search button
Open Access

NEDD4 attenuates oxidized low‑density lipoprotein‑induced inflammation and dysfunction in vascular endothelial cells via regulating APEX1 expression

  • Authors:
    • Huiyu Xu
    • Lijuan Tan
    • Qiaofang Qu
    • Wutang Zhang

  • View Affiliations

  • Published online on: January 4, 2023     https://doi.org/10.3892/etm.2023.11787
  • Article Number: 88

  • Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Atherosclerosis chiefly results from inflammation as well as vascular endothelial cell dysfunction. Methylation levels of neuronally expressed developmentally downregulated 4 (NEDD4) were found to be fortified in atherosclerosis patients and NEDD4 deficiency enhanced vascular calcification. However, the exact function of NEDD4 in inflammation and vascular endothelial dysfunction remains to be elucidated. In the present study, CCK‑8 assay was used to estimate cell viability. Reverse transcription‑quantitative PCR was adopted to examine the expression of NEDD4, inflammation‑associated enzymes and apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1). Western blotting was used to test NEDD4, endothelial nitric oxide synthase, inducible nitric oxide synthase and APEX1 protein levels. Cytotoxicity was detected by a lactate dehydrogenase (LDH) kit. Reactive oxygen species level was tested by a corresponding kit. Vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 contents were examined with ELISA. Cell adhesion assays evaluated the adhesion of endothelial cells. Co‑immunoprecipitation assay was used to test the relationship between NEDD4 and APEX1. The data revealed that NEDD4 expression rapidly declined in oxidized low density lipoprotein (ox‑LDL)‑induced human umbilical vein endothelial cells (HUVECs). Following NEDD4 overexpression, the active damage, inflammatory release and endothelial cell dysfunction in ox‑LDL‑induced HUVECs were attenuated. After co‑transfection of APEX1 interference plasmids and NEDD4 overexpression plasmids, cell damage, inflammatory release and endothelial cell dysfunction in ox‑LDL‑induced HUVECs were improved again. Taken together, NEDD4 attenuated ox‑LDL‑induced inflammation and endothelial dysfunction by regulating APEX1 expression.
View Figures
View References

Related Articles

Journal Cover

February-2023
Volume 25 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

  • Journal Metrics
  • Impact Factor: 2.7
  • Ranked Medicine Research and Experimental
    (total number of cites)
International Symposium on Molecular Medicine Conference Banner
The Cancer Story
World Congress on Advances in Oncology and International Symposium on Molecular Medicine Conference Banner
World Academy Of Sciences Banner
Heyday Road Banner

0

Copy and paste a formatted citation
x
Spandidos Publications style
Xu H, Tan L, Qu Q and Zhang W: NEDD4 attenuates oxidized low‑density lipoprotein‑induced inflammation and dysfunction in vascular endothelial cells via regulating APEX1 expression. Exp Ther Med 25: 88, 2023
APA
Xu, H., Tan, L., Qu, Q., & Zhang, W. (2023). NEDD4 attenuates oxidized low‑density lipoprotein‑induced inflammation and dysfunction in vascular endothelial cells via regulating APEX1 expression. Experimental and Therapeutic Medicine, 25, 88. https://doi.org/10.3892/etm.2023.11787
MLA
Xu, H., Tan, L., Qu, Q., Zhang, W."NEDD4 attenuates oxidized low‑density lipoprotein‑induced inflammation and dysfunction in vascular endothelial cells via regulating APEX1 expression". Experimental and Therapeutic Medicine 25.2 (2023): 88.
Chicago
Xu, H., Tan, L., Qu, Q., Zhang, W."NEDD4 attenuates oxidized low‑density lipoprotein‑induced inflammation and dysfunction in vascular endothelial cells via regulating APEX1 expression". Experimental and Therapeutic Medicine 25, no. 2 (2023): 88. https://doi.org/10.3892/etm.2023.11787