Journal
VASCULAR PHARMACOLOGY
Volume 62, Issue 3, Pages 150-161Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.vph.2014.05.010
Keywords
Endothelial regeneration and repair; LXR; EPCs; Proliferation; Migration
Categories
Funding
- National Natural Science Foundation of China [81100112, 81300153]
- Chongqing Key Laboratory (CSTC) [2011C253]
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Vascular endothelial injury is a major cause of many cardiovascular diseases. The proliferation and migration of endothelial progenitor cells (EPCs) play a pivotal role in endothelial regeneration and repair after vascular injury. Recently, liver X receptor (LXR) activation has been suggested as a potential target for novel therapeutic interventions in the treatment of cardiovascular disease. However, the effects of LXR activation on endothelial regeneration and repair, as well as EPC function, have not been investigated. In the present study, we demonstrate that LXRs, including LXR alpha and LXR beta, are expressed and functional in rat bone marrow-derived EPCs. Treatment with an LXR agonist, TO901317 (TO) or GW3965 (GW), significantly increased the proliferation and migration of EPCs, as well as Akt and eNOS phospholylation in EPCs. Moreover, LXR agonist treatment enhanced the expression and secretion of vascular endothelial growth factor in EPCs. LXR agonists accelerated re-endothelialization in injured mouse carotid arteries in vivo. These data confirm that LXR activation may improve EPC function and endothelial regeneration and repair after vascular injury by activating the PI3K/Akt/eNOS pathway. We conclude that LXRs may be attractive targets for drug development in the treatment of cardiovascular diseases associated with vascular injury. (C) 2014 Elsevier Inc. All rights reserved.
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