Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/114097
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Type: Journal article
Title: The aquaporin 1 inhibitor bacopaside II reduces endothelial cell migration and tubulogenesis and induces apoptosis
Author: Palethorpe, H.
Tomita, Y.
Smith, E.
Pei, J.
Townsend, A.
Price, T.
Young, J.
Yool, A.
Hardingham, J.
Citation: International Journal of Molecular Sciences, 2018; 19(3):653-1-653-10
Publisher: MDPI AG
Issue Date: 2018
ISSN: 1661-6596
1422-0067
Statement of
Responsibility: 
Helen M. Palethorpe, Yoko Tomita, Eric Smith, Jinxin V. Pei, Amanda R. Townsend, Timothy J. Price, Joanne P. Young, Andrea J. Yool and Jennifer E. Hardingham
Abstract: Expression of aquaporin-1 (AQP1) in endothelial cells is critical for their migration and angiogenesis in cancer. We tested the AQP1 inhibitor, bacopaside II, derived from medicinal plant Bacopa monnieri, on endothelial cell migration and tube-formation in vitro using mouse endothelial cell lines (2H11 and 3B11) and human umbilical vein endothelial cells (HUVEC). The effect of bacopaside II on viability, apoptosis, migration and tubulogenesis was assessed by a proliferation assay, annexin-V/propidium iodide flow cytometry, the scratch wound assay and endothelial tube-formation, respectively. Cell viability was reduced significantly for 2H11 at 15 μM (p = 0.037), 3B11 at 12.5 μM (p = 0.017) and HUVEC at 10 μM (p < 0.0001). At 15 μM, the reduced viability was accompanied by an increase in apoptosis of 38%, 50% and 32% for 2H11, 3B11 and HUVEC, respectively. Bacopaside II at ≥10 μM significantly reduced migration of 2H11 (p = 0.0002) and 3B11 (p = 0.034). HUVECs were most sensitive with a significant reduction at ≥7.5 μM (p = 0.037). Tube-formation was reduced with a 15 μM dose for all cell lines and 10 μM for 3B11 (p < 0.0001). These results suggest that bacopaside II is a potential anti-angiogenic agent.
Keywords: angiogenesis; aquaporin-1 (AQP1); bacopaside II; endothelial cell migration
Description: Published: 26 February 2018
Rights: © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
RMID: 0030083310
DOI: 10.3390/ijms19030653
Grant ID: http://purl.org/au-research/grants/arc/DP160104641
Appears in Collections:IPAS publications
Medicine publications

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