetes.
  • The role of long non-coding RNAs (lncRNAs) in DN pathogenesis is largely unknown.
  • lincRNA-p21 is a potential factor in DN development.

Purpose of the Study:

  • To investigate the expression and mechanism of lincRNA-p21 in diabetic nephropathy.
  • To explore lincRNA-p21 as a potential therapeutic target for DN.

Main Methods:

  • Studied lincRNA-p21 levels in a mouse model of DN and in vitro cell cultures.
  • Utilized cell proliferation assays and molecular techniques (e.g., 3'-UTR targeting) to examine interactions.
  • Assessed extracellular matrix accumulation under high glucose conditions.

Main Results:

  • lincRNA-p21 expression was upregulated in DN models and high glucose conditions.
  • Down-regulation of lincRNA-p21 ameliorated DN pathological changes.
  • lincRNA-p21 promoted mesangial cell proliferation and extracellular matrix accumulation.
  • miR-18b targeted lincRNA-p21 and connective tissue growth factor (CTGF), mediating the effects.

Conclusions:

  • lincRNA-p21 plays a critical role in DN progression.
  • The lincRNA-p21/miR-18b axis influences kidney cell behavior and extracellular matrix deposition.
  • Targeting lincRNA-p21 offers a novel therapeutic strategy for diabetic nephropathy.
Keywords:
Diabetic nephropathylincRNA-p21miR-18bmouse mesangial cells

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