Retinopathy of prematurity (ROP) is the primary cause of visual impairment and vision loss in premature infants, which results from the formation of aberrant retinal neovascularization (NV). An emerging body of evidence has shown that Müller cells are the predominant source of vascular endothelial growth factor (VEGF), which also serves as a chemoattractant for monocyte/macrophage lineage. The recruitment of macrophages is increased during retinal NV, and they exert a pro-angiogenic role in ROP. We have shown that lymphocytic microparticles (microvesicles; LMPs) derived from apoptotic human T lymphocytes possess strong angiogenesis-inhibiting properties. Here, we investigated the effect of LMPs on the chemotactic capacity of Müller cells in vitro using rat Müller cell rMC-1 and mouse macrophage RAW 264.7. In addition, the impact of LMPs was determined in vivo using a mouse model of oxygen-induced ischemic retinopathy (OIR). The results revealed that LMPs were internalized by rMC-1 and reduced their cell proliferation dose-dependently without inducing cell apoptosis. LMPs inhibited the chemotactic capacity of rMC-1 on RAW 264.7 via reducing the expression of VEGF. Moreover, LMPs attenuated pathological retinal NV and the infiltration of macrophages in vivo. LMPs downregulated ERK1/2 and HIF-1α both in vitro and in vivo. These findings expand our understanding of the effects of LMPs, providing evidence of LMPs as a promising therapeutic approach for the treatment of retinal NV diseases.

早产儿视网膜病变（ROP）是早产儿视力障碍和视力丧失的主要原因，其原因是视网膜新血管形成异常（NV）的形成。越来越多的证据表明，穆勒细胞是血管内皮生长因子（VEGF）的主要来源，而血管内皮生长因子也可作为单核细胞/巨噬细胞谱系的趋化因子。在视网膜NV中巨噬细胞的募集增加，并且它们在ROP中发挥促血管生成作用。我们已经表明，从凋亡的人T淋巴细胞衍生的淋巴细胞微粒（微囊泡； LMP）具有很强的血管生成抑制特性。在这里，我们研究了LMP对Müller细胞体外趋化能力的影响使用大鼠Müller细胞rMC-1和小鼠巨噬细胞RAW 264.7。另外，使用氧诱导的缺血性视网膜病（OIR）小鼠模型在体内确定了LMP的影响。结果表明，LMPs被rMC-1内在化，并在不诱导细胞凋亡的情况下剂量依赖性地降低了其细胞增殖。LMPs通过降低VEGF的表达抑制rMC-1在RAW 264.7上的趋化能力。而且，LMPs减弱了病理性视网膜NV和体内巨噬细胞的浸润。LMP的下调ERK1 / 2和HIF-1α都在体外和体内。这些发现扩大了我们对LMPs作用的理解，提供了LMPs作为治疗视网膜NV疾病的有前途的治疗方法的证据。