Dihydroartemisinin up-regulates VE-cadherin expression in human renal glomerular endothelial cells.

J Cell Mol Med

Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong, China.

Published: March 2018

The antimalarial agent dihydroartemisinin (DHA) has been shown to be anti-inflammatory. In this study, we found that DHA increased the expression of the junctional protein vascular endothelial (VE)-cadherin in human renal glomerular endothelial cells. In addition, DHA inhibited TGF-β RI-Smad2/3 signalling and its downstream effectors SNAIL and SLUG, which repress VE-cadherin gene transcription. Correspondingly, DHA decreased the binding of SNAIL and SLUG to the VE-cadherin promoter. Together, our results suggest an effect of DHA in regulating glomerular permeability by elevation of VE-cadherin expression.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824371PMC
http://dx.doi.org/10.1111/jcmm.13448DOI Listing

Publication Analysis

Top Keywords

ve-cadherin expression
8
human renal
8
renal glomerular
8
glomerular endothelial
8
endothelial cells
8
snail slug
8
ve-cadherin
5
dha
5
dihydroartemisinin up-regulates
4
up-regulates ve-cadherin
4

Similar Publications

GPR68 Mediates Lung Endothelial Dysfunction Caused by Bacterial Inflammation and Tissue Acidification.

Cells

December 2024

Division of Pulmonary and Critical Care, Department of Medicine, UMSOM Lung Biology Program, University of Maryland School of Medicine, 20 Penn Street, HSF-2, Room S143, Baltimore, MD 21201, USA.

Tissue acidification resulting from dysregulated cellular bioenergetics accompanies various inflammatory states. GPR68, along with other members of proton-sensing G protein-coupled receptors, responds to extracellular acidification and has been implicated in chronic inflammation-related diseases such as ischemia, cancer, and colitis. The present study examined the role of extracellular acidification on human pulmonary endothelial cell (EC) permeability and inflammatory status per se and investigated potential synergistic effects of acidosis on endothelial dysfunction caused by bacterial lipopolysaccharide (LPS, ).

View Article and Find Full Text PDF

Dihydrotanshinone I (DHT) is an active ingredient derived from Salvia miltiorrhiza. Previous studies have demonstrated that DHT can improve cardiac function in rats with myocardial ischemia-reperfusion injury (IR). However, the mechanism by which DHT improves myocardial injury in rats still requires further research.

View Article and Find Full Text PDF

Background: Oesophageal cancer (EC) is one of the common malignant tumors, and the prognosis of patients is poor. Further exploration of EC pathogenesis remains warranted.

Objective: The relationship between vascular epithelial cadherin (VE-cadherin) and chitinase-3-like protein 1 (CHI3L1) in EC is currently unknown.

View Article and Find Full Text PDF

Background: Preeclampsia (PE) is a pregnancy complication characterized by hypertension, proteinuria, endothelial dysfunction, and complement dysregulation. Placenta-derived extracellular vesicles (EVs), necessary in maternal-fetal communication, might contribute to PE pathogenesis. Moreover, neutrophil extracellular traps (NETs) play a pathogenic role in other complement-mediated pathologies, and their contribution in PE remains unexplored.

View Article and Find Full Text PDF

[GSK484, a PAD4 inhibitor, improves endothelial dysfunction in mice with sepsis-induced lung injury by inhibiting H3Cit expression].

Nan Fang Yi Ke Da Xue Xue Bao

December 2024

Department of Emergency Medicine, Affiliated Changsha Hospital of Xiangya School of Medicine, Central South University (Changsha First Hospital), Changsha 410005, China.

Objectives: To investigate the inhibitory effect of GSK484, a PAD4 inhibitor, on H3Cit expression following sepsis and its effects for improving sepsis-induced endothelial dysfunction.

Methods: Eighteen C57BL/6 mice were randomized into sham-operated group, sepsis model group and GSK484 treatment group (6), and in the latter two groups, models of sepsis were established by cecal ligation and puncture (CLP). The mice in GSK484 treatment group were given an intraperitoneal injection of GSK484 (4 mg/kg) on the second day following the surgery.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!