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Uric acid induced the phenotype transition of vascular endothelial cells via induction of oxidative stress and glycocalyx shedding

Title
Uric acid induced the phenotype transition of vascular endothelial cells via induction of oxidative stress and glycocalyx shedding
Authors
Ko, JiyeonKang, Hyun-JungKim, Dal-AhKim, Mi-JinRyu, Eun-SunLee, ShinaRyu, Jung-HwaRoncal, CarlosJohnson, Richard J.Kang, Duk-Hee
Ewha Authors
강덕희김달아류정화
SCOPUS Author ID
강덕희scopus; 김달아scopus
Issue Date
2019
Journal Title
FASEB JOURNAL
ISSN
0892-6638JCR Link

1530-6860JCR Link
Citation
FASEB JOURNAL vol. 33, no. 12, pp. 13334 - 13345
Keywords
EndoMTreactive oxygen specieshyperuricemiasyndecan-1
Publisher
FEDERATION AMER SOC EXP BIOL
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
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.
DOI
10.1096/fj.201901148R
Appears in Collections:
의과대학 > 의학과 > Journal papers
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