ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
MARCKS silencing differentially affects human vascular smooth muscle and endothelial cell phenotypes to inhibit neointimal hyperplasia in saphenous vein.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- Unveiling the Genetic Landscape of Coronary Artery Disease Through Common and Rare Structural Variants.Journal of the American Heart Association · 2025Article
- Role for the PIPJournal of cell communication and signaling · 2024Review
- Advancements in Omics and Breakthrough Gene Therapies: A Glimpse into the Future of Peripheral Artery Disease.Annals of vascular surgery · 2024Review
- Integrated analysis of tRNA-derived small RNAs in proliferative human aortic smooth muscle cells.Cellular & molecular biology letters · 2022Article
- Extracellular vesicles derived from ascitic fluid enhance growth and migration of ovarian cancer cells.Scientific reports · 2021Article
- MARCKS mediates vascular contractility through regulating interactions between voltage-gated CaVascular pharmacology · 2020Article
- The myristoylated alanine-rich C kinase substrate differentially regulates kinase interacting with stathmin in vascular smooth muscle and endothelial cells and potentiates intimal hyperplasia formation.Journal of vascular surgery · 2019Article
- Small GTPases and Their Role in Vascular Disease.International journal of molecular sciences · 2019Review
- Delivery of targeted gene therapies using a hybrid cryogel-coated prosthetic vascular graft.PeerJ · 2019Article
- The MARCKS protein amount is differently regulated by calpain during toxic effects of methylmercury between SH-SY5Y and EA.hy926 cells.The Journal of veterinary medical science · 2017Article
- RNAi therapy to the wall of arteries and veins: anatomical, physiologic, and pharmacological considerations.Journal of translational medicine · 2017Review
- Intraluminal delivery of thrombospondin-2 small interfering RNA inhibits the vascular response to injury in a rat carotid balloon angioplasty model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells.The Journal of veterinary medical science · 2016Article
- The effects of transfection reagent polyethyleneimine (PEI) and non-targeting control siRNAs on global gene expression in human aortic smooth muscle cells.BMC genomics · 2016Article
- Myristoylated Alanine-Rich Protein Kinase Substrate (MARCKS) Regulates Small GTPase Rac1 and Cdc42 Activity and Is a Critical Mediator of Vascular Smooth Muscle Cell Migration in Intimal Hyperplasia Formation.Journal of the American Heart Association · 2015Article
- Article
- 6q21-22 deletion syndrome with interrupted aortic arch.Human genome variation · 2015Article
- Current siRNA targets in the prevention and treatment of intimal hyperplasia.Discovery medicine · 2014Review
- Gene silencing in human aortic smooth muscle cells induced by PEI-siRNA complexes released from dip-coated electrospun poly(ethylene terephthalate) grafts.Biomaterials · 2014Article
- Fibroblast Migration Is Regulated by Myristoylated Alanine-Rich C-Kinase Substrate (MARCKS) Protein.PloS one · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Intimal hyperplasia (IH) limits the patency of all cardiovascular vein bypass grafts. We previously found the myristoylated alanine-rich C kinase substrate (MARCKS), a key protein kinase C (PKC) substrate, to be up-regulated in canine models of IH. Here, we further characterize the role of MARCKS in IH and examine the phenotypic consequences of MARCKS silencing by small interfering RNA (siRNA) transfection in human vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) in vitro and use a rapid 10-min nonviral siRNA transfection technique to determine the effects of MARCKS silencing in human saphenous vein cultured ex vivo. We demonstrate MARCKS silencing attenuates VSMC migration and arrests VSMC proliferation in part through the up-regulation of the cyclin-dependent kinase inhibitor p27(kip1). Conversely, MARCKS silencing had little or no effect on EC migration or proliferation. These phenotypic changes culminated in reduced neointimal formation in cultured human saphenous vein. These data identify MARCKS as a pathogenic contributor to IH and indicate therapeutic MARCKS silencing could selectively suppress the "atherogenic," proliferative phenotype of VSMCs without collateral harm to the endothelium. This approach could be readily translated to the clinic to silence MARCKS in vein bypass grafts prior to implantation.
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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.