ArticleBiochimica et biophysica acta2009
Morelloflavone blocks injury-induced neointimal formation by inhibiting vascular smooth muscle cell migration.
Article in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
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- Physiological and Metabolic Effects of Yellow Mangosteen (International journal of molecular sciences · 2019Article
- Plant-Derived Products for Treatment of Vascular Intima Hyperplasia Selectively Inhibit Vascular Smooth Muscle Cell Functions.Evidence-based complementary and alternative medicine : eCAM · 2018Review
- Natural Biflavonoids Modulate Macrophage-Oxidized LDL InteractionFrontiers in immunology · 2017Article
- Fortilin potentiates the peroxidase activity of Peroxiredoxin-1 and protects against alcohol-induced liver damage in mice.Scientific reports · 2016Article
- Total saponins from Albizia julibrissin inhibit vascular endothelial growth factor-mediated angiogenesis in vitro and in vivo.Molecular medicine reports · 2015Article
- Fortilin reduces apoptosis in macrophages and promotes atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2013Article
- Enterolobium contortisiliquum trypsin inhibitor (EcTI), a plant proteinase inhibitor, decreases in vitro cell adhesion and invasion by inhibition of Src protein-focal adhesion kinase (FAK) signaling pathways.The Journal of biological chemistry · 2012Article
- Morelloflavone, a biflavonoid inhibitor of migration-related kinases, ameliorates atherosclerosis in mice.American journal of physiology. Heart and circulatory physiology · 2012Article
- Methyl 2-cyano-3,11-dioxo-18-olean-1,12-dien-30-oate (CDODA-Me), a derivative of glycyrrhetinic acid, functions as a potent angiogenesis inhibitor.The Journal of pharmacology and experimental therapeutics · 2010Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIn-stent restenosis, or renarrowing within a coronary stent, is the most ominous complication of percutaneous coronary intervention, caused by vascular smooth muscle cell (VSMC) migration into and proliferation in the intima. Although drug-eluting stents reduce restenosis, they delay the tissue healing of the injured arteries. No promising alternative anti-restenosis treatments are currently on the horizon.
methodsIn endothelium-denudated mouse carotid arteries, oral morelloflavone-an active ingredient of the Thai medicinal plant Garcinia dulcis-significantly decreased the degree of neointimal hyperplasia, without affecting neointimal cell cycle progression or apoptosis as evaluated by Ki-67 and TUNEL staining, respectively. At the cellular level, morelloflavone robustly inhibited VSMC migration as shown by both scratch wound and invasion assays. In addition, morelloflavone prevented VSMCs from forming lamellipodia, a VSMC migration apparatus. Mechanistically, the inhibition by morelloflavone of VSMC migration was through its negative regulatory effects on several migration-related kinases, including FAK, Src, ERK, and RhoA. Consistently with the animal data, morelloflavone did not affect VSMC cell cycle progression or induce apoptosis.
resultsThese data suggest that morelloflavone blocks injury-induced neointimal hyperplasia via the inhibition of VSMC migration, without inducing apoptosis or cell cycle arrest. GENERAL SIGNIFICANCE: We propose morelloflavone to be a viable oral agent for the prevention of restenosis, without compromising effects on the integrity and healing of the injured arteries.
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