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Cannabinoid‐1 receptor activation induces reactive oxygen species‐dependent and ‐independent mitogen‐activated protein kinase activation and cell death in human coronary artery endothelial cells
Author(s) -
Rajesh Mohanraj,
Mukhopadhyay Partha,
Haskó György,
Liaudet Lucas,
Mackie Ken,
Pacher Pál
Publication year - 2010
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2010.00712.x
Subject(s) - mapk/erk pathway , microbiology and biotechnology , cannabinoid receptor , signal transduction , p38 mitogen activated protein kinases , programmed cell death , protein kinase a , reactive oxygen species , biology , chemistry , kinase , receptor , biochemistry , apoptosis , agonist
Impaired endothelial activity and/or cell death play a critical role in the development of vascular dysfunction associated with congestive heart failure, diabetic complications, hypertension, coronary artery disease and atherosclerosis. Increasing evidence suggests that cannabinoid 1 (CB(1)) receptor inhibition is beneficial in atherosclerosis and cardiovascular inflammation both in experimental models, as well as in humans. Here, we investigated the effects of CB(1) receptor activation with the endocannabinoid anandamide (AEA) or synthetic agonist HU210 on cell death and interrelated signal transduction pathways in human primary coronary artery endothelial cells (HCAECs).