![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
Abstract
Background
Keratoconus manifests as a conical protrusion of the cornea and is characterised by stromal thinning. This causes debilitating visual impairment, which may necessitate corneal transplantation. Hypothetically, many of the pathological features in keratoconus may be manifestations of defects in wound healing; however, as the pathobiology remains unclear, therapeutic targets related to disease mechanisms are currently lacking. This study investigated the protein expression of cytokines which may control stromal wound healing and the effect of an induced secondary injury (SI) on stromal cells from ex vivo human keratoconus and control corneas.
Methods
Total protein was extracted from stromal cells from human keratoconic and non‐keratoconic central corneas (n = 12) with (+SI) and without (‐SI) an ex vivo corneal incision wound. The levels of interleukin 1 alpha (IL‐1α), fibroblast growth factor 2 (FGF‐2), nerve growth factor beta (β‐NGF), insulin‐like growth factor 1 (IGF‐1), tumour necrosis factor alpha (TNF‐α), epidermal growth factor (EGF), transforming growth factor beta 1 (TGF‐β1), platelet‐derived growth factor (PDGF) and hepatocyte growth factor (HGF) were quantified using chemiluminescence‐based immunoarrays.
Results
In stromal cells from ‐SI keratoconic corneas (compared with ‐SI normal corneas), the levels of IL‐1α, IGF‐1, TNF‐α and TGF‐β1 were increased and the levels of HGF and β‐NGF were reduced. These alterations were also observed in +SI non‐keratoconic corneas (compared with ‐SI non‐keratoconic corneas). In stromal cells from +SI keratoconic corneas (compared with ‐SI keratoconic corneas), the quantities of IL‐1α, FGF‐2, TNF‐a, EGF, TGF‐a1 and PDGF were decreased.
Conclusion
The repair‐modulating milieu in keratoconic corneas appears comparable to that in wounded normal corneas. Moreover, wounded keratoconic corneas may be less capable of orchestrating a normal reparative response. These novel findings may improve our understanding of the pathobiology and may facilitate the identification of potential biological targets and therapeutic agents to advance the clinical management of this disorder.
Key words:
Acknowledgements
This study was funded by the Maurice and Phyllis Paykel Trust, Lottery Health New Zealand and the Save Sight Society of New Zealand.
The authors wish to thank the tissue donors and their families for supporting this project.