Send to

Choose Destination
See comment in PubMed Commons below
Sci Rep. 2013 Nov 20;3:3274. doi: 10.1038/srep03274.

Cysteinyl leukotrienes regulate endothelial cell inflammatory and proliferative signals through CysLT₂ and CysLT₁ receptors.

Author information

Department of Chemistry, University of Akron, OH 44325.


Cysteinyl leukotrienes (cys-LTs), LTC₄, LTD₄, LTE₄ are potent inflammatory lipid mediators that act through two distinct G-protein-coupled receptors, CysLT₁R and CysLT₂R. Although cys-LTs are shown to induce vascular leakage and atherosclerosis, the molecular mechanism by which cys-LTs modulate endothelial function is not known. Here, we show that cys-LTs (LTC₄ and LTD₄) induce robust calcium influx in human umbilical vein endothelial cells (HUVECs) through CysLT₂R, but not CysLT₁R. Further, cys-LT treatment induced endothelial cell (EC) contraction leading to monolayer disruption via CysLT₂R/Rho kinase dependent pathway. Furthermore, stimulation with cys-LTs potentiated TNFα-induced VCAM-1 expression and leukocyte recruitment to ECs through CysLT₂R. In contrast, we found that both LTC₄ and LTD₄ stimulated EC proliferation through CysLT₁R. Taken together, these results suggest that cys-LTs induce endothelial inflammation and proliferation via CysLT₂R/Rho kinase and CysLT₁R/Erk dependent pathways, respectively, which play critical role in the etiology of cardiovascular diseases such as atherosclerosis and myocardial infarction.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group Icon for PubMed Central
    Loading ...
    Support Center