July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Differential regulation of prokineticin 2 and its receptor in traumatic optic neuropathy.
Author Affiliations & Notes
  • Ornella Adeyanju Oluwole
    Ophthalmology, Medical College of Georgia, Augusta, Georgia, United States
  • Christian Kim
    Ophthalmology, Medical College of Georgia, Augusta, Georgia, United States
  • Menaka Thounaojam
    Ophthalmology, Medical College of Georgia, Augusta, Georgia, United States
  • Pamela M Martin
    Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, Georgia, United States
  • Diana Gutsaeva
    Ophthalmology, Medical College of Georgia, Augusta, Georgia, United States
  • Manuela Bartoli
    Ophthalmology, Medical College of Georgia, Augusta, Georgia, United States
  • Footnotes
    Commercial Relationships   Ornella Oluwole, None; Christian Kim, None; Menaka Thounaojam, None; Pamela Martin, None; Diana Gutsaeva, None; Manuela Bartoli, None
  • Footnotes
    Support  Department of Ophthamology phylanthropic gift
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 5515. doi:
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      Ornella Adeyanju Oluwole, Christian Kim, Menaka Thounaojam, Pamela M Martin, Diana Gutsaeva, Manuela Bartoli; Differential regulation of prokineticin 2 and its receptor in traumatic optic neuropathy.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5515.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Traumatic optic neuropathy (TON) is a sight-threatening condition occurring as consequence of direct trauma to the optic nerve or resulting from traumatic brain injury (indirect). Specific neuroprotective strategies to prevent TON-related vision loss are presently lacking. Prokineticin 2 (PKN2) is a vascular endothelial growth factor (VEGF)-related protein displaying angiogenic and neuroprotective properties. PKN2 expression and activity in the diseased retina and in TON is poorly understood. Using a mouse model of TON we have studied the expression pattern and retinal distribution of PKN2 and its receptor, prokineticin receptor 2 (PKNR2), and compared them to VEGFA expression and tissue distribution in a mouse model of TON.

Methods : C57/Bl6J mice were subjected to optic nerve crush (ONC). Seven and 14 days after injury mice were sacrificed and retinas and optic nerve were collected and processed to perform morphological and biochemical analysis. QPCR and immunoblotting were done to assess VEGFA, PKN2 and PKNR2 expression at mRNA and protein level. Immunohistochemical analysis was performed to analyze retinal tissue distribution of VEGFA, PKN2 and PKNR2.

Results : Expression of VEGFA was slightly but significantly up-regulated in the injured eye compared to control at 7 and 14 days post-ONC. VEGFA –specific immunoreactivity was localized primarily in Muller cells of normal uninjured retinas. However, in response to ONC, VEGFA expression was mostly localized in blood vessels and in microglia cells infiltrating the optic nerve. At day 7 post-injury, the expression of PKN2 was significantly increased (p<0.05, n=6) (protein and mRNA). Immunohistochemistry further showed that PKN2 up-regulation was higher in both the peripheral retina and the optic nerve. At day 14 post-injury PKN2 expression was still up-regulated but in lesser extent than day 7. Interestingly, PKNR2 expression, which was primarily localized in the optic nerve, was significantly decreased in the injured eye at day 7 post-ONC (p<0.05 versus control, n=6). At day 14 post-ONC, expression of PKN2R was still lower than control, but it was increased compared to day 7.

Conclusions : Our data demonstrate a differential regulation of PKN2 and its receptor PKN2R as consequence of ONC, thus, suggesting a potential pathogenic role for loss PKN2R in TON.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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