ArticleJournal of the American College of Cardiology
SOCS1 prevents graft arteriosclerosis by preserving endothelial cell function.
Article in Journal of the American College of Cardiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 43 citations in OpenAlex.
- SRF SUMOylation modulates smooth muscle phenotypic switch and vascular remodeling.Nature communications · 2024Article
- Species-specific responses during Seoul orthohantavirus infection in human and rat lung microvascular endothelial cells.PLoS neglected tropical diseases · 2024Article
- Endothelial RIPK1 protects artery bypass graft against arteriosclerosis by regulating SMC growth.Science advances · 2023Article
- Integrated single-cell RNA-seq analysis reveals the vital cell types and dynamic development signature of atherosclerosis.Frontiers in physiology · 2023Article
- Proteomimetics of Natural Regulators of JAK-STAT Pathway: Novel Therapeutic Perspectives.Frontiers in molecular biosciences · 2021Review
- Antioxidant Effects of PS5, a Peptidomimetic of Suppressor of Cytokine Signaling 1, in Experimental Atherosclerosis.Antioxidants (Basel, Switzerland) · 2020Article
- Diminished expression of major histocompatibility complex facilitates the use of human induced pluripotent stem cells in monkey.Stem cell research & therapy · 2020Article
- FGF signaling contributes to atherosclerosis by enhancing the inflammatory response in vascular smooth muscle cells.Molecular medicine reports · 2019Article
- Surface Modification of Electrospun Scaffolds for Endothelialization of Tissue-Engineered Vascular Grafts Using Human Cord Blood-Derived Endothelial Cells.Journal of clinical medicine · 2019Article
- Article
- ASK1-dependent endothelial cell activation is critical in ovarian cancer growth and metastasis.JCI insight · 2017Article
- The critical role of SENP1-mediated GATA2 deSUMOylation in promoting endothelial activation in graft arteriosclerosis.Nature communications · 2017Article
- The Potential Therapeutic Application of Peptides and Peptidomimetics in Cardiovascular Disease.Frontiers in pharmacology · 2016Review
- AIP1-mediated stress signaling in atherosclerosis and arteriosclerosis.Current atherosclerosis reports · 2015Review
- A Novel ASK Inhibitor AGI-1067 Inhibits TLR-4-Mediated Activation of ASK1 by Preventing Dissociation of Thioredoxin from ASK1.Cardiovascular pharmacology: open access · 2015Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
objectivesThe aim of this study was to determine the role of suppressor of cytokine signaling 1 (SOCS1) in graft arteriosclerosis (GA).
backgroundGA, the major cause of late cardiac allograft failure, is initiated by immune-mediated endothelial activation resulting in vascular inflammation and consequent neointima formation. SOCS1, a negative regulator of cytokine signaling, is highly expressed in endothelial cells (ECs) and may prevent endothelial inflammatory responses and phenotypic activation.
methodsClinical specimens of coronary arteries with GA, with atherosclerosis, or without disease were collected for histological analysis. SOCS1 knockout or vascular endothelial SOCS1 (VESOCS1) transgenic mice were used in an aorta transplant model of GA. Mouse aortic ECs were isolated for in vitro assays.
resultsDramatic but specific reduction of endothelial SOCS1 was observed in human GA and atherosclerosis specimens, which suggested the importance of SOCS1 in maintaining normal endothelial function. SOCS1 deletion in mice resulted in basal EC dysfunction. After transplantation, SOCS1-deficient aortic grafts augmented leukocyte recruitment and neointima formation, whereas endothelial overexpression of SOCS1 diminished arterial rejection. Induction of endothelial adhesion molecules in early stages of GA was suppressed by the VESOCS1 transgene, and this effect was confirmed in cultured aortic ECs. Moreover, VESOCS1 maintained better vascular function during GA progression. Mechanistically, endothelial SOCS1, by modulating both basal and cytokine-induced expression of the adhesion molecules platelet/endothelial cell adhesion molecule-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1, restrained leukocyte adhesion and transendothelial migration during inflammatory cell infiltration.
conclusionsSOCS1 prevents GA progression by preserving endothelial function and attenuating cytokine-induced adhesion molecule expression in vascular endothelium.
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