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Myo/Nog Cells Give Rise to Myofibroblasts During Epiretinal Membrane Formation in a Mouse Model of Proliferative
Mara Crispin1, Jacquelyn Gerhart1, Alison Heffer2
1Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania, United States.
Purpose:
Myo/Nog cells are the source of myofibroblasts in the lens and synthesize muscle proteins in human epiretinal membranes (ERMs). In the current study, we examined the response of Myo/Nog cells during ERM formation in a mouse model of proliferative vitreoretinopathy (PVR).
Methods:
PVR was induced by intravitreal injections of gas and ARPE-19 cells. PVR grade was scored by fundus imaging, optical coherence tomography, and histology. Double label immunofluorescence localization was performed to quantify Myo/Nog cells, myofibroblasts, and leukocytes.
Results:
Myo/Nog cells, identified by co-labeling with antibodies to brain-specific angiogenesis inhibitor 1 (BAI1) and Noggin, increased throughout the eye with induction of PVR and disease progression. They were present on the inner surface of the retina in grades 1/2 PVR and were the largest subpopulation of cells in grades 3 to 6 ERMs. All α-SMA-positive (+) cells and all but one striated myosin+ cell expressed BAI1 in grades 1 to 6 PVR. Folds and areas of retinal detachment were overlain by Myo/Nog cells containing muscle proteins. Low numbers of CD18, CD68, and CD45+ leukocytes were detected throughout the eye. Small subpopulations of BAI1+ cells expressed leukocyte markers. ARPE-19 cells were found in the vitreous but were rare in ERMs. Pigmented cells lacking Myo/Nog and muscle cell markers were present in ERMs and abundant within the retina by grade 5/6.
Conclusions:
Myo/Nog cells differentiate into myofibroblasts that appear to contract and produce retinal folds and detachment. Targeting BAI1 for Myo/Nog cell depletion may be a pharmacological approach to preventing and treating PVR.
Insights
Myo/Nog cells, identified by BAI1 and Noggin, are key myofibroblasts in epiretinal membranes (ERMs). Targeting BAI1 may offer a new treatment for proliferative vitreoretinopathy (PVR).
Area of Science:
- Ophthalmology
- Cell Biology
- Retinal Diseases
Background:
- Myofibroblasts in the lens and epiretinal membranes (ERMs) synthesize muscle proteins.
- Myo/Nog cells are identified as the source of these myofibroblasts.
Purpose of the Study:
- To investigate the role and response of Myo/Nog cells during epiretinal membrane (ERM) formation in a mouse model of proliferative vitreoretinopathy (PVR).
Main Methods:
- Proliferative vitreoretinopathy (PVR) was induced in mice using intravitreal injections.
- Fundus imaging, OCT, and histology were used for PVR grading.
- Double label immunofluorescence quantified Myo/Nog cells, myofibroblasts, and leukocytes.
Main Results:
- Myo/Nog cells, marked by BAI1 and Noggin, increased with PVR progression and ERM formation.
- These cells expressed muscle proteins and were found on retinal folds and detachments.
- Leukocyte infiltration was low, and ARPE-19 cells were rare in ERMs.
Conclusions:
- Myo/Nog cells differentiate into myofibroblasts, contributing to retinal folds and detachment in PVR.
- Targeting BAI1 for Myo/Nog cell depletion presents a potential therapeutic strategy for PVR.
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