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Investigating The Use Of Bone Marrow Transplantation To Study And Treat Polycystic Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$349,250.00
Summary
Polycystic kidney disease (PKD) is a common genetic condition that causes fluid filled cysts to form in the kidney. In many cases, these cysts lead to kidney failure. Once the kidneys fail irreversibly, the only treatments available are dialysis and kidney transplantation. Dialysis to remove waste products from the blood is time consuming and does not completely replace all functions of the kidney. Kidney transplantation is limited by the availability of donor organs. At present, there are no re ....Polycystic kidney disease (PKD) is a common genetic condition that causes fluid filled cysts to form in the kidney. In many cases, these cysts lead to kidney failure. Once the kidneys fail irreversibly, the only treatments available are dialysis and kidney transplantation. Dialysis to remove waste products from the blood is time consuming and does not completely replace all functions of the kidney. Kidney transplantation is limited by the availability of donor organs. At present, there are no reliable ways to prevent the onset or slow the progression of PKD. The kidney consists of a complex system of tubules and ducts. PKD causes the cells that make up these tubules and ducts to grow uncontrollably and form cysts. We are using mice to study how mutations affect the mechanisms that control cell growth in the kidney and cause PKD. Bone marrow cells can move to the kidney and repair it after damage. We will test if bone marrow cells carrying a PKD mutation can cause PKD when transplanted into a healthy mouse. This will help us learn how mutations cause PKD in humans. We will also see if normal bone marrow can prevent disease when transplanted into a mutant mouse that spontaneously develops PKD. This experiment may lay the basis for a way to treat human PKD.Read moreRead less
Vitamin D3 Receptor Signalling To Prevent Kidney Failure Due To Polycystic Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$468,009.00
Summary
Polycystic kidney disease (PKD) is the most common fatal inherited kidney disease in the world. Kidney failure is the most serious and life-threatening complication of PKD, but currently there is no treatment to prevent this problem. The aim of this project is to determine whether vitamin D3 can prevent kidney failure and hypertension due to PKD. The results of this project could lead to simple and cost-effective treatments to prevent kidney failure in patients suffering from PKD.
We have identified a novel gene, Inpp5e, that when mutated causes a disease similar to Joubert syndrome and MORMS disease which leads to abnormal movements, developmental delays, mental retardation, abnormal breathing and eye movement. We have identified a candidate gene for these diseases and have shown that deletion of this gene in mice results in similar pathology. We aim to determine the mechanism by which Inpp5e regulates human development and disease.
A lack of oxygen in the kidney (hypoxia) is a primary cause of kidney disease, but the mechanisms are not clear. To determine the processes involved, we will take a new approach; combining a mathematical model with studies of kidney oxygen regulation in both normal and diseased kidneys. We will determine the causes of hypoxia in kidney disease, and find out if preventing hypoxia has the potential to be a treatment for kidney disease.
The proposal builds on innovative technologies patented and published by my group. The project has two specific objectives: 1) to deliver the new generation of intelligent biomedical devices that have the capacity to control infections, inflammation and foreign body response; and 2) to develop a novel, non-invasive and affordable point of care diagnostic technology for early detection of chronic kidney diseases, and kidney and bladder cancers that is much needed in this space of healthcare.
Billions of cells are destined to die everyday as a part of normal development and tissue homeostasis. A failure to clear dying cells rapidly and efficiently can lead to chronic inflammation, autoimmunity and developmental defects. This research project aims to investigate how the immune system detects the presence of dying cells and removes them efficiently.
Effects Of Exercise And Lifestyle Management On Reproductive Function In Overweight Women With Polycystic Ovary Syndrome
Funder
National Health and Medical Research Council
Funding Amount
$379,719.00
Summary
Polycystic ovary syndrome (PCOS) is a complex disorder present in 5-10% of women of reproductive age. It is associated with obesity, increased menstrual dysfunction and infertility and metabolic conditions such as increased serum insulin, high cholesterol, diabetes and heart disease. Lifestyle interventions aimed at reducing obesity and insulin resistance, which include dietary weight loss and physical activity, are advocated for the management of PCOS. However, while research indicates that wei ....Polycystic ovary syndrome (PCOS) is a complex disorder present in 5-10% of women of reproductive age. It is associated with obesity, increased menstrual dysfunction and infertility and metabolic conditions such as increased serum insulin, high cholesterol, diabetes and heart disease. Lifestyle interventions aimed at reducing obesity and insulin resistance, which include dietary weight loss and physical activity, are advocated for the management of PCOS. However, while research indicates that weight loss through diet improves many symptoms, there is a paucity of research evaluating the combined role of physical exercise in managing this condition. In addition, there is no research examining the optimal form of exercise that should be undertaken to achieve long-term reproductive fitness and metabolic health and consequently there is a lack of evidence-based exercise guidelines for patients with PCOS. We plan to perform a clinical study to investigate whether combining exercise with weight loss by diet in patients with PCOS provides any additional benefit for improving menstrual function, fertility and metabolic health beyond those that can be achieved using dietary restriction alone. We will also assess whether, when combined with dietary restriction, a program of physical activity incorporating both endurance and resistance exercise provides a greater benefit than the more common prescription of endurance exercise alone. This information will be used to assist in the development of guidelines for the effective management of reproductive dysfunction in patients with PCOS.Read moreRead less
E-cadherin is one of the major proteins responsible for mediating cell-to-cell adhesion in the body. During development, E-cadherin is essential for establishing the cellular architecture of epithelial organs and for maintaining epithelial function in the adult. In this context, E-cadherin acts to establish and maintain the polarity of epithelial cells. E-cadherin is also a powerful tumour suppressor and the loss of E-cadherin expression or function is a primary event in metastasis and cancer in ....E-cadherin is one of the major proteins responsible for mediating cell-to-cell adhesion in the body. During development, E-cadherin is essential for establishing the cellular architecture of epithelial organs and for maintaining epithelial function in the adult. In this context, E-cadherin acts to establish and maintain the polarity of epithelial cells. E-cadherin is also a powerful tumour suppressor and the loss of E-cadherin expression or function is a primary event in metastasis and cancer invasion. Proteins at the surface of epithelial cells must be sorted and trafficked, or transported, to different membrane domains. E-cadherin, for instance, must be trafficked to the lateral domain of cells in order to function in cell-cell adhesion. We recently discovered that cell surface E-cadherin is re-internalized and recycled back to the surface via a pathway that is poised to contribute to the regulation of cell adhesion. Our proposed studies aim to reveal how newly-synthesized E-cadherin and recycling E-cadherin are trafficked, which molecules and which vesicle carriers accomplish this transport. E-cadherin has specific amino acids that act as targeting signals for its sorting and trafficking; we have recently identified one such signal and will now seek the signal responsible for its endocytosis. Using specifically engineered mutants of E-cadherin we will also study other proteins that interact with E-cadherin during its trafficking for sorting and regulation. One of these is polycystin, a protein that is mutated in a common inherited kidney disease. Insights into this disease and normal kidney epithelial function will emerge from this work. A growing understanding of E-cadherin function and regulation is essential for the health of epithelial organs and for controlling and preventing cancer.Read moreRead less
Microtubule Capture By E-cadherin: A Novel Mechanism For Dynamic Cell-cell Adhesion.
Funder
National Health and Medical Research Council
Funding Amount
$439,500.00
Summary
This project studies the molecular mechanisms responsible for holding cells together in normal tissues. Such cell-to-cell adhesion is mediated by the cadherin family of molecules, which reside at the surfaces of cells. Cadherins allow cells to recognize one another and, upon recognition, adhere to one another. By this means populations of individual cells can be linked together into cohesive populations (i.e. the tissues or organs of the body). The importance of cadherin adhesion is exemplified ....This project studies the molecular mechanisms responsible for holding cells together in normal tissues. Such cell-to-cell adhesion is mediated by the cadherin family of molecules, which reside at the surfaces of cells. Cadherins allow cells to recognize one another and, upon recognition, adhere to one another. By this means populations of individual cells can be linked together into cohesive populations (i.e. the tissues or organs of the body). The importance of cadherin adhesion is exemplified by the well-documented observation that disruption of cadherin adhesion contributes to many important diseases, including inflammation of epithelia and cancers. Thus understanding the mechanisms by which cadherins hold cells together is necessary for us to understand the molecular basis of commondisease. It has long been known that cadherins work in cooperation with elements within the cell, called the cytoskeleton. My lab has recently made the novel discovery that microtubules, specific components of the cytoskeleton, can regulate the functionof cadherin adhesion molecules. Inparticular, microtubules appear to affect how cadherins can participate in dynamic cell processes necessary for cells to be properly organized in tissues. In this project we will probe the molecular mechanisms responsible for this effect of microtubules. The information obtained will provide important new insights into how dynamic cadherin adhesion is controlled, to help our understanding of the cellular mechanisms that couple cells into tissues, and how they may be disrupted in diesase.Read moreRead less