Downregulated expression of miR-142-3p in macrophages contributes to increased IL-6 levels in aged mice
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Updated: Mar 13, 2026
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Yin Liu1, Xiaoqi Song1, Shu Meng1
1National Key Laboratory of Medical Molecular Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100005, China.
Abstract:
Macrophages are innate immune cells that are important contributors to age-related functional impairment of the immune system. During the cell aging process, microRNAs are differentially expressed and participate in the regulation of aging-related immune responses. However, the role of aging-associated changes in miRNA expression in macrophages remains unclear. Here, we found that miR-142-3p expression is downregulated 50% in peritoneal macrophages from aged mice compared with young mice and is not upregulated by cell treatment with lipopolysaccharide (LPS), CpG, or polyinosinic-polycytidylic acid. Serum levels of miR-142-3p are also lower in aged mice than in young mice by q-PCR. Luciferase reporter analysis showed that IL-6 is a target of miR-142-3p in macrophages. In addition, the histone deacetylase inhibitor trichostatin A increased miR-142-3p expression by more than 3-fold in LPS-treated macrophages from aged mice compared with young mice, which in turn suppressed LPS-stimulated IL-6 production, suggesting that inhibition of miR-142-3p by histone deacetylation may be involved in the lack of response to LPS stimulation in macrophages of aged mice. These findings suggest that downregulation of miR-142-3p in macrophages of aged mice might contribute to IL-6-associated aging disorders and that epigenetic modification might be involved in age-related inflammatory diseases.
Insights
MicroRNA-142-3p (miR-142-3p) is downregulated in aged macrophages, impairing immune response. Epigenetic modifications may reverse this, potentially treating age-related inflammatory diseases.
Area of Science:
- Immunology
- Molecular Biology
- Aging Research
Background:
- Macrophages are key innate immune cells implicated in age-related immune dysfunction.
- MicroRNAs (miRNAs) are differentially expressed during cellular aging and regulate immune responses.
- The specific role of aging-associated miRNA changes in macrophages is not fully understood.
Purpose of the Study:
- To investigate the expression and function of miR-142-3p in aged macrophages.
- To explore the potential mechanisms regulating miR-142-3p in aging.
- To determine the contribution of miR-142-3p to age-related immune disorders.
Main Methods:
- Quantitative PCR (q-PCR) to measure miR-142-3p levels in peritoneal macrophages and serum from young and aged mice.
- Luciferase reporter assays to identify miR-142-3p targets.
- Treatment of macrophages with stimuli (LPS, CpG, poly(I:C)) and a histone deacetylase inhibitor (trichostatin A).
Main Results:
- miR-142-3p expression was significantly downregulated (50%) in macrophages and serum of aged mice compared to young mice.
- miR-142-3p directly targets Interleukin-6 (IL-6) in macrophages.
- Trichostatin A treatment upregulated miR-142-3p in aged macrophages, suppressing LPS-induced IL-6 production.
Conclusions:
- Downregulation of miR-142-3p in aged macrophages may contribute to IL-6-associated aging disorders.
- Epigenetic mechanisms, specifically histone deacetylation, may inhibit miR-142-3p expression in aged macrophages, leading to impaired response to stimuli.
- These findings suggest potential therapeutic targets for age-related inflammatory diseases through epigenetic modulation.
