Bibliographic Details
| Title: |
TRPV1 mediates cellular uptake of anandamide and thus promotes endothelial cell proliferation and network-formation |
| Authors: |
Nicole A. Hofmann, Sonja Barth, Markus Waldeck-Weiermair, Christiane Klec, Dirk Strunk, Roland Malli, Wolfgang F. Graier |
| Source: |
Biology Open, Vol 3, Iss 12, Pp 1164-1172 (2014) |
| Publisher Information: |
The Company of Biologists, 2014. |
| Publication Year: |
2014 |
| Collection: |
LCC:Science
LCC:Biology (General) |
| Subject Terms: |
transient receptor potential vanilloid 1, TRPV1, anandamide, AEA, endothelial colony-forming cells, ECFC, anandamide transport, proliferation, network-formation, angiogenesis, Science, Biology (General), QH301-705.5 |
| More Details: |
Anandamide (N-arachidonyl ethanolamide, AEA) is an endogenous cannabinoid that is involved in various pathological conditions, including cardiovascular diseases and tumor-angiogenesis. Herein, we tested the involvement of classical cannabinoid receptors (CBRs) and the Ca2+-channel transient receptor potential vanilloid 1 (TRPV1) on cellular AEA uptake and its effect on endothelial cell proliferation and network-formation. Uptake of the fluorescence-labeled anandamide (SKM4-45-1) was monitored in human endothelial colony-forming cells (ECFCs) and a human endothelial-vein cell line (EA.hy926). Involvement of the receptors during AEA translocation was determined by selective pharmacological inhibition (AM251, SR144528, CID16020046, SB366791) and molecular interference by TRPV1-selective siRNA-mediated knock-down and TRPV1 overexpression. We show that exclusively TRPV1 contributes essentially to AEA transport into endothelial cells in a Ca2+-independent manner. This TRPV1 function is a prerequisite for AEA-induced endothelial cell proliferation and network-formation. Our findings point to a so far unknown moonlighting function of TRPV1 as Ca2+-independent contributor/regulator of AEA uptake. We propose TRPV1 as representing a promising target for development of pharmacological therapies against AEA-triggered endothelial cell functions, including their stimulatory effect on tumor-angiogenesis. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2046-6390 |
| Relation: |
http://bio.biologists.org/content/3/12/1164; https://doaj.org/toc/2046-6390 |
| DOI: |
10.1242/bio.20149571 |
| Access URL: |
https://doaj.org/article/cae6cf2799d94644b226c608992c7f4e |
| Accession Number: |
edsdoj.6cf2799d94644b226c608992c7f4e |
| Database: |
Directory of Open Access Journals |
