Abstract

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.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.