ArticleAnnals of translational medicine2022
Oncostatin M promotes the ox-LDL-induced activation of NLRP3 inflammasomes via the NF-κB pathway in THP-1 macrophages and promotes the progression of atherosclerosis.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Neutrophil-derived oncostatin m contributes to endothelial cell dysfunction during Treponema denticola interaction.PloS one · 2026Article
- Development of stem cell therapy for atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Study on the Anti-Atherosclerotic Mechanisms of Xin-Tong-Tai Granule Through Network Pharmacology, Molecular Docking, and Experimental Validation.Journal of inflammation research · 2024Article
- Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023Review
- MALT1 accelerates proatherogenic vascular smooth muscle cell growth, invasion and synthetic phenotype switching via nuclear factor‑κB signaling‑dependent way.Experimental and therapeutic medicine · 2023Article
- Moxonidine Increases Uptake of Oxidised Low-Density Lipoprotein in Cultured Vascular Smooth Muscle Cells and Inhibits Atherosclerosis in Apolipoprotein E-Deficient Mice.International journal of molecular sciences · 2023Article
- Effects of frog skin peptide temporin-1CEa and its analogs on ox-LDL induced macrophage-derived foam cells.Frontiers in pharmacology · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Oncostatin M (OSM) is reported to be involved in many stages of atherosclerosis, including endothelial dysfunction, chronic inflammation, and smooth muscle cell migration. This study explored the effects of OSM on foam cell formation and its corresponding molecular mechanisms. Methods: THP-1 cells were treated with phorbol-12-myristate-13-acetate (PMA) to induce macrophage differentiation and were then exposed to oxidized low-density lipoprotein (ox-LDL). OSM expression was analyzed by quantitative reverse transcription-polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay (ELISA). OSM-specific small interfering RNAs (siRNAs) were transfected into THP-1 macrophages. The effects of OSM silencing were evaluated by Oil Red O staining, ELISA, and Western blotting. Moreover, the activation of NLR family pyrin domain containing 3 (NLRP3) inflammasomes was detected by western blotting and immunofluorescence. Results: OSM was highly expressed in THP-1 macrophages in a time- and dose-dependent fashion. Silencing OSM significantly reduced the total cholesterol content and Oil Red O staining levels in ox-LDL-treated macrophages. Silencing OSM significantly inhibited ox-LDL-induced cytokine release, including TNF-α, IL-1β, IL-6, and IL-18. Ox-LDL activated p65 and NLRP3, which further induced caspase-1 cleavage, apoptosis-associated, speck-like protein containing a caspase-1 recruitment domain (ASC) upregulation, and gasdermin-D (GSDMD)-N fragmentation. Overexpression of NLRP3 significantly reversed the effects of OSM silencing on ox-LDL-induced foam cell formation and inflammation. Conclusions: OSM was highly expressed in the cell model of atherosclerosis. OSM has a promoting role in ox-LDL-induced foam cell formation and inflammation via the activation of p65-NLRP3 signaling pathways. Silencing OSM may be has benefit in treating atherosclerosis.
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