Our group is investigating mechanisms that cause heart attacks and strokes, with a specific focus on discovering new therapies that can prevent them.
Heart attacks and strokes occur when cardiac or brain tissue is deprived of blood due to the blockage of a coronary or cerebral artery, respectively. Our research is aimed at identifying the disease pathways within the blood vessel wall that lead to arterial blockages, as well as the inflammatory mechanisms in the ischaemic organs that eventually lead to cell death. We are particularly interested in determining whether modulating the trafficking or activation of immune cells, either with novel chemokine receptor antagonists, inhibitors of NADPH oxidase, or immune-suppressing stem cell therapies, can prevent vascular disease and stroke.
Lab members
Lab heads
Postdoctoral fellows
- Dr Brad Broughton
- Dr Sophocles Chrissobolis
- Dr Courtney Judkins
- Dr Barbara Kemp-Harper
- Dr Alyson Miller
- Dr Stavros Selemidis
Research assistants
Postgraduate students
- Ms Michelle Bullen
- Ms Jacqueline Ku
- Mr Jeffrey Moore
- Ms Sandy Lee
- Mr Chris Chan
- Ms Shalini Krishnan
- Ms Hannah Chu
Honours students
Current Research Projects
- Characterising the leukocyte subsets that cause brain and blood vessel pathology in stroke, hypertension and atherosclerosis.
Contacts: Chris Sobey, Grant Drummond, Klaudia Budzyn, Stephanie de Dios - Chemokine ligand-receptor interactions as novel therapeutic targets to prevent leukocyte trafficking in vascular disease and stroke.
Contacts: Grant Drummond, Chris Sobey, Klaudia Budzyn - Exploring the therapeutic potential of amnion-derived stem cells in stroke, hypertension and atherosclerosis.
Contacts: Chris Sobey, Grant Drummond, Klaudia Budzyn - Defining which isoforms of NADPH oxidase are the causes of oxidative stress and tissue damage in vascular disease and stroke.
Contacts: Grant Drummond, Chris Sobey, Stavros Selemidis, Sophocles Chrissobolis - Discovery, development and preclinical testing of novel small molecule inhibitors of NADPH oxidase.
Contacts: Grant Drummond, Chris Sobey, Stavros Selemidis - Investigating the influence of gender and estrogen receptor subtypes on outcomes after stroke.
Contacts: Chris Sobey, Brad Broughton, Alyson Miller - Characterising the roles of different redox forms of nitric oxide and soluble guanylyl cyclase in vascular physiology and pathophysiology.
Contacts: Barbara Kemp-Harper, Chris Sobey, Alyson Miller
Opportunities exist for new PhD and Honours students to work under any one of the research projects outline above. For further information please contact either Chris Sobey or Grant Drummond, or the relevant project leader.
Most Recent Research Publications
Bullen ML, Miller AA, Andrews KL, Irvine JC, Ritchie RH, Sobey CG, Kemp-Harper BK. Nitroxyl (HNO) as a vasoprotective signaling molecule. Antioxidants and Redox Signaling:in press, 2011.
Chrissobolis S, Miller AA, Drummond GR, Kemp-Harper BK, Sobey CG. Oxidative stress and endothelial dysfunction in cerebrovascular disease. Frontiers in Bioscience 16:1733-1745, 2011.
Brait VH, Rivera J, Broughton BRS, Lee S, Sobey CG. Chemokine-related gene expression in the brain following ischemic stroke: no role for CXCR2 in outcome. Brain Research 1372:169-179, 2011.
Dharmarajah J, Arthur JF, Sobey CG, Drummond GR. The anti-platelet effects of apocynin in mice are not mediated by inhibition of NADPH oxidase activity. Naunyn Schmiedeberg’s Archives of Pharmacology 382:377-84, 2010.
Rivera R, Sobey CG, Walduck A, Drummond GR. Nox isoforms in vascular pathophysiology: insights from transgenic and knockout mouse models. Redox Report 15:50-63, 2010.
Miller AA, De Silva TM, Judkins CP, Diep H, Drummond GR, Sobey CG. Augmented superoxide production by Nox2-containing NADPH oxidase causes cerebral artery dysfunction during hypercholesterolemia. Stroke 41:784-789, 2010.
Judkins CP, Diep H, Broughton BRS, Mast AE, Hooker EU, Miller AA, Selemidis S, Dusting GJ, Sobey CG, Drummond GR. Direct evidence of a role for Nox2 in superoxide production, reduced nitric oxide bioavailability and early atherosclerotic plaque formation in ApoE-/- mice. American Journal of Physiology (Heart Circulatory Physiology) 298:H24-H32, 2010.
