Publications by authors named "Muris Cabaravdic"
The etiology of atherosclerosis and restenosis involves aberrant inflammation and proliferation, rendering compounds with both anti-inflammatory and anti-mitogenic properties as promising candidates for combatting vascular diseases. A recent study identified the iridoid plumericin as a new scaffold inhibitor of the pro-inflammatory NF-κB pathway in endothelial cells. We here examined the impact of plumericin on the proliferation of primary vascular smooth muscle cells (VSMC).
View Article and Find Full Text PDFArticle Synopsis
- The study investigates how NR4A1, a nuclear receptor involved in vascular protection, is affected by various immune responses during vascular injury.* -
- Researchers found that the protein ISG12 interacts with NR4A1, inhibiting its transcriptional activity by promoting its exit from the nucleus, which decreases its protective effects.* -
- The absence of ISG12 in mice led to reduced neointima formation, suggesting that targeting this feedback loop could offer new treatments for diseases influenced by interferons.*
Objective: Our goal was to examine the influence of indirubin-3'-monoxime (I3MO), a natural product-derived cyclin-dependent kinase inhibitor, on vascular smooth muscle cell (VSMC) proliferation in vitro, experimentally induced neointima formation in vivo, and related cell signaling pathways.
Methods And Results: I3MO dose-dependently inhibited platelet-derived growth factor (PDGF)-BB-induced VSMC proliferation by arresting cells in the G(0)/G(1) phase of the cell cycle as assessed by 5-bromo-2'-deoxyuridine incorporation and flow cytometry. PDGF-induced activation of the kinases Akt, Erk1/2, and p38(MAPK) was not affected.