PMID- 20649563
OWN - NLM
STAT- MEDLINE
DCOM- 20101130
LR  - 20211020
IS  - 1476-5381 (Electronic)
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 160
IP  - 7
DP  - 2010 Aug
TI  - Endocannabinoid-like N-arachidonoyl serine is a novel pro-angiogenic mediator.
PG  - 1583-94
LID - 10.1111/j.1476-5381.2010.00841.x [doi]
AB  - BACKGROUND AND PURPOSE: N-arachidonoyl serine (ARA-S) is a recently identified 
      endocannabinoid-like lipid with weak affinity for the fully characterized 
      cannabinoid receptors (CB(1) and CB(2)) and the transient receptor potential 
      vanilloid receptor 1 (TRPV-1). ARA-S induces vasodilatation and shows 
      vasoprotective potential via activation of key signalling pathways in endothelial 
      cells. Based on these findings, the effect of ARA-S on endothelial functions was 
      further studied. EXPERIMENTAL APPROACH: Primary human dermal microvascular 
      endothelial cells (HMVEC) were used to investigate effects of ARA-S (0-10 microM) 
      on certain endothelial functions, using cell proliferation, migration and wound 
      repair models in vitro, and angiogenesis assays in vitro and ex vivo. Selective 
      CB receptor antagonists and specific siRNAs were deployed to block individual CB 
      receptors. KEY RESULTS: We found that ARA-S stimulated angiogenesis and 
      endothelial wound healing through induction of vascular endothelial growth factor 
      C and its cognate receptor expression in primary HMVEC. Moreover, knock-down of G 
      protein-coupled receptor 55 (GPR55) partly inhibited ARA-S-induced signal 
      transduction and endothelial functions. CONCLUSIONS AND IMPLICATIONS: Our results 
      indicate that ARA-S is a pro-angiogenic factor in addition to a vessel dilator. 
      The GPR55 receptor may serve as one target of ARA-S.
FAU - Zhang, X
AU  - Zhang X
AD  - Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard 
      Medical School, Boston, MA 02115, USA.
FAU - Maor, Y
AU  - Maor Y
FAU - Wang, J F
AU  - Wang JF
FAU - Kunos, G
AU  - Kunos G
FAU - Groopman, J E
AU  - Groopman JE
LA  - eng
GR  - R01 DA015008/DA/NIDA NIH HHS/United States
GR  - 1R01 DA15008-01/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Arachidonic Acids)
RN  - 0 (Cannabinoid Receptor Modulators)
RN  - 0 (Endocannabinoids)
RN  - 0 (N-arachidonoyl L-serine)
RN  - 0 (Receptor, Cannabinoid, CB1)
RN  - 0 (Receptor, Cannabinoid, CB2)
RN  - 452VLY9402 (Serine)
SB  - IM
CIN - Br J Pharmacol. 2010 Aug;160(7):1580-2. PMID: 20649562
MH  - Animals
MH  - Arachidonic Acids/*pharmacology
MH  - Cannabinoid Receptor Modulators/*pharmacology
MH  - Cattle
MH  - Cell Line
MH  - Cell Movement/drug effects
MH  - Cell Proliferation/drug effects
MH  - Chick Embryo
MH  - Chorioallantoic Membrane/blood supply/drug effects
MH  - Dose-Response Relationship, Drug
MH  - *Endocannabinoids
MH  - Endothelial Cells/drug effects/metabolism
MH  - Endothelium, Vascular/cytology/drug effects/metabolism
MH  - Humans
MH  - Neovascularization, Physiologic/*drug effects
MH  - Receptor, Cannabinoid, CB1/antagonists & inhibitors/metabolism
MH  - Receptor, Cannabinoid, CB2/antagonists & inhibitors/metabolism
MH  - Serine/*analogs & derivatives/pharmacology
MH  - Wound Healing/drug effects
PMC - PMC2936832
EDAT- 2010/07/24 06:00
MHDA- 2010/12/14 06:00
PMCR- 2011/08/01
CRDT- 2010/07/24 06:00
PHST- 2010/07/24 06:00 [entrez]
PHST- 2010/07/24 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
PHST- 2011/08/01 00:00 [pmc-release]
AID - BPH841 [pii]
AID - 10.1111/j.1476-5381.2010.00841.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 2010 Aug;160(7):1583-94. doi: 10.1111/j.1476-5381.2010.00841.x.