Biomedical subjects

Beatriz Martínez-Poveda

Publications and source records attributed to Beatriz Martínez-Poveda.

5 recordsLinked to original sources

PubMed2006

Hyperforin: more than an antidepressant bioactive compound?

Hyperforin is a lipophilic compound that is present in great amounts in St. John's wort and that has been described as the main responsible for the antidepressant effects of this medicinal plant. In the last few years, evidence has accumulated pointing to other different effects of hyperforin with potential pharmacological interest. They include other neurological effects, effects on inflammation, as well as antibacterial, antitumoral and antiangiogenic effects.

Angiogenesis Inhibitors↗

PubMed2005

Hyperforin, a bio-active compound of St. John's Wort, is a new inhibitor of angiogenesis targeting several key steps of the process.

Hyperforin, a phloroglucinol derivative found in St. John's wort related mainly to its antidepressant effects, has been reported recently to induce apoptosis in tumour cells and to inhibit cancer invasion and metastasis. We show that hyperforin inhibits angiogenesis in vitro in bovine aortic endothelial cells and in vivo in the chorioallantoic membrane assay. In a variety of experimental systems representing the sequential events of the angiogenic process, hyperforin treatment of endothelial cells resulted in strong inhibitory effects. Hyperforin inhibited the growth of endothelial cells in culture. Capillary tube formation on Matrigel was abrogated completely by addition of hypeforin at the low micromolar range. Hyperforin also exhibited a clear inhibitory effect on the invasive capabilities of endothelial cells. Zymographic assays showed that hyperforin treatment produced a complete inhibition of urokinase and a remarkable inhibition of matrix metalloproteinase 2. Our data indicates that hyperforin is a compound that interferes with key events in angiogenesis, confirming the recent and growing evidence about a potential role of this compound in cancer and metastasis inhibition and making it a promising drug for further evaluation in the treatment of angiogenesis-related pathologies.

3T3 Cells↗

PubMed2005

Hypericin in the dark inhibits key steps of angiogenesis in vitro.

Photoactivated hypericin has a potent cytotoxic effect over a wide range of cells. However, very recently hypericin has been shown to have antitumoral and antimetastatic effects in the dark. The aim of this study was to test whether hypericin in the dark affects angiogenesis. Different in vitro assays were used to study the potential effects of this compound on key steps of angiogenesis, namely, a colorimetric assay of cell proliferation/viability, a tubular formation on Matrigel assay, zymographic assays for gelatinases and urokinase, a wound assay for migration and a fluorometric assay for invasion through Matrigel. In this report, we show for the first time that hypericin kept in the dark inhibits several key steps of the angiogenic process, namely, bovine endothelial cell proliferation, formation of tubular-like structures on Matrigel, migration and invasion, as well as extracellular matrix degrading urokinase.

Angiogenesis Inhibitors↗

PubMed2003

An in vitro evaluation of the effects of homocysteine thiolactone on key steps of angiogenesis and tumor invasion.

Homocysteine thiolactone is a highly reactive homocysteine derivative that can react easily with proteins. Protein homocysteinylation has been suggested as a possible mechanism underlying the pathological consequences of impaired homocysteine metabolism. Homocysteine inhibits key steps of angiogenesis and tumor invasion. It can be hypothesized that homocysteine thiolactone could mimic the described anti-angiogenic and anti-invasive effects of homocysteine. Therefore, we studied the effects of homocysteine thiolactone on different key steps of angiogenesis and tumor invasion, using model endothelial and tumor cell lines. This study demonstrates that homocysteine thiolactone, in high contrast to homocysteine, is not an anti-angiogenic compound. Furthermore, our results suggest that homocysteine thiolactone could behave as a pro-angiogenic compound.

Angiogenesis Inducing Agents↗

PubMed2002

Anti-angiogenic effects of homocysteine on cultured endothelial cells.

High levels of homocysteine induce a sustained injury on arterial endothelial cells which accelerates the development of thrombosis and atherosclerosis. Some of the described effects of homocysteine on endothelial cells are features shared with an anti-angiogenic response. Therefore, we studied the effects of homocysteine on key steps of angiogenesis using bovine aorta endothelial cells as a model. Homocysteine decreased proliferation and induced differentiation. Furthermore, 5 mM homocysteine produced strong inhibitions of matrix metalloproteinase-2 and urokinase, two proteolytic activities that play a key role in extracellular matrix re-modeling, and decreased migration and invasion, other two key steps of angiogenesis. This study demonstrates that homocysteine can inhibit several steps of the angiogenic process.

Animals↗