Hyperuricemia Is Associated With Endothelial Dysfunction and Morphological Abnormalities of Neointima After 2nd Generation Drug-Eluting Stents Deployment Assessed by Optical Coherence Tomography

Yoshino, Satoshi; Tabata, Hiroyuki; Miyata, Masaaki; Kanda, Daisuke; Ohmure, Kenta; Uchikado, Yoshihiro; Ohishi, Mitsuru

doi:10.1016/s0735-1097(18)31791-1

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“…Hyperuricemia has been connected with hypertension, coronary heart disease, and other CVDs [2,3]. Biologically active uric acid can stimulate endothelial dysfunction, inflammation, oxidative stress, and vasoconstriction [4–6]. High uric acid levels usually occur when the kidneys cannot balance uric acid levels, resulting in slow removal of uric acid.…”

Section: Introductionmentioning

confidence: 99%

Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism

Liu

et al. 2019

Med Sci Monit

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BackgroundHyperuricemia has a pathogenic role in the development of hypertension and other cardiovascular diseases (CVD). Uric acid has been reported to activate Nod-like receptor protein 3 (NLRP3)-inflammasome and alter vascular smooth muscle cells (VSMC). However, the potential mechanisms underlying this association are still not understood. The aim of this study was to investigate the role and potential mechanisms of uric acid in proliferation of VSMC.Material/MethodsCell Counting Kit-8 (CCK-8) proliferation assay and colony formation assay were performed to determine the proliferative ability of VSMC under uric acid stimulation. Immunofluorescence microscopy was carried out to determine the expression of Alpha-smooth muscle actin (α-SMA). In addition, real-time PCR and Western blot were used to detect the expression of NLRP3-inflammasome, and ELISA was performed to measure the levels of IL-18 and IL-1β.ResultsThe results showed that uric acid increases the proliferation of VSMC and induces α-SMA accumulation. We also found that uric acid increases the level of NLRP3 and induces NLRP3-inflammasome activation. The expressions of uric acid-induced inflammatory markers IL-1β and IL-18 were decreased by the inhibitor MCC950.ConclusionsOur findings revealed that uric acid induces inflammation through NLRP3-inflammasome-mediated VSMC proliferation. NLRP3 may be a new therapeutic target for hypertension.

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Section: Introductionmentioning

confidence: 99%

Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism

Liu

et al. 2019

Med Sci Monit

View full text Add to dashboard Cite

show abstract

Hyperuricemia Is Associated With Endothelial Dysfunction and Morphological Abnormalities of Neointima After 2nd Generation Drug-Eluting Stents Deployment Assessed by Optical Coherence Tomography

Cited by 1 publication

References 0 publications

Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism

Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism

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