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Updated: Aug 14, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Selected life-extending interventions reduce arterial CXCL10 and macrophage colony-stimulating factor in aged mouse
Daniel W Trott1, Lisa A Lesniewski2, Anthony J Donato3
1University of Utah, Department of Internal Medicine, Division of Geriatrics, Salt Lake City, UT, USA.
Insights
Lifespan-extending interventions like caloric restriction and Rapamycin can reduce age-related arterial inflammation and associated cardiovascular disease risk in mice. These findings highlight potential strategies for mitigating aging-related vascular changes.
Area of Science:
- Cardiovascular Research
- Aging and Longevity
- Immunology and Inflammation
Background:
- Cardiovascular disease (CVD) is a leading cause of death, with aging as a primary risk factor.
- Aging is linked to arterial inflammation, increasing CVD risk, but key inflammatory mediators remain under-identified.
- Limited research exists on how lifespan-extending interventions impact age-related arterial inflammation.
Purpose of the Study:
- To investigate if lifespan-extending interventions (crowded litter nutrient deprivation, caloric restriction, Rapamycin) attenuate age-related arterial inflammation.
- To identify specific inflammatory mediators affected by these interventions in mouse aortas.
- To assess the impact on cytokines and chemokines involved in immune cell recruitment.
Main Methods:
- Utilized Luminex Multi Analyte Profiling to assess cytokine and chemokine concentrations in mouse aortas.
- Compared aortas from Young (4-6 months) and Old (22 months) mice, including Old mice subjected to lifespan-extending interventions.
- Analyzed specific chemokines (CCL2, CXCL9, CXCL10, GMCSF, MCSF) and interleukins (IL-1α, IL-1β, IL-10).
Main Results:
- Old mice exhibited increased levels of immune cell-recruiting chemokines (CCL2, CXCL9, CXCL10, GMCSF, MCSF) and interleukins (IL-1α, IL-1β, IL-10) compared to Young mice.
- Caloric restriction (CR) prevented the age-related increase in CXCL10.
- Rapamycin treatment lowered MCSF concentrations in aged aortas.
- Crowded litter nutrient deprivation did not significantly alter the measured inflammatory mediators compared to Old controls.
Conclusions:
- Selected lifespan-extending interventions, specifically CR and Rapamycin, can prevent or reduce age-related increases in specific aortic inflammatory mediators.
- These findings suggest potential therapeutic targets for mitigating vascular aging and associated cardiovascular disease risk.
- Further research is warranted to explore the mechanisms underlying these protective effects.
Abstract:
Cardiovascular disease (CVD) is the leading cause of death in the industrialized world. Aging is the most predictive risk factor for CVD and is associated with arterial inflammation which contributes to increased CVD risk. Although age-related arterial inflammation has been described in both humans and animals, only a limited number of inflammatory mediators, cytokines and chemokines have been identified. In this investigation we sought to determine whether lifespan extending interventions, including crowded litter early life nutrient deprivation (CL), traditional lifelong caloric restriction (CR) and lifelong Rapamycin treatment (Rap) would attenuate age-related arterial inflammation using multi analyte profiling. Aortas from Young (4-6months), Old (22months), Old CL, Old CR and Old Rap mice were homogenized and cytokine concentrations were assessed using Luminex Multi Analyte Profiling. Chemokines involved in immune cell recruitment, such as CCL2, CXCL9, CXCL10, GMCSF and MCSF, were increased in Old vs. Young (p<0.05). The age-related increase of CXCL10 was prevented by CR (p<0.05 vs. Old). MSCF concentrations were lower in aortas of Rap treated mice (p<0.05 vs. Old). Interleukins (IL), IL-1α, IL-1β and IL-10, were also greater in Old vs. Young mice (p<0.05). These data demonstrate selected lifespan extending interventions can prevent or limit age-related increases in selected aortic chemokines.
