ZD6474 attenuates TGF-β1-induced fibrosis in human Tenon fibroblasts and inhibits neovascularization via AKT-mTOR signaling pathway

Int Ophthalmol. 2023 May;43(5):1523-1536. doi: 10.1007/s10792-022-02548-3. Epub 2022 Oct 13.

Abstract

Purpose: To investigate the anti-fibrotic effect of ZD6474 (a novel inhibitor of VEGF and EGF) in TGF-β1 stimulated human Tenon's capsule fibroblasts (HTFs) and the anti-angiogenetic role in HUVECs, compared to that of mitomycin C (MMC).

Methods: The effects of ZD6474 on cell proliferation or migration in TGF-β1-stimulated HTFs and HUVECs were determined, using CCK8 or wound healing assay, respectively. The typical markers of fibrosis in TGF-β1-stimuated HTFs were detected, vimentin by immunofluorescence, α-SMA and snail by western blot. Tube formation was applied to validate the anti-angiogenesis effect in HUVECs following ZD6474 treatment. Furthermore, phosphorylated AKT and mTOR (p-AKT and p-mTOR) were evaluated, compared to the standardized total AKT and mTOR, using western blot.

Results: There was almost no decreased cell viability in HTFs following ZD6474 (≤ 1 μM/mL) treatment, but MMC (> 50 μg/mL) significantly impaired cell viability. ZD6474 significantly inhibited TGF-β1-stimulated proliferation and migration in HTFs, compared to control group (**P < 0.01). ZD6474 also significantly attenuated the TGF-β1-stimulated expression of vimentin, α-SMA and snail in HTFs. Tube formation was notably interrupted in HUVECs following ZD6474 treatment (**P < 0.01). P-AKT and p-mTOR were significantly decreased in response to ZD6474 treatment in TGF-β1- induced HTFs and HUVECs.

Conclusions: ZD6474 exerts anti-proliferation and anti-fibrotic effects in TGF-β1-stimulated HTFs perhaps via regulating AKT-mTOR signaling pathway. ZD6474 also inhibited proliferation, migration and tube formation in HUVECs via the same signaling pathway. We concluded that ZD6474 may be potentially a novel agent in preventing bleb dysfunction following glaucoma filtration surgery (GFS).

Keywords: Anti-angiogenesis; Anti-fibrosis; Glaucoma surgery; ZD6474.

MeSH terms

  • Cell Proliferation
  • Fibrosis
  • Humans
  • Proto-Oncogene Proteins c-akt* / metabolism
  • Proto-Oncogene Proteins c-akt* / pharmacology
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism
  • TOR Serine-Threonine Kinases / pharmacology
  • Tenon Capsule / pathology
  • Transforming Growth Factor beta1* / metabolism
  • Transforming Growth Factor beta1* / pharmacology
  • Vimentin / metabolism

Substances

  • Transforming Growth Factor beta1
  • Proto-Oncogene Proteins c-akt
  • Vimentin
  • TOR Serine-Threonine Kinases
  • MTOR protein, human