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

NHMRC

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
Collapse -
Expand +
Investigating cell death pathways in the proinflammatory function of platelets and leukocytes during ischaemia-reperfusion injury

Recent studies from our laboratory have made the unexpected observation that a specific form of platelet cell death, termed programmed necrosis, plays a major role in promoting leukocyte recruitment and tissue damage following I/R injury. Notably, this pathway is resistant to the inhibitory effects of conventional anti-platelet and anti-inflammatory agents. We are examining the thrombo-inflammatory response of mice that are resistant to apoptotic cell death (Bak:Bax knock-out mice) or necrosis (Cyclophilin D knock-out mice), in in vivo models of inflammation and I/R injury. Our aim is to investigate the role of specific cell death pathways in regulating platelet proinflammatory function and leukocyte recruitment, with the ultimate aim of identifying new therapeutic targets to improve microvascular perfusion and reduce inflammation and organ injury.

Identifying new pathways regulating platelet hyperactivity and thrombosis in diabetes

Our laboratory has recently defined a new pathway promoting platelet aggregation and thrombus development that involves biomechanical platelet activation. More recently, we have identified that this pathway is dysregulated in diabetes and leads to enhanced platelet-endothelial interaction through a molecular process that is linked to atherogenesis. This project aims to identify the molecular mechanisms by which hyperglycemia leads to enhanced biomechanical platelet activation, and the relevance of this pathway to platelet-endothelial and platelet-platelet adhesive interactions linked to atherothrombosis.

Investigating a new innovative approach to the treatment of ischaemic stroke

Our laboratory has a longstanding interest in identifying pathways in platelets that are important for arterial thrombus formation, but less critical for haemostasis. One of these pathways involves shear activation of platelets through activation of the p110 isoform of PI 3-kinase (PI3K). We have developed isoform-selective inhibitors against PI3K and demonstrated that these inhibitors are highly effective at promoting and facilitating thrombus dissolution and complete vascular reperfusion, without markedly increasing tail bleeding times. Preliminary studies have revealed that PI3K inhibitors lead to localised regions of thrombus instability, that lead to the development of channels within the body of the thrombus. This project will examine the mechanisms by which PI3K inhibitors enhance reperfusion, examining the impact of thrombus channel formation on blood flow, thrombus porosity and thrombus dissolution. Moreover, the impact of PI3Kinhibitors on end-organ damage, particularly in the stroke context, will also be examined. These studies will not only provide important insight into our understanding of blood clot formation, but may also lead to new approaches to regulate the size and stability of blood clots forming in the body, providing major clinical benefit in the delivery of thrombolytic therapy (blood clot removal).

Investigating novel regulators of platelet procoagulant activity –targeting safer anticoagulation

The intracellular pathways that mediate procoagulant platelet function are only starting to be elucidated. Our laboratory has recently demonstrated that platelet PS exposure and procoagulant function is regulated by programmed cell death pathways, including apoptosis and necrosis. Utilising several novel mouse lines that specifically lack Bak, Bax and CypD in platelets, we have made the unexpected observation that these pathways only contribute to approximately 50% of the platelet procoagulant response. In this project, we are examining a new pathway we have identified to play an important role in regulating the platelet procoagulant response – which involves the signalling adaptor protein 14-3-3 regulating metabolic ATP. We have found that this pathway plays an important role in regulating platelet PS exposure and thrombin generation, necessary for thrombus growth and stability. We aim to determine whether therapeutic targeting of this pathway represents a safe and effective way of reducing thrombin generation in vivo without increasing bleeding risk.

Featured Publication
Collapse -
Expand +
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
Collapse -
Expand +
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
Collapse -
Expand +
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
Collapse -
Expand +
Clinical

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.

 
Commercial

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.