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This project addresses the problem of how diabetes complications develop, specifically the effect of vascular endothelial dysfunction in diabetes on the regulation of the anti-inflammatory cell surface protein CD163 as well as the relationship between these changes and the development of diabetes complications.
Camperdown - Central Clinical School
There is considerable evidence to show that macrophage accumulation in certain tissues is a pathogenic feature of diabetes complications. However few studies have investigated the effects of diabetes on monocytes, the precursor cell of macrophages. Our studies in people with diabetes have provided novel data showing that diabetes can affect monocyte phenotype and moreover this change is related to the presence of diabetes complications. These novel findings of differing relationships between monocyte profiles in particular the anti-inflammatory CD163+ monocytes, the proteases known as the matrix metalloproteinases (MMPs), and diabetes complication status underpin this project. How these changes are associated with diabetes complications, in particular the effect of diabetes on the interaction between monocytes and vascular endothelial cells, and the regulation of MMPs and CD163, will be studied in detail. This study will allow us to improve and extend our knowledge of the causes of diabetes complications and may provide potential new treatment strategies to benefit patients in the future.
This project will use a variety of techniques including molecular biology, cell biology, pathology and immunology. Both in vivo and in vitro study models used in this project are well-established in our laboratory.
Program Type: Master/PHD
Co-Supervisor: Stephen Twigg,
The opportunity ID for this research opportunity is 3026