Abstract
BackgoundTo identify and compare specific protein levels between overacting inferior oblique (IO) muscles in superior oblique (SO) palsy patients and normal IO muscles.MethodsWe obtained 20 IO muscle samples from SO palsy patients with IO overaction ≥ + 3 who underwent IO myectomies (IOOA group), and 20 IO samples from brain death donors whose IO had functioned normally, according to their ophthalmological chart review (control group). We used MyoD for identifying satellite cell activation, insulin-like growth factor binding protein 5 (IGFBP5) for IGF effects, thioredoxin for oxidative stress, and p27 for satellite cell activation or oxidative stress in both groups. Using immunohistochemistry and Western blot, we compared expression levels of the four proteins (MyoD, IGFBP5, thioredoxin, and p27).ResultsLevels of thioredoxin and p27 were decreased significantly in the IOOA group. MyoD and IGFBP5 levels showed no significant difference between the groups.ConclusionsBased on these findings, the overacting IOs of patients with SO palsy had been under oxidative stress status versus normal IOs. Pathologically overacting extraocular muscles may have an increased risk of oxidative stress compared with normal extraocular muscles.
Highlights
Inferior oblique (IO) muscle overaction may occur as a primary condition or develop secondarily to specific events such as superior oblique (SO) palsy
Overacting extraocular muscles may have an increased risk of oxidative stress compared with normal extraocular muscles
Prolonged oxidative stress can result in reduced antioxidant capacity in extraocular muscles, and a previous report revealed that the medial rectus muscles (MRM) of patients with exotropia had a redox imbalance status compared with normal MRMs [6]
Summary
Inferior oblique (IO) muscle overaction may occur as a primary condition or develop secondarily to specific events such as superior oblique (SO) palsy. Bagheri et al [2] reported that there was no detectable correlation between IOOA and muscle position or Extraocular muscles have different metabolic and structural components compared with other skeletal muscles, both molecularly and microscopically [3]. Both extraocular muscles and other skeletal muscles generate free radicals with repetitive contraction, which can result in cellular oxidative damage in severe or prolonged state [4,5,6]. Prolonged oxidative stress can result in reduced antioxidant capacity in extraocular muscles, and a previous report revealed that the medial rectus muscles (MRM) of patients with exotropia had a redox imbalance status compared with normal MRMs [6]
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