Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
CYP39A1 protein structure abnormalities correspond to altered enzymatic activity in Exfoliation Glaucoma
Author Affiliations & Notes
  • Nicholas Mueller
    SUNY Upstate Medical University, Syracuse, New York, United States
  • Audrey M Bernstein
    SUNY Upstate Medical University, Syracuse, New York, United States
    Syracuse VA Medical Center, Syracuse, New York, United States
  • Arunkumar Venkatesan
    SUNY Upstate Medical University, Syracuse, New York, United States
  • Footnotes
    Commercial Relationships   Nicholas Mueller None; Audrey Bernstein None; Arunkumar Venkatesan None
  • Footnotes
    Support  NIH EY024942, NIH EY030567, Merit Review Award (I01 BX005360) from the United States Department of Veteran’s Affairs, Biomedical Laboratory Research and Development Service, SUNY Upstate Start-up Funds, Unrestricted Grant to the Department of Ophthalmology & Visual Sciences from Research to Prevent Blindness, The Mayer Family Foundation, and The Lion's District 20-Y.
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 4060. doi:
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    • Get Citation

      Nicholas Mueller, Audrey M Bernstein, Arunkumar Venkatesan; CYP39A1 protein structure abnormalities correspond to altered enzymatic activity in Exfoliation Glaucoma. Invest. Ophthalmol. Vis. Sci. 2024;65(7):4060.

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

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Abstract

Purpose : Exfoliation Syndrome (XFS) is a prevalent age-related disorder defined by the accumulation of extracellular fibrillar aggregates in the anterior segment of the eye. These aggregates are a major risk factor for the development of Exfoliation Glaucoma (XFG), a secondary open-angle glaucoma affecting about 70 million people worldwide. A genome-wide association study (GWAS) uncovered a linkage between XFG and Cytochrome P450 gene CYP39A1 variants. The objective of this study is to investigate the structural changes of CYP39A1 protein variants that may contribute to altered enzymatic activity.

Methods : cDNAs containing five nonsynonymous single nucleotide polymorphisms of CYP39A1 (Arg103His, Leu174Pro, Phe175Leu, Asn324Lys, and Phe385Val) were compared to WT cDNA. cDNAs were overexpressed in Human Embryonic Kidney (HEK) cells. The structural changes of CYP39A1 variants were studied using SDS-PAGE western blotting from cell lysates and membrane fractions. Microscopy was used to detect differences in cell localization in immortalized hTERT fibroblasts.

Results : Each CYP39A1 point mutation has varying enzymatic activity. A cell lysing protocol was optimized to enhance extraction of the target protein into the soluble fraction for the purpose of analyzing differences in post-translational modifications. The CYP39A1 variants were normalized to WT enzymatic activity. CYP39A1 Leu174Pro and Phe385Val have a greater than 95% reduction in enzymatic activity compared to WT. These variants displayed an increase in molecular weight (MW) and also have an aggregated phenotype in hTERT-immortalized fibroblasts compared to WT.

Conclusions : CYP39A1 variants Leu174Pro and Phe385Val have increased MW and altered cellular distribution suggesting that structural changes or post-translational modification may contribute to the loss of WT enzymatic activity.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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