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Peer-reviewedCC BY 4.0Graefe's Archive for Clinical and Experimental Ophthalmology

Loss of DNA-PK complex in recurrent pterygium suggests a role for defective double-strand break repair

  • Leonardo Lupacchini1
  • Marco Marenco2
  • Marco Rosina3
  • Fabiana Mallone2,4
  • Cristiana Mollinari3,5
  • Angelina Pernazza6
  • Alessandro Lambiase2
  • Daniela Merlo3
6 affiliations
  1. 1Laboratory of Molecular and Cellular Neurobiology, IRCCS San Raffaele Roma, Via di Val Cannuta 247, Rome, 00166 Italy
  2. 2Department of Sense Organs, Sapienza - University of Rome, Viale del Policlinico 155, Rome, 00161 Italy
  3. 3Department of Neuroscience, Italian National Institute of Health (ISS), Viale Regina Elena 299, Rome, 00161 Italy
  4. 4IRCCS-G.B. Bietti Foundation, Via Livenza 3, Rome, 00198 Italy
  5. 5Institute of Translational Pharmacology (IFT), National Research Council, Via Fosso del Cavaliere 100, Rome, 00133 Italy
  6. 6Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Corso della Repubblica 79, Latina, 04100 Italy
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Abstract

Purpose: Pterygium is a common ocular surface disorder strongly associated with ultraviolet (UV) radiation exposure and oxidative stress. Double-strand breaks (DSBs) are among the most deleterious forms of DNA damage, and their repair mainly relies on the non-homologous end joining (NHEJ) pathway, in which the DNA-dependent protein kinase (DNA-PK) complex plays a central role. This study investigated the expression of the DNA-PK complex components—DNA-PKcs, Ku70, and Ku86—in pterygium compared with healthy conjunctiva.

Methods: Conjunctival tissues were obtained from six patients undergoing surgical excision of recurrent pterygium and 6 age- and sex-matched controls undergoing ocular surgery without surface disease. Protein and transcript expression of DNA-PKcs, Ku70, and Ku86 were assessed by immunofluorescence, Western blotting, and real-time PCR.

Results: Immunofluorescence revealed markedly reduced DNA-PKcs immunoreactivity in the epithelium of pterygium conjunctiva compared with marked staining in controls. Western blot analysis demonstrated a significant decrease of DNA-PKcs protein, paralleled by a ~ 13-fold reduction of its mRNA. Similarly, Ku70 and Ku86 protein levels were dramatically reduced (by ~ 93.5% and ~ 92.0%, respectively) in pterygium compared with controls.

Conclusions: This study provides the first evidence of profound down-regulation of the DNA-PK complex in pterygium. The loss of DNA-PKcs and its regulatory subunits Ku70 and Ku86 suggests impaired DSB repair capacity, potentially driven by chronic UV-induced oxidative stress. These alterations may contribute to pterygium pathogenesis and recurrence, highlighting DNA-PK complex proteins as potential biomarkers of disease susceptibility and progression.

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s00417-026-07283-4.

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Cite

BibTeXRIS
BibTeX
@article{lupacchini2026loss,
  title = {{Loss of DNA-PK complex in recurrent pterygium suggests a role for defective double-strand break repair}},
  author = {Leonardo Lupacchini and Marco Marenco and Marco Rosina and Fabiana Mallone and Cristiana Mollinari and Angelina Pernazza and Alessandro Lambiase and Daniela Merlo},
  journal = {Graefe's Archive for Clinical and Experimental Ophthalmology},
  year = {2026},
  month = may,
  doi = {10.1007/s00417-026-07283-4},
  url = {https://doi.org/10.1007/s00417-026-07283-4},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Loss of DNA-PK complex in recurrent pterygium suggests a role for defective double-strand break repair
AU  - Leonardo Lupacchini
AU  - Marco Marenco
AU  - Marco Rosina
AU  - Fabiana Mallone
AU  - Cristiana Mollinari
AU  - Angelina Pernazza
AU  - Alessandro Lambiase
AU  - Daniela Merlo
PY  - 2026
DA  - 2026/05/26
JO  - Graefe's Archive for Clinical and Experimental Ophthalmology
DO  - 10.1007/s00417-026-07283-4
UR  - https://doi.org/10.1007/s00417-026-07283-4
AB  - Purpose: Pterygium is a common ocular surface disorder strongly associated with ultraviolet (UV) radiation exposure and oxidative stress. Double-strand breaks (DSBs) are among the most deleterious forms of DNA damage, and their repair mainly relies on the non-homologous end joining (NHEJ) pathway, in which the DNA-dependent protein kinase (DNA-PK) complex plays a central role. This study investigated the expression of the DNA-PK complex components—DNA-PKcs, Ku70, and Ku86—in pterygium compared with healthy conjunctiva.  Methods: Conjunctival tissues were obtained from six patients undergoing surgical excision of recurrent pterygium and 6 age- and sex-matched controls undergoing ocular surgery without surface disease. Protein and transcript expression of DNA-PKcs, Ku70, and Ku86 were assessed by immunofluorescence, Western blotting, and real-time PCR.  Results: Immunofluorescence revealed markedly reduced DNA-PKcs immunoreactivity in the epithelium of pterygium conjunctiva compared with marked staining in controls. Western blot analysis demonstrated a significant decrease of DNA-PKcs protein, paralleled by a ~ 13-fold reduction of its mRNA. Similarly, Ku70 and Ku86 protein levels were dramatically reduced (by ~ 93.5% and ~ 92.0%, respectively) in pterygium compared with controls.  Conclusions: This study provides the first evidence of profound down-regulation of the DNA-PK complex in pterygium. The loss of DNA-PKcs and its regulatory subunits Ku70 and Ku86 suggests impaired DSB repair capacity, potentially driven by chronic UV-induced oxidative stress. These alterations may contribute to pterygium pathogenesis and recurrence, highlighting DNA-PK complex proteins as potential biomarkers of disease susceptibility and progression.  Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s00417-026-07283-4.
SN  - 0721-832X
SN  - 1435-702X
ER  -