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Development Of Endogenous Granulocyte Colony Stimulating Factor (G-CSF) Antagonism As A New Therapeutic Approach To Inflammatory Disease
Funder
National Health and Medical Research Council
Funding Amount
$401,561.00
Summary
Neutrophils play a pivotal role in inflammatory diseases including rheumatoid arthritis (RA). G-CSF is a growth factor that is important to neutrophil survival and function. We have shown that in the absence of G-CSF the incidence and severity of experimental autoimmune arthritis are reduced. We will investigate the mechanisms by which this occurs as well as studying the effects of G-CSF blockade on function and survival of human neutrophils from healthy donors and RA patients.
This proposal aims to examine central mechanisms important in stress related hypertension. My team will focus on the role of tissue plasminogen activator in mediating inhibitory effects of chronic stress on neural plasticity and examine inhibitory dysfunction in GABAergic and nitric oxide pathways that lead to increased sympathetic activity and elevated blood pressure. Importantly, we will investigate the potential of three interventions directed at each as therapies for hypertension.
Control Of TGF-beta Superfamily Signalling In Human Disease
Funder
National Health and Medical Research Council
Funding Amount
$443,946.00
Summary
Members of the transforming growth factor ? (TGF-?) family of proteins play crucial roles in adult tissue homeostasis. In recent years a new paradigm has emerged suggesting that inhibition of TGF-? signalling could be an effective strategy for restoring homeostasis in disease-affected tissues. Dr Harrison’s overall research strategy is based on this concept, and is particularly focussed on developing specific antagonists of individual TGF-? proteins.
The Inflammasome In Host Defence And Autoinflammation
Funder
National Health and Medical Research Council
Funding Amount
$408,388.00
Summary
Inflammation is one of the bodies first responses to infection. The inflammasome is a protein complex that activates pro-inflammatory cytokines as part of this process. We are investigating pathogens that activate a specific inflammasome complex, and also an inflammatory disease it may cause when activated accidentally, in the absence of infection. We are also investigating pathways that keep this inflammation in check, and how pathogens might hijack these anti-inflammatory pathways to promote i ....Inflammation is one of the bodies first responses to infection. The inflammasome is a protein complex that activates pro-inflammatory cytokines as part of this process. We are investigating pathogens that activate a specific inflammasome complex, and also an inflammatory disease it may cause when activated accidentally, in the absence of infection. We are also investigating pathways that keep this inflammation in check, and how pathogens might hijack these anti-inflammatory pathways to promote infection.Read moreRead less
Nerve cell survival is dependent on both growth-promoting factors and factors released by neurotransmission, which can promote recovery in neurodegenerative conditions by overriding cell death pathways. The molecule responsible for activating death pathways in the nervous system is called p75. This project will investigate how p75 results in cell death, how synaptic signals can prevent the activation of the p75 death pathway and whether blocking p75 function can limit neurodegeneration.
The Role Of Insulin Hypersecretion In Beta Cell Dysfunction In Type 2 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$318,622.00
Summary
The treatment of diabetes involves the use of drugs that stimulate the release of insulin from the pancreas to reduce the high blood sugar levels. However, we believe that while in the short term this is a good strategy, in the long-term it damages the cells that produce insulin leading to a worsening state of diabetes. It is the aim of this application to understand the mechanisms by which the insulin producing cells are damaged when forced to oversecrete insulin.
This research proposal will identify changes in liver-secreted proteins during the development of fatty liver, and in the transition from fatty liver to the more advanced form of liver disease, non-alcoholic steatohepatitis (NASH). Understanding the differences in protein secretion between NASH patients and patients with normal/fatty liver will provide the opportunity to identify disease biomarkers that could be determined from a blood sample. This will provide a major shift in clinical care.