ArticleExperimental and clinical cardiology2007
The proteasome inhibitor lactacystin attenuates growth and migration of vascular smooth muscle cells and limits the response to arterial injury.
Article in Experimental and clinical cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells.The Kaohsiung journal of medical sciences · 2024Article
- Targeting endothelial vascular cell adhesion molecule-1 in atherosclerosis: drug discovery and development of vascular cell adhesion molecule-1-directed novel therapeutics.Cardiovascular research · 2023Review
- Gallic Acid Attenuates Angiotensin II-Induced Hypertension and Vascular Dysfunction by Inhibiting the Degradation of Endothelial Nitric Oxide Synthase.Frontiers in pharmacology · 2020Article
- Dysfunction of the ubiquitin-proteasome system in atherosclerotic cardiovascular disease.American journal of cardiovascular disease · 2015Review
- Integrated analysis of microarray data of atherosclerotic plaques: modulation of the ubiquitin-proteasome system.PloS one · 2014Article
- The ubiquitin-proteasome system and cardiovascular disease.Progress in molecular biology and translational science · 2012Review
- Inhibition of ubiquitin proteasome function suppresses proliferation of pulmonary artery smooth muscle cells.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Regulation of posttranscriptional modification as a possible therapeutic approach for retinal neuroprotection.Journal of ophthalmology · 2011Article
- On to the road to degradation: atherosclerosis and the proteasome.Cardiovascular research · 2010Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThere is emerging evidence that the ubiquitin-proteasome system plays a role in vascular proliferative disorders such as restenosis after percutaneous coronary interventions. The present study examined the effect of proteasome inhibition on cultured vascular smooth muscle cell (VSMC) growth and migration, as well as on vascular lesion formation, following balloon arterial injury in the rat.
methodsThe effect of the proteasome inhibitor clasto-lactacystin beta-lactone (lactacystin) on cultured VSMC proliferation was assessed using cell proliferation assays and immunohistochemical assessment of S-phase entry. To test the effect of proteasome inhibition on lesion formation and to confirm the role of p21(Cip1/Waf1) (p21) in this effect in vivo, carotid injury was performed on anesthetized male Sprague-Dawley rats, followed by local treatment with either lactacystin or vehicle.
resultsTreatment of VSMCs with the proteasome inhibitor lactacystin resulted in a 60% and 80% decrease in cell number versus controls at day 3 and day 5 after treatment, respectively. This effect was accompanied by an 86% decrease in S-phase entry and an increased level of the cyclin-dependent kinase inhibitor p21. Additionally, lactacystin significantly inhibited VSMC migration in a modified Boyden chamber assay. Lactacystin resulted in a 59% reduction of neointimal formation at 14 days following balloon injury. This effect was associated with an early increase in p21 protein in the arterial wall.
conclusionsInhibition of the ubiquitin-proteasome system resulted in the attenuation of VSMC growth both in cultured cells and in an animal model of vascular injury, possibly via a mechanism involving upregulation of the p21 cyclin-dependent kinase inhibitor. These data provide support for a role of the proteasome in the vascular response to injury, and suggest an important role for p21 and attenuation of cellular migration in the mechanism of this effect.
Indexed as
Identifiers
18650992PMC2323756W342775215What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.