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Vitreous M2 Macrophage-Derived Microparticles Promote RPE Cell Proliferation and Migration in Traumatic Proliferative
Yinting Song1, Mengyu Liao1, Xiao Zhao1
1Department of Ophthalmology, Tianjin Medical University General Hospital, Tianjin, China.
Purpose:
To characterize vitreous microparticles (MPs) in patients with traumatic proliferative vitreoretinopathy (PVR) and investigate their role in PVR pathogenesis.
Methods:
Vitreous MPs were characterized in patients with traumatic PVR, patients with rhegmatogenous retinal detachment (RRD) complicated with PVR, and control subjects by flow cytometry. The presence of M2 macrophages in epiretinal membranes was measured by immunostaining. Vitreous cytokines were quantified by ELISA assay. For in vitro studies, MPs isolated from THP-1 cell differentiated M1 and M2 macrophages, termed M1-MPs and M2-MPs, were used. The effects and mechanisms of M1-MPs and M2-MPs on RPE cell proliferation, migration, and epithelial to mesenchymal transition were analyzed.
Results:
Vitreous MPs derived from photoreceptors, microglia, and macrophages were significantly increased in patients with traumatic PVR in comparison with control and patients with RRD (PVR), whereas no significance was identified between the two control groups. M2 macrophages were present in epiretinal membranes, and their signature cytokines were markedly elevated in the vitreous of patients with traumatic PVR. Moreover, MPs from M2 macrophages were increased in the vitreous of patients with traumatic PVR. In vitro analyses showed that M2-MPs promoted the proliferation and migration of RPE cells via activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. However, M2-MPs did not induce the expression of fibrotic proteins, including fibronectin, α-smooth muscle actin, and N-cadherin in RPE cells.
Conclusions:
This study demonstrated increased MP shedding in the vitreous of patients with traumatic PVR; specifically, MPs derived from M2 polarized macrophages may contribute to PVR progression by stimulating RPE cell proliferation and migration.
Insights
Microparticle shedding in the vitreous is elevated in traumatic proliferative vitreoretinopathy (PVR). M2 macrophage-derived microparticles may drive PVR by increasing retinal pigment epithelium cell proliferation and migration.
Area of Science:
- Ophthalmology
- Cell Biology
- Immunology
Background:
- Proliferative vitreoretinopathy (PVR) is a sight-threatening complication of retinal detachment.
- Microparticles (MPs) are small vesicles released from cell membranes, implicated in intercellular communication.
- The specific role of vitreous MPs in traumatic PVR pathogenesis remains unclear.
Purpose of the Study:
- To characterize vitreous microparticles (MPs) in patients with traumatic proliferative vitreoretinopathy (PVR).
- To investigate the role of these MPs in PVR pathogenesis.
- To explore the contribution of specific MP subtypes to PVR progression.
Main Methods:
- Vitreous MPs were analyzed using flow cytometry in patients with traumatic PVR, rhegmatogenous retinal detachment (RRD) with PVR, and controls.
- Immunostaining assessed M2 macrophages in epiretinal membranes.
- ELISA quantified vitreous cytokines. In vitro studies used M1 and M2 macrophage-derived MPs (M1-MPs, M2-MPs) to assess effects on retinal pigment epithelium (RPE) cells.
Main Results:
- Vitreous MPs from photoreceptors, microglia, and macrophages were significantly increased in traumatic PVR compared to controls.
- M2 macrophages and their associated cytokines were elevated in traumatic PVR vitreous.
- In vitro, M2-MPs promoted RPE cell proliferation and migration via the PI3K/AKT/mTOR pathway, but did not induce fibrosis.
Conclusions:
- Traumatic PVR is associated with increased shedding of vitreous MPs.
- MPs derived from M2 polarized macrophages are implicated in PVR progression.
- M2-MPs stimulate RPE cell proliferation and migration, contributing to PVR pathogenesis.
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