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Caffeine-induced endothelial cell death and the inhibition of angiogenesis
Numerous studies have shown that adenosine or adenosine agonists can stimulate angiogenesis. However, the effect of caffeine (a known adenosine receptor antagonist) on angiogenesis has not been previously studied. Accordingly, this study was undertaken to examine the effect of caffeine on angiogenes...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Association of Anatomists
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3615613/ https://www.ncbi.nlm.nih.gov/pubmed/23560237 http://dx.doi.org/10.5115/acb.2013.46.1.57 |
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author | Li, Hua Jin, Sheng-Yu Son, Hyun-Joon Seo, Je Hoon Jeong, Goo-Bo |
author_facet | Li, Hua Jin, Sheng-Yu Son, Hyun-Joon Seo, Je Hoon Jeong, Goo-Bo |
author_sort | Li, Hua |
collection | PubMed |
description | Numerous studies have shown that adenosine or adenosine agonists can stimulate angiogenesis. However, the effect of caffeine (a known adenosine receptor antagonist) on angiogenesis has not been previously studied. Accordingly, this study was undertaken to examine the effect of caffeine on angiogenesis and to clarify the mechanism involved. Chick chorioallantoic membrane assays were used to investigate the effect of caffeine on angiogenesis and proliferation assays using human umbilical vein endothelial cells (HUVECs), were used to study its effects on specific aspects of angiogenesis. The expressions of caspase-3 and Bcl-2 were examined by western blotting, immunofluorescence staining was used to identify HUVEC morphological changes, and fluorescence activated cell sorting (FACS) and DAPI staining were used to detect HUVEC apoptosis. Caffeine was found to inhibit blood vessel formation dose-dependently and to inhibit the proliferation of HUVECs time- and dose-dependently. FACS analysis and DAPI staining showed that inhibitory effect of caffeine on HUVEC proliferation was the result of apoptosis and the up-regulation of thrombospondin-1 (TSP-1). Furthermore, TSP-1 levels were down-regulated by NECA but were unaffected by CGS21680, indicating that caffeine regulated TSP-1 expression via adenosine A(2B) receptor. In addition, caffeine up-regulated caspase-3 and down-regulated Bcl-2 at the protein level. These results suggest that the inhibitory effect of caffeine on angiogenesis is associated, at least in part, with its induction of endothelial cell apoptosis, probably mediated by a caspase-3 dependent mechanism. |
format | Online Article Text |
id | pubmed-3615613 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Korean Association of Anatomists |
record_format | MEDLINE/PubMed |
spelling | pubmed-36156132013-04-04 Caffeine-induced endothelial cell death and the inhibition of angiogenesis Li, Hua Jin, Sheng-Yu Son, Hyun-Joon Seo, Je Hoon Jeong, Goo-Bo Anat Cell Biol Original Article Numerous studies have shown that adenosine or adenosine agonists can stimulate angiogenesis. However, the effect of caffeine (a known adenosine receptor antagonist) on angiogenesis has not been previously studied. Accordingly, this study was undertaken to examine the effect of caffeine on angiogenesis and to clarify the mechanism involved. Chick chorioallantoic membrane assays were used to investigate the effect of caffeine on angiogenesis and proliferation assays using human umbilical vein endothelial cells (HUVECs), were used to study its effects on specific aspects of angiogenesis. The expressions of caspase-3 and Bcl-2 were examined by western blotting, immunofluorescence staining was used to identify HUVEC morphological changes, and fluorescence activated cell sorting (FACS) and DAPI staining were used to detect HUVEC apoptosis. Caffeine was found to inhibit blood vessel formation dose-dependently and to inhibit the proliferation of HUVECs time- and dose-dependently. FACS analysis and DAPI staining showed that inhibitory effect of caffeine on HUVEC proliferation was the result of apoptosis and the up-regulation of thrombospondin-1 (TSP-1). Furthermore, TSP-1 levels were down-regulated by NECA but were unaffected by CGS21680, indicating that caffeine regulated TSP-1 expression via adenosine A(2B) receptor. In addition, caffeine up-regulated caspase-3 and down-regulated Bcl-2 at the protein level. These results suggest that the inhibitory effect of caffeine on angiogenesis is associated, at least in part, with its induction of endothelial cell apoptosis, probably mediated by a caspase-3 dependent mechanism. Korean Association of Anatomists 2013-03 2013-03-25 /pmc/articles/PMC3615613/ /pubmed/23560237 http://dx.doi.org/10.5115/acb.2013.46.1.57 Text en Copyright © 2013. Anatomy & Cell Biology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Li, Hua Jin, Sheng-Yu Son, Hyun-Joon Seo, Je Hoon Jeong, Goo-Bo Caffeine-induced endothelial cell death and the inhibition of angiogenesis |
title | Caffeine-induced endothelial cell death and the inhibition of angiogenesis |
title_full | Caffeine-induced endothelial cell death and the inhibition of angiogenesis |
title_fullStr | Caffeine-induced endothelial cell death and the inhibition of angiogenesis |
title_full_unstemmed | Caffeine-induced endothelial cell death and the inhibition of angiogenesis |
title_short | Caffeine-induced endothelial cell death and the inhibition of angiogenesis |
title_sort | caffeine-induced endothelial cell death and the inhibition of angiogenesis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3615613/ https://www.ncbi.nlm.nih.gov/pubmed/23560237 http://dx.doi.org/10.5115/acb.2013.46.1.57 |
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