2008 Grants

The Association funded the following two grants in 2008: -

• Dr Helen Young at the University of Manchester. Do alterations in cutaneous vascular biology identify those patients who have increased risk of cardiovascular co-morbidity?
Psoriasis is a common skin disease which confers immense suffering on those it afflicts. Recent work indicates that psoriasis is an independent risk factor for ischaemic hear disease. The growth of new blood vessels, a process known as angiogenesis, may be a causative factor for both psoriasis and heart disease.
A key promoter of angiogenesis, a protein called vascular endothelial growth factor (VEGF) is produced in skin and is found in increased amounts in ischaemic heart disease (atherosclerosis) and in patients with psoriasis. On the basis of our previous research we believe that VEGF may be particularly relevant to the development of psoriasis in some patients. It is this group of patients with psoriasis who may be at greatest risk of developing heart disease.
This study will examine the magnitude of the increased risk of hear disease in patients with psoriasis. It will also identify key risk factors and investigate the biological pathway for the development of hear disease in these patients. The project will use an integrated research approach and translate findings from studies of the function of genes and cells into improved identification and management of heart disease in patients with psoriasis.

• Dr Julia Reichelt at Newcastle University. Signal transduction of stress in normal and psoriatic keratinocytes.
Psoriatic plaques are characterised by a strong thickening of the skin. This thickening is due to excessive proliferation of cells (keratinocytes) which constitute the epidermis, the uppermost layer of the skin. The cause for the increase in keratinocyte proliferation and hence the development of the psoriatic plaques is unknown. A common observation, however, is that psoriatic plaques tend to localize to the knees and elbows, areas that are particularly subject to mechanical stress resulting to the action of bending. Moreover, plaques often develop at sites of trauma or injury. It is well established that most tissues react with increased growth following mechanical stress. Some of the molecular signals for this phenomenon are known and interestingly these are also activated in psoriatic skin.
We therefore aim to test the hypothesis that psoriatic skin and particularly the epidermal keratinocytes are oversensitive to mechanical stress. To this aim we will evaluate the signals regulating the development of psoriatic plaques leading to the definition of novel therapeutic targets for psoriasis treatment.