To understand the role of MPs in the pathogenesis of PVR, we first isolated MPs from the vitreous of the sampled patients and then assessed the MPs by transmission electron microscope (TEM) and nanoparticle tracking analysis. Under the TEM, we found that the isolated MPs appeared as double-layer membrane structures with a diameter between 100 and 1000 nm (
Fig. 1A). Furthermore, nanoparticle tracking analysis confirmed that the isolated MPs had a diameter primarily distributed between 100 and 500 nm (
Fig. 1B). Next, we determined the expression of cell type–specific markers in isolated vitreous MPs by flow cytometry analysis. Specifically, photoreceptor-derived MPs defined as FITC-PNA
+, microglial-derived MPs defined as FITC-ILB4
+, and macrophage-derived MPs defined as CD14-APC
+ were identified (
Figs. 1C–
1G). Vitreous levels of photoreceptor PNA
+, microglial ILB4
+, macrophage CD14
+, and Annexin V
+ MPs were markedly increased in patients with traumatic PVR in comparison with control patients (
P = 0.0002,
P = 0.0012,
P < 0.0001, and
P = 0.0003, respectively) (
Fig. 1H,
Table) and in patients with RRD complicated with PVR (
P = 0.0042,
P = 0.0109,
P = 0.0003, and
P = 0.0030, respectively) (
Fig. 1H,
Table). There was no significant difference in the concentrations of vitreous MPs labeled with PNA
+, ILB
+, CD14
+, or Annexin V
+ between patients with RRD with PVR and control patients (
P = 0.5306,
P = 0.7066,
P = 0.5406, and
P = 0.7520, respectively) (
Fig. 1H,
Table). In addition, MPs of macrophage origin were further confirmed by dual-labeling with macrophage markers CD14 and CD68. We found that CD14 and CD68 double-positive MPs were significantly higher in patients with traumatic PVR compared with control patients and patients with RRD with PVR (
P = 0.0052 and
P = 0.0030, respectively) (
Figs. 1I–
1L), suggesting increased shedding of MPs from macrophages in patients with traumatic PVR. Altogether, these results indicate that MPs were increased significantly in the vitreous of patients with traumatic PVR, and the increased MPs may have originated from photoreceptors, microglial cells, and macrophages.