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Updated: Jan 20, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Oncostatin M reduces atherosclerosis development in APOE*3Leiden.CETP mice and is associated with increased survival
Danielle van Keulen1,2,3,4, Marianne G Pouwer4,5, Valur Emilsson6,7
1Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Objective:
Previous studies indicate a role for Oncostatin M (OSM) in atherosclerosis and other chronic inflammatory diseases for which inhibitory antibodies are in development. However, to date no intervention studies with OSM have been performed, and its relation to coronary heart disease (CHD) has not been studied.
Approach And Results:
Gene expression analysis on human normal arteries (n = 10) and late stage/advanced carotid atherosclerotic arteries (n = 127) and in situ hybridization on early human plaques (n = 9) showed that OSM, and its receptors, OSM receptor (OSMR) and Leukemia Inhibitory Factor Receptor (LIFR) are expressed in normal arteries and atherosclerotic plaques. Chronic OSM administration in APOE*3Leiden.CETP mice (n = 15/group) increased plasma E-selectin levels and monocyte adhesion to the activated endothelium independently of cholesterol but reduced the amount of inflammatory Ly-6CHigh monocytes and atherosclerotic lesion size and severity. Using aptamer-based proteomics profiling assays high circulating OSM levels were shown to correlate with post incident CHD survival probability in the AGES-Reykjavik study (n = 5457).
Conclusions:
Chronic OSM administration in APOE*3Leiden.CETP mice reduced atherosclerosis development. In line, higher serum OSM levels were correlated with improved post incident CHD survival probability in patients, suggesting a protective cardiovascular effect.
Insights
Oncostatin M (OSM) plays a role in atherosclerosis. Studies show OSM administration reduced atherosclerosis in mice and higher OSM levels correlate with better coronary heart disease survival in humans, suggesting a protective cardiovascular effect.
Area of Science:
- Cardiovascular Biology
- Inflammation Research
Background:
- Oncostatin M (OSM) is implicated in atherosclerosis and chronic inflammatory diseases.
- Inhibitory antibodies targeting OSM are under development.
- No prior intervention studies or direct investigation into OSM's role in coronary heart disease (CHD) existed.
Purpose of the Study:
- To investigate the role of Oncostatin M (OSM) in atherosclerosis and coronary heart disease (CHD).
- To assess the effects of OSM intervention in a mouse model of atherosclerosis.
- To determine the correlation between circulating OSM levels and CHD outcomes in humans.
Main Methods:
- Gene expression and in situ hybridization analyzed OSM and its receptors (OSMR, LIFR) in human arterial tissues.
- Chronic OSM administration was performed in APOE*3Leiden.CETP mice.
- Aptamer-based proteomics profiled OSM levels in the AGES-Reykjavik cohort (n=5457).
Main Results:
- OSM and its receptors are expressed in normal and atherosclerotic human arteries.
- In mice, OSM administration reduced atherosclerotic lesion size and inflammatory monocyte presence, despite increased E-selectin and monocyte adhesion.
- Elevated serum OSM levels in humans correlated with improved post-incident CHD survival probability.
Conclusions:
- Chronic OSM administration demonstrates a protective effect against atherosclerosis development in a mouse model.
- Higher circulating OSM levels are associated with improved CHD survival in patients.
- These findings suggest a potentially protective cardiovascular role for OSM.
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