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

Authors
  • Mai, Weiqian1, 2
  • Chen, Minfeng1, 2
  • Huang, Maohua1, 2
  • Zhong, Jincheng1, 2
  • Chen, Jian3
  • Liu, Xiaoyong4
  • Deng, Juan5
  • Yang, Xiaoxi6
  • Ye, Wencai1, 2
  • Zhang, Rijia4
  • Zhou, Qing4
  • Zhang, Dongmei1, 2
  • 1 College of Pharmacy, Jinan University , Guangzhou , China. , (China)
  • 2 Guangdong Province Key Laboratory of Pharmacodynamic Constituents of Traditional Chinese Medicine and New Drugs Research, Jinan University , Guangzhou , China. , (China)
  • 3 Eye Institute, Jinan University , Guangzhou , China. , (China)
  • 4 The First Affiliated Hospital of Jinan University , Guangzhou , China. , (China)
  • 5 The Third Affiliated Hospital of Sun Yat-sen University , Guangzhou , China. , (China)
  • 6 The Sixth Affiliated Hospital of Sun Yat-sen University , Guangzhou , China. , (China)
Type
Published Article
Journal
Expert Opinion on Therapeutic Targets
Publisher
Informa UK (Taylor & Francis)
Publication Date
Sep 01, 2019
Volume
23
Issue
9
Pages
805–817
Identifiers
DOI: 10.1080/14728222.2019.1653281
PMID: 31385548
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Background: 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. Methods: The cell proliferation and motility were studied in both the primary human pterygial fibroblasts (hPFs) and an ex vivo pterygium model. hPFs transfected with the pCMV3-PDGFRB plasmid, PDGFRB 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. Results: 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 ex vivo model, the knockout of PDGFRB and sunitinib treatment blocked the proliferation and motility of fibroblasts in the pterygial stroma via the suppression of PDGFR-β/ERK pathway. Conclusion: 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.

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