These results indicated that M2 macrophages, rather than M1, play an important role in promoting retinal pathological neovascularization probably by producing secreted factors. Thus, targeting M2 macrophages could be a potential therapeutic option for inhibiting retinal pathological neovascularization.

Background: Silver-Russell syndrome (SRS) is characterized by growth failure and dysmorphic features. Major (epi)genetic causes of SRS are loss of methylation on chromosome 11p15 (11p15 LOM) and maternal uniparental disomy of chromosome 7 (upd(7)mat). However, IGF2, CDKN1C, HMGA2, and PLAG1 mutations infrequently cause SRS. In addition, other imprinting disturbances, pathogenic copy number variations (PCNVs), and monogenic disorders sometimes lead to SRS phenotype. This study aimed to clarify the frequency and clinical features of the patients with gene mutations among etiology-unknown patients with SRS phenotype.

Our data indicate that extracellular matrix-related molecules such as POSTN, TNC, TGFβ, and angiogenic factors have important roles in promoting the development of FVMs associated with PDR.

Choroidal neovascularization (CNV) is a serious complication of age-related macular degeneration. The aim of the present study was to investigate the expression and distribution of M1 and M2 macrophages in a laser-induced CNV adult mouse model. The mRNA expression levels of M1, M2 and pan macrophage markers, and macrophage-associated angiogenic cytokines, were determined by reverse transcription-quantitative polymerase chain reaction. Immunofluorescence studies were performed to determine the location of the macrophages. The expression levels of M1 macrophage markers increased to a greater extent compared with M2 markers in the retinal pigment epithelium (RPE)-choroid complexes following laser photocoagulation. By contrast, the expression levels of M2 macrophage markers increased primarily in the retinas. Immunofluorescence studies revealed that the increased number of cluster of differentiation (CD)206-positive cells were located primarily in the retina, whereas the CD80-positive cells were located around the site of CNVs in the RPE-choroid. In addition, the M1-associated cytokines increased to a greater extent in the RPE-choroid complexes, whereas the M2-associated cytokines were highly expressed in the retinas. These findings indicate that M1 and M2 macrophage numbers increased following CNV; however, the locations were different in this mouse model of laser-induced CNV. The results of the present study suggest that M1 macrophages have a more direct role in inhibiting the development of CNV.

The elevated levels of MCP-1 and IL-6 may indicate prolonged inflammation even after successful vitrectomy, which can cause postoperative DME.