| ORIGINAL ARTICLE |
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| Year : 2022 | Volume
: 5
| Issue : 3 | Page : 80-87 |
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The role of RAGE, MAPK and NF-κB pathway in the advanced glycation end-products induced HUVECs dysfunction
Xun Wang, Yi-Shu Wang, Qing-Long Zeng, Chen-Yang Qiu, Yang-Yan He, Zi-Heng Wu, Yun-Jun He, Tao Shang, Hong-Kun Zhang, Qian-Qian Zhu, Dong-Lin Li
Department of Vascular Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
Correspondence Address:
Dr. Dong-Lin Li
Department of Vascular Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou
China
Dr. Qian-Qian Zhu
Department of Vascular Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou
China
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/2589-9686.360874
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OBJECTIVE: The objective of this study was to investigate how receptor for advanced glycation end-products–mitogen-activated protein kinase–nuclear factor-kappa B (MAPK-NF-κB) pathway is involved in advanced glycation end-product (AGE)-induced human umbilical venous endothelial cell (HUVEC) dysfunction.
MATERIALS AND METHODS: HUVECs were cultured with AGEs, anti-RAGE, inhibitors of MAPK or NF-κB respectively. Then we detected endothelial nitric oxide synthase (eNOS) activation, nitric oxide (NO) concentration, cell migration ability, and RAGE expression of HUVECs.
RESULTS: AGEs depressed eNOS activation, decreased NO concentration, impaired endothelial cell (EC) migration, and upregulated RAGE expression, which could be recovered by p38 inhibitor and extracellular regulated protein kinases (ERK) inhibitor. However, these effects could not be recovered by NF-κB inhibitor.
CONCLUSIONS: AGEs increase RAGE expression and decrease NO release and migration of HUVECs through RAGE-MAPK pathway, but not NF-κB pathway.
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