miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis
Open accessAbstract
Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-α. Downregulation of miR-155 and PDCD4 and upregulation of SOCS1 obviously decreased the IL-6 and TNF-α expression. In addition, inhibition of miR-155 levels in atherosclerotic mice could notably reduce the IL-6 and TNF-α level in plasma and aortic tissue, accompanied with increased p-STAT3 and PDCD4 and decreased SOCS1. Thus, miR-155 might mediate the inflammation in AS via the SOCS1-STAT3-PDCD4 axis. These results provide a rationale for intervention of intracellular miR-155 as possible antiatherosclerotic targets.
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PDCD4 is an important factor for inflammatory diseases such as asthma and atherosclerosis.
“Recently, it was shown that PDCD4 is also an important factor for inflammatory diseases such as asthma [86] and atherosclerosis [87,88].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [88]
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- Authors
- Ye, J., Guo, R., Shi, Y., Qi, F., Guo, C., & Yang, L.
- Affiliations
- Army Medical University (CN)
- Kunming General Hospital of Chengdu Military Command (CN)
- Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China
- Corresponding author
- Yang, Lixia
- Venue
- Mediators of Inflammation
- Publisher
- Wiley
- Published
- 2016
- Volume
- 2016
- Pages
- 1-14
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC5098093
- OpenAlex
- W2533066341
- Cited by
- 127
- References
- 49
- Citations by year
- 2026: 11 · 2025: 11 · 2024: 14 · 2023: 19 · 2022: 11 · 2021: 9 · 2020: 21 · 2019: 18 · 2018: 8 · 2017: 5
- FWCI
- 4.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- miR-155, atherosclerosis, atherogenesis, inflammation, SOCS1, STAT3, PDCD4, macrophages, interleukin-6, TNF-α, oxidized LDL, microRNA
- MeSH terms
- RAW 264.7 Cells, Suppressor of Cytokine Signaling 1 Protein, Animals, Aorta, Apolipoproteins E, Inflammation, Male, Tumor Necrosis Factor-alpha, Signal Transduction, RNA-Binding Proteins, RNA, Small Interfering, MicroRNAs, Atherosclerosis, STAT3 Transcription Factor, Apoptosis Regulatory Proteins, Mice
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