Positive feedback regulation of proliferation in vascular smooth muscle cells stimulated by lipopolysaccharide is mediated through the TLR 4/Rac1/Akt pathway.
basic_science · Level V
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- Record sourced from PubMed, PMID 24667766.
- Also identified by DOI 10.1371/journal.pone.0092398 and PMC identifier 3965409.
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Abstract
Toll-like receptor 4 (TLR4) are important in inflammation and regulating vascular smooth muscle cells (VSMCs) proliferation, which are related to atherosclerosis and restenosis. We have investigated the mechanisms involved in Lipopolysaccharide (LPS)-induced proliferation of VSMCs. Stimulation of rat aortic VSMCs with LPS significantly increases the proliferation of VSMCs. This effect is regulated by Rac1 (Ras-related C3 botulinum toxin substrate l), which mediates the activation of phosphatidylinositol 3-kinase/Akt (PI3K/Akt) signaling pathways. Inhibition of Rac1 activity by NSC23766 is associated with inhibition of Akt activity. Treatment with NSC23766 or LY294002 significantly decreases LPS-induced TLR4 protein and mRNA expression. The data show that positive feedback regulation of proliferation in VSMCs is mediated through the TLR4/Rac1/Akt pathway.
Medical subject headings
- Aorta
- Cell Proliferation
- Lipopolysaccharides
- Muscle, Smooth, Vascular
- Proto-Oncogene Proteins c-akt
- Toll-Like Receptor 4
- rac1 GTP-Binding Protein