June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
ROLE OF INFLAMMATION MARKERS AND EFFECTS OF HUMANIN G IN AMD
Author Affiliations & Notes
  • Sonali R Nashine
    Ophthalmology, University of California Irvine, Irvine, California, United States
  • M. Cristina Kenney
    Ophthalmology, University of California Irvine, Irvine, California, United States
    Pathology, University of California Irvine, Irvine, California, United States
  • Footnotes
    Commercial Relationships   Sonali Nashine, None; M. Cristina Kenney, None
  • Footnotes
    Support  NEI R01 EY0127363, Arnold and Mabel Beckman foundation, UCI School of Medicine, Discovery Eye Foundation, Polly and Michael Smith, Edith and Roy Carver, Iris and B. Gerald Cantor Foundation, Unrestricted Departmental Grant from Research to Prevent Blindness, and support of the Institute for Clinical and Translational Science (ICTS) at University of California Irvine. S.N. is a recipient of the 2017 Genentech/ ARVO AMD Translational Research Fellowship and the 2016 RPB pilot research grant.
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 299. doi:
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    • Get Citation

      Sonali R Nashine, M. Cristina Kenney; ROLE OF INFLAMMATION MARKERS AND EFFECTS OF HUMANIN G IN AMD. Invest. Ophthalmol. Vis. Sci. 2021;62(8):299.

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

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Abstract

Purpose : Inflammation is a critical player in the etiology and pathogenesis of Age-related Macular Degeneration (AMD). Humanin G (HNG) is a Mitochondrial Derived Peptide (MDP) that is cytoprotective in AMD. The goal of this study was to test our hypothesis that the inflammation markers- CD62P i.e., P Selectin and CD62E i.e., E Selectin proteins, are increased in AMD and HNG treatment in vitro leads to reduction in their protein levels.

Methods : In this study, we used: 1) blood plasma isolated from AMD patients and age-matched control subjects, and 2) AMD and control transmitochondrial RPE cybrid cell lines. HNG was exogenously added to AMD cybrids, which have identical nuclei from the mitochondria-deficient ARPE-19 cells but differed in mitochondrial DNA (mtDNA) content derived from clinically characterized AMD patients and control subjects. Cell lysates were extracted from untreated and HNG-treated AMD and control cybrids, and then analyzed using the Luminex multiplex assay to determine the protein levels of CD62P and CD62E.

Results : The CD62P protein levels were 152% higher in AMD plasma samples (2.52±0.41, n=3) vs. Controls (1±0.2, n=3) (p=0.03). Treatment with HNG led to a 37% decrease in CD62P protein levels in control cybrid cell lysates (Untreated: 1±0.34; HNG-treated: 0.63±0.04) and a 21% decrease in CD62P protein levels in AMD cybrid cell lysates (Untreated: 1±0.24; HNG-treated: 0.79±0.09). Furthermore, CD62E protein levels were 176% higher in AMD plasma samples (2.76±0.48, n=3) vs. Controls (1±0.28, n=3) (p=0.03). Treatment with HNG led to 18% decrease in CD62E protein levels in AMD cell lysates (Untreated:1±0.02; HNG-treated: 0.82±0.02). No difference was found in CD62E protein levels between untreated vs. HNG-treated control cell lysates.

Conclusions : In summary, we observed: 1) significantly higher levels of CD62P and CD62E proteins in AMD plasma samples compared with control plasma samples, and 2) HNG reduced the CD62P and CD62E protein levels in cell lysates, thereby suggesting that HNG may rescue the mtDNA-mediated inflammation in AMD cybrids. In conclusion, this study presents novel findings that suggest the role of 1) CD62P and CD62E in AMD pathogenesis and 2) HNG as a potential target for reducing Selectins-associated inflammation in AMD. Further studies are required to establish the role of HNG in reducing inflammation by decreasing the protein levels of Selectins in AMD.

This is a 2021 ARVO Annual Meeting abstract.

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