期刊
AGING-US
卷 13, 期 9, 页码 12359-12377出版社
IMPACT JOURNALS LLC
关键词
miR-142-3p; age-related macular degeneration; angiogenesis; inflammation; microglia
资金
- University of Liege
- Maastricht University
- Fondation Leon Fredericq, FEDER
- FNRS-PDR [T.1080.15]
- Fonds Speciaux de l'Universite de Liege
- ERA-Net-CVD project MacroERA [01KL1706]
- Netherlands Cardiovascular Research Initiative
- Dutch Heart Foundation
- CVON2016-Early HFPEF [2015-10]
- CVON ShePREDICTS
- CVON Arena-PRIME
Age-related macular degeneration (AMD) is a leading cause of blindness in individuals over 50 years old worldwide, with wet AMD being the most aggressive form characterized by specific features and pathological processes. MiR-142-3p plays a key role in CNV formation, highlighting its importance in the progression of the disease.
Age-related macular degeneration (AMD) is a worldwide leading cause of blindness affecting individuals over 50 years old. The most aggressive form, wet AMD, is characterized by choroidal neovascularization (CNV) and inflammation involving microglia recruitment. By using a laser-induced CNV mouse model, we provide evidence for a key role played by miR-142-3p during CNV formation. MiR-142-3p was overexpressed in murine CNV lesions and its pharmacological inhibition decreased vascular and microglia densities by 46% and 30%, respectively. Consistently, miR-142-3p overexpression with mimics resulted in an increase of 136% and 126% of blood vessels and microglia recruitment. Interestingly, miR-142-3p expression was linked to the activation state of mouse microglia cells as determined by morphological analysis (cell solidity) through a computational method. In vitro, miR-142-3p overexpression in human microglia cells (HMC3) modulated microglia activation, as shown by CD68 levels. Interestingly, miR142-3p modulation also regulated the production of VEGF-A, the main pro-angiogenic factor. Together, these data strongly support the unprecedented importance of miR-142-3p-dependent vascular-inflammation axis during CNV progression, through microglia activation.
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