Targeting platelet-derived growth factor receptor β inhibits the proliferation and motility of human pterygial fibroblasts.

: Pterygium, a common eye disease with high postoperative recurrence, lacks effective therapeutic strategies. Therefore, it's urgent to identify specific targets to develop rationally targeted molecular drugs for the pterygial therapy. : The cell proliferation and motility were studied in both the primary human pterygial fibroblasts (hPFs) and an pterygium model. hPFs transfected with the pCMV3- plasmid, siRNA and CRISPR/Cas9 system were used to determine the role of PDGFR-β in pterygial fibroblasts functions. Western blotting, immunohistochemistry and immunofluorescence were performed to evaluate the expression of the key proteins. : PDGFR-β expression in the pterygial stroma and primary hPFs was significantly higher than that in the conjunctiva and human conjunctival fibroblasts. PDGF-BB promoted the proliferation, migration and invasion of hPFs, which can be significantly suppressed by sunitinib via inhibition of the PDGFR-β/extracellular signal-regulated kinase (ERK) pathway. In the model, the knockout of and sunitinib treatment blocked the proliferation and motility of fibroblasts in the pterygial stroma via the suppression of PDGFR-β/ERK pathway. : This study demonstrates that PDGFR-β may be a potential therapeutic target for pterygium, and inhibition of PDGFR-β by sunitinib is a promising and effective approach for pterygium treatment.