2. Academic Validation
  3. Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling

Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling

  • Exp Ther Med. 2022 May;23(5):355. doi: 10.3892/etm.2022.11282.
Xiaorui Li 1,  Xiao Li 2,  Rong Sun 3 4,  Mei Gao 5,  Hui Wang 6
Affiliations

Affiliations

  • 1 Public Health Clinical Center Affiliated to Shandong University, Jinan, Shandong 250100, P.R. China.
  • 2 Department of Pathophysiology, School of Traditional Chinese Medicine, Shandong University of Traditional Medicine, Jinan, Shandong 250014, P.R. China.
  • 3 Advanced Medical Research Institute, Shandong University, Jinan, Shandong 250014, P.R. China.
  • 4 Institute of Basic Medical Sciences, The Second Hospital of Shandong University, Jinan, Shandong 250031, P.R. China.
  • 5 Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Department of Cardiology, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Jinan, Shandong 250014, P.R. China.
  • 6 Key Laboratory of Molecular and Nano Probes, Institute of Biomedical Sciences, Collaborative Innovation Center of Functionalized Probes for Chemical Imaging in Universities of Shandong, College of Chemistry, Chemical Engineering and Materials Science, Shandong Normal University, Ministry of Education, Jinan, Shandong 250014, P.R. China.
PMID: 35481222 DOI: 10.3892/etm.2022.11282
Abstract

Vascular endothelium is a target of cadmium (Cd), which is a global pollutant of the environment. However, the detailed effects and underlying mechanisms remain to be elucidated. In the present study, human umbilical vein endothelial cells (HUVECs) were treated with 0.1, 1, 5, 10, 50 µM cadmium chloride (CdCl2) for 12 h. It was found that vascular endothelial (VE)-cadherin mRNA and protein expression was upregulated by Cd in HUVECs in a dose-dependent manner. Higher levels of VE-cadherin were detected at cell-to-cell junctions in HUVECs treated with 10 µM CdCl2 compared with normal condition. The phosphorylation level of myosin-binding subunit of myosin Phosphatase, a downstream substrate of Rho-associated protein kinase (ROCK), was reduced by 10 µM CdCl2, suggesting that Cd inhibited the Rho/ROCK pathway. Activation of ROCK by narciclasine reversed the Cd-induced increase of VE-cadherin expression. By contrast, ROCK pathway inhibitor Y27632 increased VE-cadherin expression in HUVECs. Following inhibition of the ROCK pathway, Cd did not significantly alter the level of VE-cadherin. Taken together, the results suggested that Cd exposure enhanced VE-cadherin expression in endothelial cells via suppression of ROCK signaling.

Keywords

Rho-associated protein kinase; cadmium; endothelial cells; vascular endothelial cadherin.

Figures
Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-16563
    99.88%, ROCK激动剂
嗨！很高兴为您提供帮助！

尊敬的 MCE 客户您好，
请您选择所在区域，我们将转接对应客服为您服务！

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

热 A B C F G H J L N Q S T X Y Z