June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Differential Gene Expression of Extracellular Matrix Components in Response to In Vivo Corneal Cross-linking (CXL) in Rabbit Corneas
Author Affiliations & Notes
  • Sabine Kling
    Laboratory for Ocular Cell Biology, University of Zurich, Zurich, Zurich, Switzerland
  • Arthur Hammer
    Laborator of Ocular Cell Biology, University of Geneva, Geneva, Switzerland
  • Farhad Hafezi
    Laboratory for Ocular Cell Biology, University of Zurich, Zurich, Zurich, Switzerland
    ELZA Institute AG, Dietikon/Zurich, Switzerland
  • Footnotes
    Commercial Relationships   Sabine Kling, None; Arthur Hammer, None; Farhad Hafezi, None
  • Footnotes
    Support  Gelbert Foundation, Velux Foundation
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5563. doi:
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      Sabine Kling, Arthur Hammer, Farhad Hafezi; Differential Gene Expression of Extracellular Matrix Components in Response to In Vivo Corneal Cross-linking (CXL) in Rabbit Corneas. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5563.

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

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Abstract

Purpose : To study changes in gene expression after corneal cross-linking (CXL) in the rabbit cornea in vivo and to identify potential molecular signaling pathways.

Methods : 15 male New Zealand white rabbits (2.5 kg) were equally divided into 5 groups. All corneas were de-epithelialized using a hockey knife. Groups I to IV were soaked with 0.1%-riboflavin for 20 minutes, followed by UV-A irradiation at a fluence of 5.4 J/cm2, delivered at 3 mW/cm2 for 30 min (group I, standard CXL protocol), 9 mW/cm2 for 10 min (group II, accelerated), and 18 mW/cm2 for 5 min (group III, accelerated). Group IV served as riboflavin control, group V as virgin control. At one week after treatment, corneal buttons were obtained, mRNA was extracted and subjected to cDNA sequencing (RNA-seq).

Results : CXL down-regulated enzyme activity (enolase 1, transketolase, cystatin, serine/threonine kinase) and extracellular matrix components (collagen types 1A1, 1A2, 6A2, 11A1, keratocan, fibromodulin). CXL activated pathways related to protein cross-linking (transglutaminase 2, osteonectin, cysteine-rich angiogenic inducer). Interestingly, CXL at 3mW/cm2 (Group 1) induced a more distinct change in gene expression than the accelerated CXL protocols, which induce less stiffening effect.

Conclusions : Several target genes have been identified that might be related to the biomechanical stability of the cornea. The differential gene expression was dependent on the amount of biomechanical stiffening, suggesting the activation of mechano-sensitive pathways.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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