Abstract
Purpose :
To investigate UVR-B-induced NKR-1 expression in ocular tissues before and after treatment with substance P receptor antagonist, spantide I in exposed as well as non-exposed partner eyes.
Methods :
Six-week-old C57Bl/6 mice were injected intraperitoneally with 36 µg/mouse of spantide I before and after UVR-B exposure. Control mice were similarly injected with saline only. Pretreated mice were unilaterally exposed to a 5-fold cataract threshold dose (1.45 J/cm2) of UVR-B (UVR-B peak at 312nm) with a Bio-Spectra system. Three, seven, and 14 days post exposure, eyes were fixed, embedded in paraffin, sectioned and stained with a fluorescence coupled antibody for substance P receptor (NKR-1) and DAPI staining. The same was performed in animals receiving only pretreatment and anaesthesia but no UVR-exposure. NKR-1 protein levels in ocular tissue lysates of exposed and contralateral eyes were quantified by immunofluorescence and enzyme-linked immunosorbent assay (ELISA).
Results :
UVR-B exposure induces an NKR-1 upregulation in ocular tissues of exposed and contralateral eyes. Three days after UVR-B exposure NKR-1 immunoreactivity decreased in animals treated with spantide I in the exposed and contralateral cornea, iris and retina, in comparison to the control group. After an initial blocking of NKR-1 at day 3, NKR-1 is overexpressed 7 days post-exposure in the UVR-irradiated as well as the partner eye after spantide I treatment.
Conclusions :
The UVR-B induced expression of substance P receptor, NKR-1 in ocular tissues is affected by spantide I in the exposed as well as in the unexposed partner eye. SP might be the signaling molecule involved in the contralateral reaction following unilateral UVR-B exposure.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.