The tyrosine kinase inhibitor dasatinib effectively blocks PDGF-induced orbital fibroblast activation

Graefes Arch Clin Exp Ophthalmol. 2014 Jul;252(7):1101-9. doi: 10.1007/s00417-014-2674-7. Epub 2014 May 30.

Abstract

Background: Graves' ophthalmopathy (GO) remains hard to treat. Excessive orbital fibroblast activation by platelet-derived growth factor (PDGF)-BB contributes to GO. The tyrosine kinase inhibitors (TKIs) imatinib mesylate and dasatinib both target PDGF-receptor tyrosine kinase activity, albeit with a different potency. We compared the efficacy of these TKIs on PDGF-BB-induced proliferation, and on cytokine and hyaluronan production by orbital fibroblasts. Also the capacity of dasatinib to suppress GO-associated gene expression in orbital tissue was examined.

Methods: Orbital fibroblasts from four GO patients and five control subjects were used. The efficacy of the two TKIs was tested by: 1) pre-incubating orbital fibroblasts overnight with different TKI concentrations, followed by 24 h stimulation with PDGF-BB, 2) adding TKI and PDGF-BB simultaneously to the orbital fibroblasts in 24 h cultures. Proliferation was assessed by colorimetric assay. Hyaluronan and cytokine production were measured by ELISA. Furthermore, orbital tissue was obtained from a patient with active GO, and the effect of dasatinib on the expression levels of HAS2-, CCL2-, IL6-, and IL8-mRNA expression was examined by real-time quantitative PCR.

Results: Pre-incubation of orbital fibroblasts with imatinib mesylate or dasatinib resulted in significant and dose-dependent inhibition of PDGF-BB-induced orbital fibroblast proliferation, and hyaluronan and cytokine production. Dasatinib exhibited these effects at far lower concentrations. The same results were observed in the setting where TKI and PDGF-BB treatments were commenced simultaneously. In orbital tissue from active GO, dasatinib significantly suppressed HAS2-, CCL2-, IL6- and IL8-mRNA levels.

Conclusion: Dasatinib may be a promising alternative to high-dose steroids in the treatment of GO.

MeSH terms

  • Becaplermin
  • Benzamides / pharmacology
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Chemokine CCL2 / genetics
  • Dasatinib
  • Dose-Response Relationship, Drug
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Gene Expression Regulation / physiology
  • Glucuronosyltransferase / genetics
  • Graves Ophthalmopathy / drug therapy
  • Graves Ophthalmopathy / pathology
  • Humans
  • Hyaluronan Synthases
  • Imatinib Mesylate
  • Interleukin-6 / genetics
  • Interleukin-8 / genetics
  • Orbit / pathology*
  • Piperazines / pharmacology
  • Protein Kinase Inhibitors / pharmacology*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-sis / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-sis / pharmacology
  • Pyrimidines / pharmacology*
  • RNA, Messenger / genetics
  • Thiazoles / pharmacology*

Substances

  • Benzamides
  • CCL2 protein, human
  • CXCL8 protein, human
  • Chemokine CCL2
  • IL6 protein, human
  • Interleukin-6
  • Interleukin-8
  • Piperazines
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins c-sis
  • Pyrimidines
  • RNA, Messenger
  • Thiazoles
  • Becaplermin
  • Imatinib Mesylate
  • Glucuronosyltransferase
  • HAS2 protein, human
  • Hyaluronan Synthases
  • Protein-Tyrosine Kinases
  • Dasatinib