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The immune system employs a variety of strategies to combat parasites including viruses. One of them is cytolytic lymphocytes, cells that can recognize and destroy virus-infected target cells. These cells use, besides other molecules, enzymes called granzymes to kill target cells by inducing suicide in them. We intend to investigate if those granzymes can protect cytolytic lymphocytes themselves from being infected by viruses and turned into viral factories. We are going to use a model of a natu ....The immune system employs a variety of strategies to combat parasites including viruses. One of them is cytolytic lymphocytes, cells that can recognize and destroy virus-infected target cells. These cells use, besides other molecules, enzymes called granzymes to kill target cells by inducing suicide in them. We intend to investigate if those granzymes can protect cytolytic lymphocytes themselves from being infected by viruses and turned into viral factories. We are going to use a model of a natural infection, ectromelia, mouse pox. Mouse pox is fatal in resistant strains of mice if the genes for the two dominant granzymes are deleted. This indicates that granzymes are essential for fighting this viral disease. We will explore in which cells of the immune system granzymes are expressed and whether virus entry into a cell can actually trigger their expression. Furthermore, we will investigate how the granzymes inhibit virus infection within the infected cell to determine whether the mechanisms involved resemble those used by cytolytic lymphocytes in killing of target cells (i.e. degradation of DNA and mitochondrial damage), or whether they represent entirely new facets of granzyme function. Finally, using viruses from a number of different families, we will establish whether these functions of granzymes also contribute to protection from other viral infections. An understanding of the role of these granzymes in the innate immune response, i.e. before antigen specific T cell and antibody responses are fully activated, is of great significance as it may allow us to manipulate this particular anti-viral response and thus enhance survival and reduce morbidity in viral infections.Read moreRead less
Molecular Mechanisms Linking Proteinuria And Sodium Retention
Funder
National Health and Medical Research Council
Funding Amount
$211,527.00
Summary
The clinical association between protein loss in the urine and retention of salt, resulting in high blood pressure and progressive decline in kidney function, is well known. Under normal conditions, the kidneys filter 180 litres of water and reabsorb 1.7 kg of salt per day, a function which is principally performed by the kidney tubules in the kidney. Similarly the kidney tubule cells reabsorb and break down up to 3 grams of albumin per day. In the past, it has been considered that excessive pro ....The clinical association between protein loss in the urine and retention of salt, resulting in high blood pressure and progressive decline in kidney function, is well known. Under normal conditions, the kidneys filter 180 litres of water and reabsorb 1.7 kg of salt per day, a function which is principally performed by the kidney tubules in the kidney. Similarly the kidney tubule cells reabsorb and break down up to 3 grams of albumin per day. In the past, it has been considered that excessive protein loss in the urine is primarily due to problems in the filtering units of the kidneys, rather than due to abnormalities in the reabsorption of protein in the kidney tubules. However, we consider that common abnormalities in the processes within the kidney tubules that regulate both the reabsorption of salt and the excretion of acid may result in concomitant high blood pressure and increased protein loss in the kidney. Thus the overall aim of the project is to investigate the interrelationship between protein reabsorption and catabolism and Na+ reabsorption in the human kidney tubule. The project uses the combined methods of cultured human kidney tubules, biochemical and molecular biology techniques which are unavailable in other laboratories in Australia (and internationally). This project will comprehensively characterise the mechanisms of protein uptake and salt reabsorption in human kidney tubule cells when exposed to both normal and high concentrations of protein. The exact nature of the interaction of protein uptake with salt reabsorption and hence high blood pressure will be determined. As both hypertension and persistent proteinuria are the most important predictors of tubulointerstitial pathology and progressive decline in renal function in almost all renal disease, the understanding of the precise interaction between these two factors is essential in the design of renoprotective therapies.Read moreRead less
How Does The Mitochondria Regulate Cardiac L-type Ca2+ Channel Function?
Funder
National Health and Medical Research Council
Funding Amount
$328,267.00
Summary
Oxygen is vital to cellular metabolism and function. Oxygen delivery to cells is critical and a lack of oxygen such as occurs during a heart attack can be lethal. The L-type Ca2+ channel is a protein in the membrane of heart muscle cells responsible for regulating the entry of calcium into heart muscle cells. It plays a role in maintaining the heart beat and contraction. We have found that a lack of oxygen (hypoxia) alters the function of the L-type Ca2+ channel and its response to adrenergic st ....Oxygen is vital to cellular metabolism and function. Oxygen delivery to cells is critical and a lack of oxygen such as occurs during a heart attack can be lethal. The L-type Ca2+ channel is a protein in the membrane of heart muscle cells responsible for regulating the entry of calcium into heart muscle cells. It plays a role in maintaining the heart beat and contraction. We have found that a lack of oxygen (hypoxia) alters the function of the L-type Ca2+ channel and its response to adrenergic stimulation (adrenaline).This may be one of the ways that rhythm disturbances or sudden cardiac death occurs with a heart attack. The activity of the L-type Ca2+ channel is sensitive to changes in reactive oxygen species caused by changes in oxygen concentration. The reactive oxygen species are generated from a part of the cell responsible for maintaining the cell's energy requirements (the mitochondria). Oxidative stress is a feature of various cardiovascular pathologies and we are now interested in determining the effect of oxidative stress on function of the L-type Ca2+ channel and the role of the mitochondria in generating reactive oxygen species. Oxidative stress can damage mitochondria leading to an increase in production of reactive oxygen species. We will determine how oxidative stress damages the mitochondria and how this then alters the channel function, directly or indirectly. The information gained will provide insight into how reactive oxygen species influence L-type Ca2+ channel function and the mechanisms that contribute to pathology involving reactive oxygen species such as heart failure and arrhythmia.Read moreRead less
Muscle Thermogenesis In Models Of Predisposition To Obesity
Funder
National Health and Medical Research Council
Funding Amount
$469,289.00
Summary
Obesity is a major health crisis, but effective treatments remain elusive. Body weight is determined by a balance of food intake and energy expenditure. Understanding both sides of this equation is essential to combating obesity. This project will show that the rate at which muscle uses energy is an important determinant of energy balance and contributes to the propensity to become obese. The work will define muscle as a target for developing anti-obesity therapies.
Improving Successful Long-term Weight Loss By Deactivating The Human Famine Reaction
Funder
National Health and Medical Research Council
Funding Amount
$799,102.00
Summary
There are more than 7 million overweight or obese adults in Australia. With conventional methods of weight loss, only 5% of these people will be able to achieve permanent weight reduction of any significance to health outcomes. This project aims to develop more effective and permanent methods of weight management through comparing effectiveness of continuous versus intermittent dieting; and determining what metabolic, hormonal and behavioural factors predict weight regain.