Myo/Nog cells are present in the ciliary processes, on the zonule of Zinn and posterior capsule of the lens following cataract surgery.

Myo/Nog cells, named for their expression of MyoD and noggin, enter the eye during early stages of embryonic development. Their release of noggin is critical for normal morphogenesis of the lens and retina. Myo/Nog cells are also present in adult eyes. Single nucleated skeletal muscle cells designated as myofibroblasts arise from Myo/Nog cells in cultures of lens tissue. In this report we document the presence of Myo/Nog cells in the lens, ciliary body and on the zonule of Zinn in mice, rabbits and humans. Myo/Nog cells were rare in all three structures. Their prevalence increased in the lens and ciliary body of rabbits 24 h following cataract surgery. Rabbits developed posterior capsule opacification (PCO) within one month of surgery. The number of Myo/Nog cells continued to be elevated in the lens and ciliary body. Myo/Nog cells containing alpha smooth muscle actin and striated muscle myosin were present on the posterior capsule and overlaid deformations in the capsule. Myo/Nog cells also were present on the zonule fibers and external surface of the posterior capsule. These findings suggest that Myo/Nog contribute to PCO and may use the zonule fibers to migrate between the ciliary processes and lens.

Educational intervention to adopt selective laser trabeculoplasty as first-line glaucoma treatment: Randomized controlled trial: Educational intervention on selective laser trabeculoplasty.

PURPOSE: To determine the efficacy of an educational intervention on patient adoption and attitudes toward selective laser trabeculoplasty (SLT) as first-line treatment for glaucoma. METHODS: This study is a randomized controlled trial. Subjects include 33 patients within 1-year diagnosis of either primary open-angle glaucoma, ocular hypertension, or pseudoexfoliation syndrome. After informed consent, subjects were randomly assigned to a Usual Care or Educational Intervention group. All subjects completed a pre-intervention questionnaire. The Educational Intervention group was shown a slideshow presentation and a 3-min video and given a post-intervention questionnaire. Follow-up examinations were reviewed for 6 months to determine subject completion of SLT, the primary outcome. Secondary outcomes include assessment of attitude toward SLT before and after intervention. RESULTS: Age, gender, and baseline characteristics between the groups did not differ. The Usual Care group had a higher proportion of African Americans (77% vs 31%, p = 0.04). At 6 months following the intervention, 63% of subjects underwent SLT compared to 35% of Usual Care subjects (p = 0.12). Older age was associated with decreased SLT uptake (OR 0.90, 95% CI 0.82-0.99, p = 0.03). Prior to the intervention, there were no differences in attitudes of both groups regarding SLT therapy. Nineteen percent of Educational Intervention subjects changed positively toward SLT (p = 0.08) and 50% scheduled an SLT appointment after intervention (p = 0.005). CONCLUSIONS: A slideshow and video-based educational intervention may positively enhance patient adoption of SLT.Clinical trial registration name, number, URL: Educational Intervention to Adopt SLT as First-Line Glaucoma Treatment, NCT03365778, https://clinicaltrials.gov/ct2/show/NCT03365778.

Depletion of Myo/Nog Cells in the Lens Mitigates Posterior Capsule Opacification in Rabbits.

Purpose: Posterior capsule opacification (PCO) is a vision-impairing disease that occurs in some adults and most children after cataract surgery. Contractile myofibroblasts contribute to PCO by producing wrinkles in the lens capsule that scatter light. Myofibroblasts in the lens originate from Myo/Nog cells named for their expression of the MyoD transcription factor and bone morphogenetic protein inhibitor noggin. In this study we tested the effects of depleting Myo/Nog cells on development of PCO. Methods: Myo/Nog cells were eliminated by injecting the G8 antibody conjugated to 3DNA nanocarriers for the cytotoxin doxorubicin (G8:3DNA:Dox) during cataract surgery in rabbits. The severity of PCO was scored by slit lamp analysis, gross and histologic observation, and immunofluorescence localization of α-smooth muscle actin. Results: G8:3DNA:Dox specifically induced cell death in Myo/Nog cells in the lens. None of the lenses administered G8:3DNA containing 9 to 36 µM doxorubicin developed greater than trace levels of central PCO and few myofibroblasts were present on the capsule. Less than 9% of these lenses exhibited greater than mild levels of peripheral PCO. Doxorubucin itself reduced PCO; however, myofibroblasts and wrinkles were abundant in the lens, and off-target effects were observed in the ciliary processes and cornea. Conclusions: Myo/Nog cells are the primary source of myofibroblasts in the lens after cataract surgery. Targeted depletion of Myo/Nog cells has potential for preventing PCO and preserving vision.