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Vasoactive neuropeptides in clinical ophthalmology: An association with autoimmune retinopathy?

Authors Staines D, Brenu E, Marshall-Gradisnik S

Published 17 March 2009 Volume 2009:3 Pages 259—261

DOI https://doi.org/10.2147/OPTH.S5356

Review by Single-blind

Peer reviewer comments 3


Donald R Staines1,2, Ekua W Brenu2, Sonya Marshall-Gradisnik2

1Queensland Health, Gold Coast Population Health Unit, Southport, Gold Coast, Queensland, Australia; 2Faculty of Health Science and Medicine, Population Health and Neuroimmunology Unit, Bond University, Robina, Queensland, Australia

Abstract: The mammalian eye is protected against pathogens and inflammation in a relatively immune-privileged environment. Stringent mechanisms are activated that regulate external injury, infection, and autoimmunity. The eye contains a variety of cells expressing vasoactive neuropeptides (VNs), and their receptors, located in the sclera, cornea, iris, ciliary body, ciliary process, and the retina. VNs are important activators of adenylate cyclase, deriving cyclic adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). Impairment of VN function would arguably impede cAMP production and impede utilization of ATP. Thus VN autoimmunity may be an etiological factor in retinopathy involving perturbations of purinergic signaling. A sound blood supply is necessary for the existence and functional properties of the retina. This paper postulates that impairments in the endothelial barriers and the blood–retinal barrier, as well as certain inflammatory responses, may arise from disruption to VN function. Phosphodiesterase inhibitors and purinergic modulators may have a role in the treatment of postulated VN autoimmune retinopathy.

Keywords: retinopathy, autoimmune, vasoactive neuropeptides, phosphodiesterase inhibitors

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