| Autor: |
Seung Hee Yang, Yong Chul Kim, Jung Nam An, Jin Hyuk Kim, Juhoh Lee, Hee-Yoon Lee, Joo-Youn Cho, Jin Ho Paik, Yun Kyu Oh, Chun Soo Lim, Yon Su Kim, Jung Pyo Lee |
| Jazyk: |
English<br />Korean |
| Rok vydání: |
2017 |
| Předmět: |
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| Zdroj: |
Kidney Research and Clinical Practice, Vol 36, Iss 4, Pp 329-341 (2017) |
| Druh dokumentu: |
article |
| ISSN: |
2211-9132 |
| DOI: |
10.23876/j.krcp.2017.36.4.329 |
| Popis: |
Background: Soluble epoxide hydrolase (sEH) expressed by endothelial cells catalyzes the metabolism of epoxyeicosatrienoic acids (EETs), which are vasoactive agents. Methods: We used a unilateral ureteral obstruction mouse model of kidney fibrosis to determine whether inhibition of sEH activity reduces fibrosis, the final common pathway for chronic kidney disease. Results: sEH activity was inhibited by continuous release of the inhibitor 12-(3-adamantan-1-ylureido)-dodecanoic acid (AUDA) for 1 or 2 weeks. Treatment with AUDA significantly ameliorated tubulointerstitial fibrosis by reducing fibroblast mobilization and enhancing endothelial cell activity. In an in vitro model of endothelial-to-mesenchymal transition (EndMT) using human vascular endothelial cells (HUVECs), AUDA prevented the morphologic changes associated with EndMT and reduced expression of fibroblast-specific protein 1. Furthermore, HUVECs activated by AUDA prevented the epithelial-to-mesenchymal transition (EMT) of tubular epithelial cells in a co-culture system. Conclusion: Our findings suggest that regulation of sEH is a potential target for therapies aimed at delaying the progression of kidney fibrosis by inhibiting EndMT and EMT. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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