Laboratory
of Vascular BiologyLaboratory
of Vascular Biology
Highlights
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Congratulations to Srividya Velagapudi for receiving an Award in the 17th Cardiovascular research and clinical implications meeting, Murten, Switzerland, October 6-7, 2011 : "best oral presentation" |
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The study on the role of S6K1 in vascular aging and the anti-vascular aging effect of resveratrol goes to University Press: http://www.unifr.ch/scm/de/news/7045/ |
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Congratulations to Angana Gupta Rajapakse for receiving the Asher-Hess Prize at the Annual Meeting of the Swiss Physiological Society, September 9, 2009 in Berne and the best oral presentation prize at the 15th Cardiovascular Biology and Clinical Implications Meeting, October 1-2, 2009 in Muntelier. |
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Congratulations for Dr. Xiu-Fen Ming’s successful Habilitation-Thesis defence! 19.11.2008 |
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A loud thunder without storm!
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Please read (http://www.biomedcentral.com/1471-2261/5/22 or http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16018822).
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Photo gallery Cheers!!! |
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The
group of Vascular Biology received
Pfizer-Research-Prize 2005
for the domain of “Heart and Circulation
– Basic Research”. The
ceremony will take place on
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An unfair tug-of-war causes atherosclerotic endothelial dysfunction |
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Competition between arginase and eNOS for the substrate L-arginine in endothelial cells decreases NO production, which represents a novel mechanism for atherosclerotic endothelial dysfunction and may explain the controversy of supplemental L-arginine therapy in patients with coronary heart disease. Please see more details in the study published by Ming X-F. et al, Circulation. 2004;110:3708-3714 and a commentary by Yang Z published in the website of International Atherosclerosis Society (www.athero.org). |
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A Novel Vascular Protective Function of HDL Uncovered |
| High density lipoprotein
(HDL) exerts many cardiovascular protective effects beyond reverse cholesterol
transport. Our most recent study explored a novel beneficial effect on vascular
endothelial cells namely inhibition of tissue factor expression. This function
may importantly contribute to the anti-atherothrombotic effects of the lipid.
Please see more details in the study published by Viswambharan H. et al, Circ
Res. 2004;94:918-925. This study was selected to be featured on MDLinx on |
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Say NO to Venous Bypass Graft |
| The study in
collaboration with Cardiovascular Research Group, Cardiology, University
Hospital Zürich (Tanner
et al., J Thorac Cardiovasc Surg) demonstrates the efficacy of ex
vivo eNOS gene transfer in inhibition of the biological features of human
venous bypass graft disease. Local overexpression of eNOS gene may prove
beneficial for venous bypass graft function. This study further supports the
therapeutic rationale of eNOS gene transfer for preventing human venous bypass
graft disease in patients. |
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Too much NO in sleeping sickness |
| Excessive endothelial NO production in the unfashionable sleeping sickness. What does this mean? Please see the publication by Viswambharan et al, Inter J Parasitol. | |
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A destructive cross-talk between Rho/Rho-Kinase and Akt/eNOS causes vascular endothelial dysfunction. |
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Our recent research (Ming
et al, Mol Cell Biol and Barandier
et al, Biophy Biochem Res Comm) demonstrates that
Rho/Rho-kinase impairs endothelial function not only via suppression of the
vascular protective eNOS gene expression, but also inactivates eNOS enzyme
activity through inhibition of PKB/Akt. Statins inhibit Rho/Rho-kinase pathway,
which therefore on one hand enhances endothelial NO release acutely through
recovery of eNOS activity, and on the other hand prevents eNOS gene
down-regulation chronically. These mechanisms may contribute to the beneficial
effects of statins in patients with coronary artery disease. |
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