Welcome to the home of Vascular Research at Aston University.
Our team are dedicated to conducting high-quality research in the field of vascular medicine, with extensive experience in angiogenesis and vascular protection. We hope that our current and future research will make a lasting contribution to theoretical and clinical approaches to vascular disorders.
Here you can find information about our research team and the work they do, plus links to our published articles and media coverage of our findings. Also check out the ‘Home’ page for updates about our latest research findings and recent developments in vascular science.
Follow us on Twitter @VascularAston
Aston University is a long established research-led institution known for its world-class teaching quality and strong links to industry, government and commerce. It is based in the heart of Birmingham, home to over 65,000 students and one of Europe’s liveliest and most welcoming cities. With a burgeoning reputation for producing high-quality research and an ambitious, forward-thinking outlook, Aston is an institution with great future prospects.
“Teaching and research excellence remain focused on a select portfolio of subjects aligned to the needs of the 21st Century and which address priority areas for business and society locally, nationally and internationally. The University has continued to develop its excellent national reputation and is seeking to enhance its international standing”
In addition to maintaining a strong focus on high-quality research work, Aston is committed to widening participation in higher education. The University seeks to ensure that it is truly representative of the community it serves and that students from all backgrounds are given the opportunity to receive a first-class education.
“Aston’s policy has been to expand and widen participation without compromising academic standards. The University’s impressive track record in widening participation is one of which we are extremely proud. In 2007/08, 57% of new entrants were from ethnic minorities, 91.4% were from state schools/colleges, 11.3% were from low participation neighbourhoods, and 2.3% were in receipt of Disabled Students Allowance. Aston’s Widening Participation Strategy has been to provide support to students throughout the student life cycle, from aspiration raising in primary schools through to student graduation and employment”
At Aston we are constantly striving to approach social inequalities in new and innovative ways, providing access to education for students from hard-to-reach areas with the aim of improving routes into employment and benefiting local communities. We feel passionately about social deprivation and are keen to address health inequalities within society; we believe that one of the ways in which we can help to improve the quality of life experienced by residents of low-income areas is to facilitate the training of medical professionals from these localities.
In the future we hope to help more individuals from low-income backgrounds receive the best possible training, making higher education and the medical profession more accessible and socially representative. In doing so we hope to improve social mobility prospects and reduce the effects of social deprivation by improving local healthcare.
Vascular Research at Aston
The Vascular Research team is relatively new to the University; however it has already made a significant contribution to Aston’s research output. Our research interests are primarily focused on the vascular basis of diseases, particularly in the areas of Angiogenesis and Vascular Protection.
We are committed to translational research (“from bench to bedside”) with a view to developing our discoveries from invention through to practical application, maintaining a clear focus on helping people affected by the conditions we study. Through our research we hope to understand the pathogenesis of vascular diseases such as preeclampsia and arthrosclerosis and develop therapeutic interventions based on our findings.
The team is led by Asif Ahmed, Professor of Vascular Biology and Pro-Vice-Chancellor for Health. Professor Ahmed has an international reputation in angiogenesis and vascular protection research; his laboratory was amongst the first laboratories to signal the importance of vascular growth factors in pregnancy, and pioneered the concept of angiogenic imbalance theory in preeclampsia in the mid 1990s.
In 2000, Ahmed discovered that the enzyme placental heme oxygenase (HO) protects the human placenta against injury (Mol Med. 6:391-409, 2000) and went on to identify carbon monoxide (CO), the gaseous product of HO, as an inhibitor of anti-angiogenic proteins (soluble Flt-1 and soluble endoglin) (Circulation 115:1789-97, 2007; Natural Protein Offers New Therapeutic Potential for Pre-Eclampsia). Soluble Flt-1, the natural anti-VEGF factor in circulation, has been increasingly recognized as a major factor responsible for the clinical signs of preeclampsia. In 2004 Ahmed & Ahmad identified soluble Flt-1 as the single most important molecule responsible for angiogenic imbalance in preeclampsia, by demonstrating that the removal of sFlt-1 from preeclamptic samples restored angiogenic balance (Circ Res 95:884-91,2004), which was confirmed by others in vivo.
The discovery that increasing HO activity could provide protection against preeclampsia formed the basis for the world’s first randomized controlled clinical trial on the use of statins in pregnancy, the StAmP (Statins to Ameliorate early onset Preeclampsia) Trial (see: Heart disease drugs could treat pregnant women; Heart drugs used in pre-eclampsia pregnancy trial). This trial is currently ongoing at Aston University, and based on our discoveries two additional international clinical trials have been initiated (details here and here).
Recently the Aston Vascular Research team has identified another diatomic molecule, hydrogen sulfide (H2S), as offering the potential to treat both preeclampsia and fetal growth restriction in pregnancy. The new findings have been published in Circulation. This work was recently highlighted as being a “groundbreaking study” by Circulation and within the mainstream media (Breakthrough in fight against pre-eclampsia). This is the first time two naturally-occurring small gaseous molecules (CO and H2S) have been shown to prevent the release of the culprit proteins (sFlt-1 and sEng) which are elevated in preeclampsia. More importantly, in this new work we have shown that it is possible to restore fetal growth and fix the vascular abnormalities (angiogenesis) in placenta by restoring hydrogen sulfide.
The group will continue to evaluate the effects of anti-angiogenic growth factors that may contribute to vascular based disorders, in particular preeclampsia, and develop therapeutic targets for these conditions. It is hoped that before the end of the decade Aston’s team may have a treatment for preeclampsia.
The Aston Vascular Team
Prof Asif Ahmed, Professor of Vascular Biology
Dr Shakil Ahmad, Senior Research Fellow
Dr Keqing Wang, Aston Academic Research Fellow
Dr Meng Cai, Research Fellow
- 2013 – Dysregulation of Hydrogen Sulfide Producing Enzyme Cystathionine γ-lyase Contributes to Maternal Hypertension and Placental Abnormalities in Preeclampsia (Circulation: 127(25):2514-2522)
- 2012 – The role of heterodimerization between VEGFR-1 and VEGFR-2 in the regulation of endothelial cell homeostasis (Nature Communications 24;3:972)
- 2012 – The elevation in circulating anti-angiogenic factors is independent of markers of neutrophil activation in preeclampsia (Angiogenesis 15(3):333-40)
- 2012 – Resveratrol inhibits the release of soluble fms-like tyrosine kinase (sFlt-1) from human placenta (American Journal of Obstetrics and Gynecology 206(3):253)
- 2011 – Is inflammation the cause of pre-eclampsia? (Biochemical Society Transactions 39(6):1619-27)
- 2011 – Heparin elevates circulating soluble fms-like tyrosine kinase-1 immunoreactivity in pregnant women receiving anticoagulation therapy (Circulation 124(23):2543-53)
- 2011 – Multiple roles of angiopoietins in atherogenesis (Current Opinion in Lipidology 22(5):380-5)
- 2011 – Autocrine activity of soluble Flt-1 controls endothelial cell function and angiogenesis (Vascular Cell 3(1):15)
- 2011 – Flt1 acts as a negative regulator of tip cell formation and branching morphogenesis in the zebrafish embryo (Development 138(10):2111-20)
- 2011 – Placenta growth factor-1 exerts time-dependent stabilization of adherens junctions following VEGF-induced vascular permeability (PLoS One 6(3):e18076)
- 2011 – Loss of Akt activity increases circulating soluble endoglin release in preeclampsia: identification of inter-dependency between Akt-1 and heme oxygenase-1 (European Heart Journal 33(9):1150-8)
- 2011 – New insights into the etiology of preeclampsia: identification of key elusive factors for the vascular complications (Thrombosis Research 127 Suppl 3:S72-5)
- 2010 – Angiopoietin-1 induces migration of monocytes in a tie-2 and integrin-independent manner (Hypertension 56(3):477-83)
- 2010 – Fetal growth restriction results in remodeled and less efficient hearts in children (Circulation 121(22):2427-36)
- 2010 – Upregulation of urotensin II receptor in preeclampsia causes in vitro placental release of soluble vascular endothelial growth factor receptor 1 in hypoxia (Hypertension 56(1):172-8)
- 2010 – Activation of proteinase-activated receptor 2 stimulates soluble vascular endothelial growth factor receptor 1 release via epidermal growth factor receptor transactivation in endothelial cells (Hypertension 55(3):689-97)
- 2010 – Nitric oxide-dependent bone marrow progenitor mobilization by carbon monoxide enhances endothelial repair after vascular injury (Circulation 121(4):537-48)
- 2010 – Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor-dependent manner (Gastroenterology 138(3):1134-42)
- 2009 – Can the biology of VEGF and haem oxygenases help solve pre-eclampsia? (Biochemical Society Transactions 37(Pt 6):1237-42)
- 2009 – Reduction of circulating soluble Flt-1 alleviates preeclampsia-like symptoms in a mouse model (Journal of Cellular and Molecular Medicine 14(6B):1857-67)
- 2009 – Identification of novel serotonin 2C receptor ligands by sequential virtual screening (Bioorganic & Medicinal Chemistry 17(13):4559-68)
- 2009 – Angiopoietin-2 confers Atheroprotection in apoE-/- mice by inhibiting LDL oxidation via nitric oxide (Circulation Research 104(12):1333-6)
- 2009 – Hypoxia induces dilated cardiomyopathy in the chick embryo: mechanism, intervention, and long-term consequences (PLoS One 4(4):e5155)
- 2008 – Cardiac dysfunction and cell damage across clinical stages of severity in growth-restricted fetuses (American Journal of Obstetrics and Gynecology 199(3):254.e1-8)
- 2008 – Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia (Nature 453(7198):1117-21)
- 2008 – Autoantibody from women with preeclampsia induces soluble Fms-like tyrosine kinase-1 production via angiotensin type 1 receptor and calcineurin/nuclear factor of activated T-cells signaling (Hypertension 51(4):1010-9)
- 2007 – VEGF induces Tie2 shedding via a phosphoinositide 3-kinase/Akt dependent pathway to modulate Tie2 signaling (Arteriosclerosis, Thrombosis and Vascular Biology 27(12):2619-26)
- 2007 – Vascular endothelial growth factor promotes physical wound repair and is anti-apoptotic in primary distal lung epithelial and A549 cells (Critical Care Medicine 35(9):2164-70)
- 2007 – Negative regulation of soluble Flt-1 and soluble endoglin release by heme oxygenase-1 (Circulation 115(13):1789-97)
- 2006 – The release of nitric oxide from S-nitrosothiols promotes angiogenesis (PLoS One 1:e25)
- 2006 – Angiotensin II induces soluble fms-Like tyrosine kinase-1 release via calcineurin signaling pathway in pregnancy (Circulation Research 100(1):88-95)
- 2006 – Direct evidence for endothelial vascular endothelial growth factor receptor-1 function in nitric oxide-mediated angiogenesis (Circulation Research 99(7):715-22)
- 2006 – Selective inhibition of the human tie-1 promoter with triplex-forming oligonucleotides targeted to Ets binding sites (Molecular Medicine 12(1-3):8-16)
- 2006 – VEGF-E activates endothelial nitric oxide synthase to induce angiogenesis via cGMP and PKG-independent pathways (Biochemical and Biophysical Research Communications 345(4):1275-82)
- 2005 – Vascular endothelial growth factor-induced endothelial cell proliferation is regulated by interaction between VEGFR-2, SH-PTP1 and eNOS (Microvascular Research 71(1):20-31)
- 2005 – Antiangiogenic effect of soluble vascular endothelial growth factor receptor-1 in placental angiogenesis (Endothelium 12(1-2):89-95)
- 2004 – Elevated placental soluble vascular endothelial growth factor receptor-1 inhibits angiogenesis in preeclampsia (Circulation Research 95(9):884-91)
- 2003 – Activation of vascular endothelial growth factor receptor-1 sustains angiogenesis and Bcl-2 expression via the phosphatidylinositol 3-kinase pathway in endothelial cells (Diabetes 52(12):2959-68)
- 2003 – Bifunctional role for VEGF-induced heme oxygenase-1 in vivo: induction of angiogenesis and inhibition of leukocytic infiltration (Blood 103(3):761-6)
- 2002 – Modulation of trophoblast cell death by oxygen and EGF (Molecular Medicine 8(12):847-56)
- 2002 – Down-regulation of angiopoietin-1 expression in menorrhagia (The American Journal of Pathology 160(3):773-80)
- 2000 – Induction of placental heme oxygenase-1 is protective against TNFalpha-induced cytotoxicity and promotes vessel relaxation (Molecular Medicine 6(5):391-409)
- 1998 – Hemeoxygenase-1 inhibits human myometrial contractility via carbon monoxide and is upregulated by progesterone during pregnancy (Journal of Clinical Investigation 101(5):949-55)
- 1998 – Cellular localization of AT1 receptor mRNA and protein in normal placenta and its reduced expression in intrauterine growth restriction. Angiotensin II stimulates the release of vasorelaxants (Journal of Clinical Investigation 101(2):442–454)
- Aston University
- Vascular Aston on Twitter (@VascularAston)
- Dysregulation of Hydrogen Sulfide Producing Enzyme Cystathionine γ-lyase Contributes to Maternal Hypertension and Placental Abnormalities in Preeclampsia (Circulation, 2013)
- Daily Mail: “Breakthrough in fight against pre-eclampsia: Scientists may have found cause of the life-threatening pregnancy condition”
- Aston University: “Aston researchers help fight life-threatening pregnancy condition”
- StAmP Trial (Statins to Ameliorate early onset Pre-eclampsia)
- The Telegraph: “Heart disease drugs could treat pregnant women” (StAmP)
- BBC News: “Heart drugs used in pre-eclampsia pregnancy trial” (StAmP)
- BBC News (Video): “Statins drug trial for pre-eclampsia offers hope” (StAmP)
- Clinical Trial (Treating early onset severe preeclampsia with Pravastatin)
- Clinical Trial (Pravastatin for Prevention of Preeclampsia)