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Volume 6, Issue 6(Suppl)
J Clin Toxicol 2016
ISSN: 2161-0495, JCT an open access journal
Page 43
Notes:
Euro Toxicology 2016
October 24-26, 2016
conferenceseries
.com
Toxicology & Applied Pharmacology
October 24-26, 2016 Rome, Italy
7
th
Euro-Global Summit on
The insect repellent N,N-diethyl-m-toluamide (DEET) induces angiogenesis via allosteric
modulation of the M3 muscarinic receptor in endothelial cells
Samuel Legeay
University of Angers, France
T
he insect repellent N,N-diethyl-m-toluamide (DEET) has been reported to inhibit AChE (acetylcholinesterase) and
to be associated with increased risk of cancer. In the present paper, we demonstrate that DEET specifically stimulates
endothelial cells that promote angiogenesis which increases tumor growth
in vivo
. DEET activates cellular processes that lead
to angiogenesis including proliferation, migration and adhesion. This is associated with an enhancement of NO production
and VEGF expression in endothelial cells. M3 silencing or the use of a pharmacological M3 inhibitor abrogates all of these
effects which reveals that DEET-induced angiogenesis is M3 sensitive. The experiments involving calcium signals in both
endothelial and HEK cells overexpressing M3 receptors, as well as binding and docking studies demonstrate that DEET acts as
an allosteric modulator of the M3 receptor. In addition, DEET inhibited AChE which increased acetylcholine bioavailability
and binding to M3 receptors and also strengthened pro-angiogenic effects by an allosteric modulation.
Biography
Samuel Legeay is a PharmD PhD student at the University of Angers in France (west part of France). He worked mainly on two different subjects: In USA at
Augusta University (Georgia) on the regulation of hypertension in diabetic conditions and at the University of Angers (France) on the impact of mosquito repellents
in angiogenesis. He has 2 published articles in PubMed and 1 book chapter and is a member of the French Society of Pharmacology and Therapeutics.
salegeay@gmail.comSamuel Legeay, J Clin Toxicol 2016, 6:6(Suppl)
http://dx.doi.org/10.4172/2161-0495.C1.021