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Geniposide restricts angiogenesis in experimentary arthritis via inhibiting Dnmt1-mediated PTEN hypermethylation

Yanhong Bu1, Hong Wu1, Ran Deng1

  • 1Key Laboratory of Xin'an Medicine, Ministry of Education, Hefei 230012, China; College of Pharmacy, Anhui University of Chinese Medicine, Qian Jiang Road 1, Hefei 230012, China; Anhui Province Key Laboratory of Chinese Medicinal Formula, Hefei 230012, China; Anhui Province Key Laboratory of Research & Development of Chinese Medicine, Hefei 230012, China.

International Immunopharmacology
|July 31, 2022
PubMed

Insights

Geniposide (GE) reduces rheumatoid arthritis (RA) by inhibiting angiogenesis. It works by down-regulating DNA methyltransferase 1 (Dnmt1), which increases PTEN gene expression and reduces harmful blood vessel growth.

Area of Science:

  • Rheumatology
  • Molecular Biology
  • Cell Biology

Background:

  • Neovascularization in rheumatoid arthritis (RA) drives the progression of synovial tissue to pannus.
  • Geniposide (GE) has shown efficacy in experimental arthritis models.
  • Understanding GE's mechanism in inhibiting angiogenesis is crucial for RA treatment.

Purpose of the Study:

  • To investigate the mechanism by which Geniposide (GE) inhibits angiogenesis in rheumatoid arthritis (RA).
  • To explore the role of PTEN (phosphate and tension homology deleted on chromosome ten) gene regulation in GE's anti-angiogenic effects.
  • To examine the impact of GE on DNA methyltransferases (Dnmts) and PTEN methylation in vitro and in vivo.

Main Methods:

  • In vitro studies using human umbilical vein endothelial cells (HUVEC) and in vivo studies using adjuvant arthritis (AA) rat models.
  • Assessing the effects of GE on synovitis and angiogenesis in AA rats.
  • Analyzing PTEN expression, DNA methylation, and Dnmt1, Dnmt3a, Dnmt3b expression in response to GE treatment.

Main Results:

  • GE treatment significantly reduced synovitis and angiogenesis in AA rats.
  • GE treatment increased PTEN expression in AA rats.
  • GE inhibited angiogenesis in HUVEC by down-regulating Dnmt1, thereby reducing PTEN gene hypermethylation.

Conclusions:

  • Geniposide (GE) exhibits anti-angiogenesis effects in experimental arthritis.
  • GE inhibits angiogenesis by targeting Dnmt1-mediated PTEN gene hypermethylation.
  • These findings offer new perspectives for the prevention and research of rheumatoid arthritis (RA).
Keywords:
AngiogenesisDNA methylationDNA methyltransferasesGeniposidePTENRheumatoid arthritis

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