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Uric acid induced the phenotype transition of vascular endothelial cells via induction of oxidative stress and glycocalyx shedding
- Uric acid induced the phenotype transition of vascular endothelial cells via induction of oxidative stress and glycocalyx shedding
- Ko, Jiyeon; Kang, Hyun-Jung; Kim, Dal-Ah; Kim, Mi-Jin; Ryu, Eun-Sun; Lee, Shina; Ryu, Jung-Hwa; Roncal, Carlos; Johnson, Richard J.; Kang, Duk-Hee
- Ewha Authors
- 강덕희; 김달아; 류정화
- SCOPUS Author ID
- 강덕희; 김달아
- Issue Date
- Journal Title
- FASEB JOURNAL
- FASEB JOURNAL vol. 33, no. 12, pp. 13334 - 13345
- EndoMT; reactive oxygen species; hyperuricemia; syndecan-1
- FEDERATION AMER SOC EXP BIOL
- SCIE; SCOPUS
- Document Type
- Recent data suggested a causative role of uric acid (UA) in the development of renal disease, in which endothelial dysfunction is regarded as the key mechanism. Endothelial-to-mesenchymal transition (EndoMT) and shedding of the glycocalyx are early changes of endothelial dysfunction. We investigated whether UA induced EndoMT in HUVECs and an animal model of hyperuricemia fed with 2% oxonic acid for 4 wk. UA induced EndoMT in HUVECs with a generation of reactive oxygen species via the activation of membranous NADPH oxidase (from 15 min) and mitochondria (from 6 h) along with glycocalyx shedding (from 6 h), which were blocked by probenecid. GM6001, an inhibitor of matrix metalloproteinase, alleviated UA-induced glycocalyx shedding and EndoMT. Antioxidants including N-acetyl cysteine, apocynin, and mitotempo ameliorated EndoMT; however, they did not change glycocalyx shedding in HUVECs. In the kidney of hyperuricemic rats, endothelial staining in peritubular capillaries (PTCs) was substantially decreased with a de novo expression of alpha-smooth muscle actin in PTCs. Plasma level of syndecan-1 was increased in hyperuricemic rats, which was ameliorated by allopurinol. UA caused a phenotypic transition of endothelial cells via induction of oxidative stress with glycocalyx shedding, which could be one of the mechanisms of UA-induced endothelial dysfunction and kidney disease.
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