Abstract
The purpose of this study was to determine the relative expression of clinically-relevant components of the renin-angiotensin system (RAS) in the adult human eye. We obtained 14 post-mortem enucleated human eyes from patients whom had no history of inflammatory ocular disease nor pre-mortem ocular infection. We determined the gene expression for prorenin, renin, prorenin receptor, angiotensin-converting enzyme, angiotensinogen and angiotensin II Type 1 receptor, on tissue sections and in cultured human primary retinal pigment epithelial and iris pigment epithelial (RPE/IPE) cell lines, using both qualitative and quantitative reverse transcription polymerase chain reaction (RT-PCR). Protein expression was studied using indirect immunofluorescence (IF). Almost all components of the classical RAS were found at high levels, at both the transcript and protein level, in the eyes' uvea and retina; and at lower levels in the cornea, conjunctiva and sclera. There was a much lower level of expression in the reference cultured RPE/IPE cells lines. This study describes the distribution of RAS in the normal adult human eye and demonstrates the existence of an independent ocular RAS, with uveal and retinal tissues showing the highest expression of RAS components. These preliminary findings provide scope for examination of additional components of this system in the human eye, as well as possible differential expression under pathological conditions.
Highlights
The classical renin angiotensin system (RAS) is demonstrated to have an increasingly important role in ocular pathology and homeostasis
The cornea and conjunctiva of the 10 fresh eye specimens had been removed for use in corneal graft surgery; these tissues were unavailable for reverse transcription polymerase chain reaction (RT-PCR) testing
Qualitative PCR showed the AGTR1-transcript for the AT1 receptor to be present in RPE choroid samples from donor eyes only (Figure 2)
Summary
The classical renin angiotensin system (RAS) is demonstrated to have an increasingly important role in ocular pathology and homeostasis. It has been implicated in a variety of eye diseases, including uveitis, macular degeneration, diabetic retinopathy and glaucoma.[1] Classical RAS originates with renin (REN), an aspartyl protease derived from its inactive precursor pro-renin, within the juxtaglomerular cells of the kidney. Subsequent cleavage of Ang I by the angiotensin-converting enzyme (ACE), results in formation of angiotensin II (AngII), an important vasoconstrictor, trophic, angiogenic and pro-inflammatory octapeptide (Figure 1). ACE metabolises bradykinin, a powerful vasodilator involved in mediation of the inflammatory response.
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