Professor Shaun Jackson

MBBS (Hons), BMedSci (Hons), PhD
Our aim is to establish an entirely new and innovative approach to the prevention and treatment of heart disease and stroke.

Professor Shaun Jackson is an NHMRC Senior Principal Research Fellow (SPRF) and faculty member at the prestigious Scripps Research Institute in La Jolla, San Diego (CA, USA). Shaun was a co-founder of the Australian Centre for Blood Diseases in Melbourne and a founder of Kinacia, an Australian biotechnology company developing novel diagnostic and therapeutic products aimed at preventing blood clotting. He is currently the Head of Cardiovascular Research at the Heart Research Institute and Charles Perkins Centre, as well as Research director of Atherothrombosis services within the Department of Cardiology at the Royal Prince Alfred (RPA) hospital. Professor Jackson’s research interests are focussed in the area of atherothrombosis and cardiovascular disease. Shaun established his independent research laboratory in the Monash Department of Medicine at Box Hill Hospital (1998-2003). In 2004 he moved to the Alfred Medical Research and Education Precinct (AMREP), where he co-founded and became Research Director of the Australian Centre for Blood Diseases (ACBD). 

Current Appointments

Thrombosis Group Leader and Director of Cardiovascular Research

Heart Research Institute and Charles Perkins Centre, The University of Sydney

Senior Principal Research Fellow


Research Director, Atherothrombosis services, Department of Cardiology

Royal Prince Alfred Hospital

Faculty member, Department of Molecular & Experimental Medicine, Division of Experimental  Hemostasis & Thrombosis

The Scripps Research Institute, La Jolla, San Diego (CA, USA).

Professor Shaun Jackson leads group:
Research covers areas of:
Contact Professor Shaun Jackson

More about Professor Shaun Jackson

Research Project Opportunities
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“Bad Blood”: Unravelling the link between gut ischemia and remote organ injury

Ischaemic injury to vital organs is common in critically ill patients, producing deleterious effects on other organ systems. This is particularly common in the gut, with intestinal hypoperfusion inducing systemic inflammation and multiorgan organ dysfunction syndrome. In addition to promoting inflammation, prolonged ischemic injury to the intestines can also lead to the development of a systemic thrombotic response (pathological formation of blood clots), which is particularly common in the lung, and leads to a very poor prognosis (>90% mortality). We have identified a new mechanism of pathological blood clotting (thrombosis) and vascular occlusion that is triggered by dying platelets in the intestinal microvasculature. Our ultimate aim is to identify new therapeutic targets to improve microvascular perfusion and reduce inflammation and organ injury, which may represent an innovative approach to reduce remote organ injury in critically ill patients. This project will involve the use of animal models of ischaemia reperfusion, confocal microscopy, gut and lung histology, and other in vitro cell biology and biochemical approaches.

Solving a sticky clotting problem in diabetes

The leading cause of death in diabetes is cardiovascular disease, with up to 70% of deaths relating to the development of blood clots supplying the heart (heart attack) or brain (ischemic stroke). Diabetic individuals are more prone to develop blood clots, and these clots are more resistant to standard anticlotting therapies. Our laboratory has discovered a new biomechanical clotting mechanism severely affected by diabetes that is resistant to the beneficial effects of commonly used antithrombotic agents. Studies ongoing in our laboratory aim to identify how high blood sugar levels (hyperglycaemia) can enhance this new clotting mechanism. To achieve this, we are using Biomembrane force probe (‘BFP’) technology, which allows us to study how a single platelet senses mechanical cues at the molecular scale. We will also examine the role chronic oxidative stress plays in amplifying blood clotting in diabetes, and the mechanisms by which oxidative stress may modify platelet receptors to enhance adhesion. These studies may identify novel targets with which to treat thrombosis associated with diabetes. This project will involve the use of in vivo animal models, Biomembrane force probe (‘BFP’) technology, biochemistry and mass spectoscopy.

New approaches to the treatment of ischaemic stroke

The development of a blood clot in the cerebral circulation (ischaemic stroke) is the third most common cause of death and the most common cause of adult disability globally. The central goal of stroke therapy is the prompt reperfusion of occluded blood vessels to minimise tissue death. The delivery of fibrinolytic agents modelled on tissue-type plasminogen activator (t-PA) is the only clinically approved means available to stroke patients. Despite this, the use of t-PA is associated with significant side effects, limiting its widespread use. We are working on a novel approach to improve upon existing stroke therapies, making them safer and more effective. Ongoing studies using a novel mouse model of thrombolysis (iCAT) developed in our lab will determine whether cerebral damage and cognitive impairment associated with stroke are reduced using this approach. This project will involve the use of animal models of stroke, behavioural analysis, laser speckle contrast and Laser Doppler Flow imaging, histology, and cell biology approaches.

Investigating blood flow reductions in the brain after stroke

Acute ischemic stroke is a leading cause of death and disability worldwide. It is caused by the blockage of a major artery that supplies the brain. Injury occurs as a consequence of the reductions in blood flow and the longer the brain stays hypoperfused, the greater the damage inflicted. It has long been known that quickly restoring blood flow to the brain will limit the progression of cell death and improve patient outcome after stroke. However, there is evolving evidence that reopening the blocked artery does not always restore blood flow in the small vessels of the brain and correlates with worse prognosis for stroke patients. The causes of the continued hypoperfusion is poorly understood. Identifying the causes of these blood flow reductions despite large vessel reopening will provide targets for potential new stroke therapies. This project will involve the use of animal models of stroke, behavioural analysis, laser speckle contrast and Laser Doppler Flow imaging, histology, and cell biology approaches.

Platelet death as an important regulator of blood clot formation

The generation of a fibrin blood clot is driven by coagulation factors present in the plasma. These factors assemble on negatively charged endothelial surfaces, such as phosphatidylserine (PS), to facilitate thrombin generation and promote blood clot formation. Platelets are also capable of exposing PS on their outer membrane and promoting localised thrombin generation – a process referred to as platelet ‘procoagulant’ function. All currently employed anticoagulant agents indiscriminately inhibit blood clotting reactions at the injured vessel wall and throughout the body of a developing blood clot, resulting in increased bleeding risk for patients receiving these medications.

Our laboratory has demonstrated that procoagulant platelets are dying cells, undergoing a cell death process akin to necrosis, leading to PS exposure and thrombin generation. We have also found that the adaptor protein 14-3-3z plays an important role in regulating platelet death necessary for blood clot growth and stability. We aim to determine whether therapeutic targeting of this pathway, either alone, or in combination with necrotic cell death pathways, represents a safe and effective way of reducing thrombin generation in vivo without increasing bleeding risk.

This project will involve an array of in vitro biochemistry and platelet biology assays, along with in vivo models of thrombosis and confocal imaging techniques.

Featured Publication
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Zane S Kaplan, Alessandro Zarpellon, Imala Alwis, Yuping Yuan, James McFadyen, Mehran Ghasemzadeh, Simone M Schoenwaelder, Zaverio M. Ruggeri and Shaun P. Jackson. Thrombin-dependent Intravascular Leukocyte Trafficking Regulated by Fibrin and the Platelet Receptors, GPIb and PAR4. Nat Commun, 2015 Jul 23; 6:7835. doi: 10.1038/ncomms8835. 

Description - Unblocking blood vessels to treat heart attack and stroke can unfortunately cause a paradoxical worsening of organ damage, due to increased inflammation upon blood flow restoration. These studies have identified a novel way in which this side-effect is regulated by the small blood clotting cells platelets, and the protein fibrin. We have found that blood clots can slow down the white blood cells (neutrophils) responsible for inflammation and stop them causing damage in the brain's tissue. However, when tPA is administered, it dissolves this protective barrier, allowing neutrophils to flood in and cause damage. Using this knowledge, we can now develop new therapies which can be administered alongside tPA, potentially preventing neutrophils from rushing in and dramatically improve outcomes for patients.

Current Research Grants
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National Health and Medical Research Council (NHMRC) Project Grant 1042886, Investigation of a novel mechanism causing platelet hyperactivity in diabetes, 2013-2015
National Health and Medical Research Council (NHMRC) Project Grant 1048574, Investigation of the proinflammatory function of platelets during ischaemia-reperfusion injury, 2013-2015
National Health and Medical Research Council (NHMRC) Project Grant 1066956, A new role for growth factor c-mpl in blood clot formation, 2014-2016
National Health and Medical Research Council (NHMRC) Project Grant 1066957, Tractopods - Novel structures regulating platelet-vessel wall interactions, 2014-2016
National Health and Medical Research Council (NHMRC) Research Fellowship 1079400, Supporting Prof. Shaun Jackson, 2015-2019
Thrombosis (Schoenwaelder) National Health and Medical Research Council (NHMRC) Project Grant 1044214, PI3K beta and blood clot porosity, 2013-2015
Selected Awards for Research
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2011     Investigator Recognition Award & Medal, Awarded by the International Society on Thrombosis and Haemostasis
2010     Australia Fellowship, NHMRC
2009     Marion Barnhart Prize, Awarded by the International Society on Thrombosis and Haemostasis, 2009
2006     AMREP Research Prize
2005     AMGEN National Medical Researcher Award
2004     Rudolph Virchow Medal, Wurzburg, Germany
2001     Silver Jubilee Research Prize, Monash University
1999     Tall Poppy Award, Australian Institute of Political Science
1996     Speywood Award, Australian Society of Thrombosis & Hemostasis
1995     Inaugural Premier's Award for Excellence in Medical Research, Victoria
1994     Albert J. Baikie Memorial Medal for Haematological Research, Haematology Society of Australia
1995     PhD candidature, Dept. Medicine, Monash University
1989     MB.BS (First Class Honours), Monash University
1987     B.Med.Sci. (First Class Honours), Monash University
Skills and Expertise
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I have had a longstanding clinical interest in thrombosis. This was initially cultivated by Prof. Hatem Salem and the late Prof. Barry Firkin, whilst I was a medical student and hospital resident at the Alfred Hospital, Melbourne. I had formal training in haemostasis and thrombosis as a Pathology Registrar at Box Hill Hospital (1994-1998) and underwent Haematopathology training with the Royal College of Pathologists of Australasia during this time. Over the last 20 years I have developed considerable skills in the clinical and laboratory aspects of haemostasis and thrombosis. I have had a fractional clinical appointment in Haematology at Box Hill Hospital (1994-2004) and the Alfred Hospital (2004-2013) where my primary responsibility was to manage patients with thrombotic disorders. I also assisted with the interpretation of abnormal coagulation and platelet function tests and provided advanced diagnostic testing of patients and their families with suspected platelet disorders. I am currently Research director of Aatherothrombotic services within the Department of Cardiology, Royal Prince Alfred (RPA) Hospital in Sydney.


i) Biotechnology

(1997) Founder, Board member and Principal Scientist for Kinacia (formerly Thrombogenix Pty Ltd). Kinacia is an Australian biotechnology company developing novel diagnostic and therapeutic products aimed at preventing blood clotting. The company’s R&D program is based on the commercialisation of discoveries emanating from the Australian Centre for Blood Diseases. The company has discovered and patented two new class of anti-thrombotic drugs and has developed and patented a novel diagnostic instrument that monitors platelet reactivity.