Lubricin: translating an idea into a cure

Purpose We hypothesize that lubricin, a boundary lubricant, is transcribed, translated and expressed by the ocular surface and serves to protect the cornea and conjunctiva against significant shear forces generated during an eyelid blink. We also hypothesize that lubricin deficiency increases shear stress and promotes corneal damage. Our objective was to test these hypotheses. Methods Human tissues and cells were processed for molecular, immunochemical and/or biomechanical procedures. Techniques included the use of real‐time PCR, microarrays, sequencing, immunohistochemistry and friction analyses. Methods also involved the corneal evaluation of wildtype and lubricin knockout (KO) mice. Results Our results show that lubricin is produced by human corneal and conjunctival epithelial cells. Lubricin absence in KO mice is associated with a significant increase in corneal fluorescein staining. Our findings also demonstrate that lubricin functions as a very effective friction‐lowering boundary lubricant at the human cornea‐eyelid interface. Conclusion Our data indicate that lubricin acts as a natural boundary lubricant to reduce shear stress at the ocular surface. We thank S Richards, S Liu, A Sahin, R Rahimi Darabad and W Kam (Boston) and S Morrison (Calgary) for their help with these studies. This research was supported by NIH grant R01EY05612, the Margaret S. Sinon Scholar in Ocular Surface Research fund, the Canadian Natural Sciences and Engineering Research Council & the Centre for Bioengineering Research and Education at the University of Calgary.Commercial interest