June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
JNK Signaling Mediates CTGF Expression and Scar Formation in Corneal Wound Healing
Author Affiliations & Notes
  • Long Shi
    Ophthalmology, Qilu Hospital of Shandong University, Jinan, China
  • Xinyi Wu
    Ophthalmology, Qilu Hospital of Shandong University, Jinan, China
  • Footnotes
    Commercial Relationships Long Shi, None; Xinyi Wu, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 739. doi:
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      Long Shi, Xinyi Wu; JNK Signaling Mediates CTGF Expression and Scar Formation in Corneal Wound Healing. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):739.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: To investigate the signaling pathway mediates the expression of Connective Tissue Growth Factor (CTGF) and corneal scarring in corneal wound healing

Methods: We investigated whether TGF-β1 could induced MAPK pathways hosphorylation in Telomerase-immortalized human cornea stroma fibroblasts (THSF), and determined the effect of the MAPK pathways in TGF-β1 induced CTGF, fibronectin and collagen I expression. Then, the penetrating corneal wound model was created in vivo and the effect of JNK on CTGF expression and corneal scarring in corneal wound healing was identified.

Results: TGF-β1 activated MAPK pathways in THSF cells. JNK inhibitor significantly inhibited CTGF, fibronectin and collagen I expression induced by TGF-b1 in THSF. In corneal wound healing, the JNK inhibitor significantly inhibited CTGF expression, markedly improved the architecture of corneal stroma and reduced corneal scar formation, but did not have a measurable impact on corneal wound healing in vivo.

Conclusions: JNK mediates the expression of CTGF and corneal scarring in corneal wound healing, and might be considered as specific targets of drug therapy for corneal scarring.

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