Abstract
Purpose :
Proliferative vitreoretinopathy (PVR) is a complication of rhegmatogenous retinal detachment. The condition is characterized by the development of pre- or subretinal contractile membranes that may lead to redetachment of the retina. Membrane contraction has been attributed to skeletal muscle-like cells called myofibroblasts. Progenitors of contractile myofibrobasts in the lens are Myo/Nog cells named for their expression of mRNA for the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor noggin. The retina and choroid also contain Myo/Nog cells that respond to stress and injury. In this study we examined human PVR tissue for the presence of Myo/Nog cells and their expression of muscle proteins.
Methods :
PVR membranes were procured from patients in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of the University of California, Davis. The tissue was embedded in paraffin, sectioned and fluorescently labeled with antibodies to the G8 antigen and noggin to identify Myo/Nog cells. Double labeling also was carried with G8 and antibodies to MyoD, alpha smooth muscle actin (α-SMA) and striated muscle myosin.
Results :
G8 and noggin were co-localized in a subpopulation of cells in sections from all three patients. The numbers of G8-positive (+)/noggin+ cells varied between patients. The percentages of G8+ cells that contained MyoD, α-SMA and myosin also differed in tissue samples. However, all cells containing muscle proteins were G8+. Some G8+/myosin+ cells appeared to be multinucleated.
Conclusions :
Myo/Nog cells are present among pigmented and non-pigmented cells in human PVR tissue. Variation in the numbers of Myo/Nog cells with MyoD, α-SMA and striated myosin suggests that the progenitor cells are in different stages of differentiation and maturation. These results lay the foundation for studies of the origin of Myo/Nog cells in PVR membranes and their contribution to retinal redetachment.
This is a 2020 ARVO Annual Meeting abstract.