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1 Department of Pharmacology, Rush Presbyterian St. Luke's Medical Center, Chicago, IL, USA
2 Department of Surgery, Cook County Hospital, Chicago, IL, USA
3 Department of Medicine, Rush Presbyterian St. Luke's Medical Center, Chicago, IL, USA
4 Department of Pediatrics, The Johns Hopkins University, Baltimore, MD, USA
5 Department of Medicine, Cook County Hospital, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: hlum{at}rush.edu.
The atherogenic serum lysophosphatidylcholine (LPC) is known to mediate vascular endothelial responses ranging from upregulation of adhesion molecules and growth factors to secretion of chemokines and superoxide anion. We investigated whether endothelial cells express receptors for LPC, which may account for their actions. Human brain microvascular (HBMEC) and dermal microvascular endothelial cells (HMEC) were prepared for RT-PCR analysis for possible expression of the G protein-coupled receptors, GPR4 and G2A, which are believed to be specific LPC receptors. Results indicated that HBMEC expressed low basal GPR4 mRNA, but stimulation with TNF
(100 U/ml) or H2O2 (50 µmol/L) for 2 hr or overnight upregulated expression several-fold. In contrast, HMEC expressed high basal GPR4 mRNA, which was not further increased by either TNF nor H2O2 stimulation. Another LPC receptor, G2A, was not detected in either endothelial cell type. Competition binding studies were made to evaluate specific binding of 3H-LPC to the intact endothelial cell monolayer. Basal specific 3H-LPC binding in HBMEC was ~8-times lower than in HMEC; however, TNF or H2O2 stimulation increased 3H-LPC binding on HMBEC, but not HMEC. The results indicated that GPR4 expression was consistent with specific 3H-LPC binding. Overall, we report that endothelial cells selectively expressed GPR4, a specific LPC receptor. Further, GPR4 expression by HBMEC, but not HMEC, was increased by inflammatory stresses. We conclude that endogenous GPR4 in endothelial cells may be a potential G protein-coupled receptor by which LPC signals pro-inflammatory activities.
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