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VIP protects human retinal microvascular endothelial cells against high
glucose-induced increases in TNF-? and enhances RvD1
#MMPMID27026343
Shi H
; Carion TW
; Jiang Y
; Steinle JJ
; Berger EA
Prostaglandins Other Lipid Mediat
2016[Mar]; 123
(?): 28-32
PMID27026343
show ga
PURPOSE: The purpose of our study was to evaluate the therapeutic effect of VIP
on human retinal endothelial cells (HREC) under high glucose conditions. Diabetes
affects almost 250 million people worldwide. Over 40% of diabetics are expected
to develop diabetic retinopathy, which remains the leading cause of visual
impairment/blindness. Currently, treatment is limited to late stages of
retinopathy with no options available for early stages. To this end, the purpose
of the current study is to evaluate the therapeutic effect of vasoactive
intestinal peptide (VIP) on HREC under high glucose conditions. METHODS: Primary
HREC were cultured in normal (5mM) or high (25mM) glucose medium +/- VIP
treatment. Protein levels of TNF-?, resolvin D1 (RvD1), formyl peptide receptor 2
(FPR2), G protein-coupled receptor 32 (GPR32), VEGF, and VIP receptors, VPAC1 and
VPAC2 were measured. RESULTS: High glucose-induced changes in TNF-? and RvD1 were
restored to control levels with VIP treatment. RvD1 receptors, ALX/FPR2 and
GPR32, were partially rescued with VIP treatment. VPAC2 expression appeared to be
the major receptor involved in VIP signaling in HREC, as VPAC1 receptor was not
detected. In addition, VIP did not induce HREC secretion of VEGF under high
glucose conditions. CONCLUSIONS: Our results demonstrate that VIP's therapeutic
effect on HREC, occurs in part, through the balance between the pro-inflammatory
cytokine, TNF-?, and the pro-resolving mediator, RvD1. Although VPAC1 is
considered the major VIP receptor, VPAC2 is predominantly expressed on HREC under
both normal and high glucose conditions.
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