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J.J. Steinle; Sympathetic Nerves Regulate Inflammatory Markers in the Rat Retina . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1735.
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To determine whether loss of sympathetic neurotransmission results in alterations in inflammatory markers.
Rats were surgical sympathectomized by removal of the right superior cervical ganglion. Six weeks following surgery, the retina was removed from the eye cup of the sympathectomized (experimental) and contralateral (control) eye. Real–time PCR and western blot analysis was conducted on retinal RNA and protein to investigate expression levels of iNOS, prostaglandin E2 (PGE2) and TNFα. ELISA assay was done to evaluate TNFα protein expression following sympathectomy. Human retinal endothelial cells were grown in low glucose (5mM) and high glucose (20mM) medium and western blot analysis for iNOS was completed.
Removal of sympathetic neurotransmission resulted in a significant increase in iNOS and PGE2 steady–state mRNA and protein expression. TNFα gene and protein expression was not altered by sympathectomy. Human retinal endothelial cells grown in high glucose medium had much higher iNOS protein expression than those grown in low glucose medium.
Intact sympathetic neurotransmission is important to maintaining normal retinal homeostasis and its loss results in an inflammatory state. Since it has been suggested that diabetic retinopathy involves inflammatory processes and sympathetic nerves are damaged in diabetes, it may be that sympathetic dysfunction is a potential mechanism for the increased inflammation in diabetic retina.
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