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• W2093980767 abstract "<i>Background/Aims:</i> Despite advances in stent design, in-stent restenosis (ISR) remains a significant clinical problem. All implant metals exhibit corrosion, which results in release of metal ions. Stainless steel (SS), a metal alloy widely used in stents, releases ions to the vessel wall and induces reactive oxygen species, inflammation and fibroproliferative responses. The molecular mechanisms are unknown. TGF-β is known to be involved in the fibroproliferative responses of vascular smooth muscle cells (VSMCs) in restenosis, and TGF-β antagonists attenuate ISR. We hypothesized that SS ions induce the latent TGF-β activator, thrombospondin-1 (TSP1), through altered oxidative signaling to stimulate increased TGF-β activation and VSMC phenotype change. <i>Methods:</i> VSMCs were treated with SS metal ion cocktails, and morphology, TSP1, extracellular matrix production, desmin and TGF-β activity were assessed by immunoblotting. <i>Results:</i> SS ions stimulate the synthetic phenotype, increased TGF-β activity, TSP1, increased extracellular matrix and downregulation of desmin in VSMCs. Furthermore, SS ions increase hydrogen peroxide and decrease cGMP-dependent protein kinase (PKG) signaling, a known repressor of TSP1 transcription. Catalase blocks SS ion attenuation of PKG signaling and increased TSP1 expression. <i>Conclusions:</i> These data suggest that ions from stent alloy corrosion contribute to ISR through stimulation of TSP1-dependent TGF-β activation." @default.
• W2093980767 created "2016-06-24" @default.
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• W2093980767 date "2009-12-16" @default.
• W2093980767 modified "2023-10-12" @default.
• W2093980767 title "Stainless Steel Ions Stimulate Increased Thrombospondin-1-Dependent TGF-Beta Activation by Vascular Smooth Muscle Cells: Implications for In-Stent Restenosis" @default.
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• W2093980767 doi "https://doi.org/10.1159/000265565" @default.
• W2093980767 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2895758" @default.
• W2093980767 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20016205" @default.
• W2093980767 hasPublicationYear "2009" @default.
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