Cited by 249Angiogenesis and VEGF in CancerRetinal Diseases and TreatmentsTelomeres, Telomerase, and Senescence

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Senescence regulates macrophage activation and angiogenic fate at sites of tissue injury in mice

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Kelly, Jennifer, Khan, Aslam Ali, Yin, Jiyi, Ferguson, Thomas A., Apte, Rajendra S.·2007·Journal of Clinical Investigation

DOI 10.1172/jci32430PMC PMC2045608

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Abstract

Abnormal angiogenesis plays a key role in diseases of aging such as heart disease, certain cancers, and eye diseases including age-related macular degeneration. Macrophages have been shown previously to be both anti- and proangiogenic, and their role in regulating angiogenesis at sites of tissue injury is critical and complex. In this study, we analyzed cytokine gene expression patterns of mouse macrophages by real-time quantitative PCR and tested the functional effects of senescence on gene expression and macrophage polarization. Following laser injury to the retina, IL-10 was upregulated and Fas ligand (FasL), IL-12, and TNF-alpha were downregulated in ocular macrophages of old mice (>18 months of age). Downregulation of FasL on macrophages led to a loss of the antiangiogenic phenotype, as evidenced by the inability of these macrophages to inhibit vascular endothelial cells. Our results demonstrate that senescence, FasL, and IL-10 are key determinants of macrophage function that alter the growth of abnormal postdevelopmental blood vessels in disease processes including blinding eye disease.

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Authors: Kelly, J., Khan, A. A., Yin, J., Ferguson, T. A., & Apte, R. S.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Apte, Rajendra S.
ORCID: Khan, Aslam Ali
Apte, Rajendra S.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2007-11-01
Volume: 117
Issue: 11
Pages: 3421-3426
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci32430
PMC: PMC2045608
OpenAlex: W2000811703
Cited by: 249
References: 15
Citations by year: 2026: 12 · 2025: 11 · 2024: 12 · 2023: 14 · 2022: 20 · 2021: 12 · 2020: 9 · 2019: 15 · 2018: 24 · 2017: 14 · 2016: 9 · 2015: 13 · 2014: 13 · 2013: 16 · 2012: 11
FWCI: 4.37
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
Funders: Research to Prevent Blindness (EY02687)
National Institutes of Health (5p60dk020579-35, DK20579, P60-DK-20579, EY02687, 5 P60 DK20579, EY06765)
National Eye Institute (EY 02687, P30EY002687, EY 12826, K08EY016139, R01EY012826, F32EY006765, EY06765, R01EY006765)
National Institute of Diabetes and Digestive and Kidney Diseases (5P60 DK20579, P60-DK-020579)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Keywords: cellular senescence, macrophage activation, angiogenesis, tissue damage, Fas ligand, IL-10, macrophage polarization, cytokine gene expression, age-related macular degeneration, vascular endothelial cells, aging
MeSH terms: Aging, Animals, Gene Expression Regulation, Humans, Lasers, Macrophage Activation, Macrophages, Mice, Inbred C57BL, Retina, Cytokines, Interleukin-10, Cellular Senescence, Mice, Knockout, Choroidal Neovascularization, Mice

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Senescence regulates macrophage activation and angiogenic fate at sites of tissue injury in mice

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