ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2026
Loss of DNA-PK complex in recurrent pterygium suggests a role for defective double-strand break repair.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
purposePterygium 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.
methodsConjunctival 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.
resultsImmunofluorescence 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.
conclusionsThis 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.
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