ArticleInternational journal of molecular medicine2018
Pro‑atherogenic activation of A7r5 cells induced by the oxLDL/β2GPI/anti‑β2GPI complex.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- The Effects of the oxLDL/β2GPI/anti-β2GPI Complex on Macrophage Autophagy and its Mechanism.Immunity, inflammation and disease · 2024Article
- Review
- OxLDL/β2GPI/anti‑β2GPI Ab complex induces inflammatory activation via the TLR4/NF‑κB pathway in HUVECs.Molecular medicine reports · 2021Article
- Impaired Autophagy Induced by oxLDL/Oxidative medicine and cellular longevity · 2021Article
- The Effects ofFrontiers in immunology · 2021Review
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6 authors at 1 institution in 1 country.
Funding
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Abstract
A previous study has revealed that oxidized low‑density lipoprotein (oxLDL)/β2‑glycoprotein I (β2GPI)/anti‑β2‑glycoprotein I (anti‑β2GPI), an immune complex, is able to activate the Toll‑like receptor 4 (TLR4)/nuclear factor κβ (NF‑κβ) inflammatory signaling pathway in macrophages, and consequently enhance foam cell formation and the secretion of prothrombin activators. However, the effects of the oxLDL/β2GPI/anti‑β2GPI complex on vascular smooth muscle cells have yet to be investigated. The present study investigated whether the oxLDL/β2GPI/anti‑β2GPI complex was able to reinforce the pro‑atherogenic activities of a rat thoracic aorta smooth muscle cell line (A7r5) and examined the underlying molecular mechanisms. The results revealed that the oxLDL/β2GPI/anti‑β2GPI complex treatment significantly (P<0.05 vs. the media, oxLDL, oxLDL/β2GPI and β2GPI/anti‑β2GPI groups) enhanced the pro‑atherogenic activation of A7r5 cells, including intracellular lipid loading, Acyl‑coenzyme A cholesterol acyltransferase mRNA expression, migration, matrix metalloproteinase‑9 and monocyte chemoattractant protein 1 secretion, all via TLR4. In addition, the expression of TLR4 and the phosphorylation of NF‑κβ p65, p38 and ERK1/2 were also upregulated in oxLDL/β2GPI/anti‑β2GPI complex‑treated A7r5 cells. Pre‑treatment with TAK‑242, a TLR4 inhibitor, was able to partly attenuate the oxLDL/β2GPI/anti‑β2GPI complex‑induced phosphorylation of NF‑κβ p65; however, it had no effect on the phosphorylation of extracellular regulated kinase 1/2 (ERK1/2) and p38. Meanwhile, the NF‑κβ p65 inhibitor ammonium pyrrolidinedithiocarbamate and the ERK1/2 inhibitor U0126, but not the p38 inhibitor SB203580, were able to block oxLDL/β2GPI/anti‑β2GPI complex‑induced foam cell formation and migration in A7r5 cells. Hence, it was demonstrated that the oxLDL/β2GPI/anti‑β2GPI complex is able to enhance the lipid uptake, migration and active molecule secretion of A7r5 cells via TLR4, and finally deteriorate atherosclerosis plaques. Additionally, it was demonstrated that oxLDL/β2GPI/anti‑β2GPI complex‑induced foam cell formation and migration may be partly mediated by the TLR4/NF‑κβ signaling pathway and that ERK1/2 may also participate in the process.
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