The psoriasin (S100A7) protein has previously been identified as over-abundant in the skin of psoriasis patients in comparison to patients with normal skin, making it a key player in the development and severity of psoriasis. Now, researchers from Linköping University in Sweden have discovered that S100A7, which has also been implicated in breast cancer, interacts with oxygen free radicals and vascular endothelial growth factors (VEGF) in a way that leads to significantly increased cell division and growth of new blood vessels (angiogenesis), the underlying cause of psoriasis. The researchers now believe that inhibiting psoriasin may be a new avenue for treating psoriasis.
The research team, led by associate professor Charlotta Enerbäck, treated endothelial cells with recombinant psoriasin, which resulted in an increased proliferation comparable to that of recombinant VEGF protein. According to the paper on the study in Breast Cancer Research and Treatment, “No change in proliferation was seen when endothelial cells were infected with psoriasin-expressing adenoviruses, suggesting that the proliferative effect of psoriasin was mediated by a specific receptor.”
In the course of the study, Enerbäck and colleagues also blocked the formation of psoriasin, which correlated to a decrease in VEGF expression. Because the first steps of the study determined that the relationship between psoriasin, oxygen free radicals and VEGF led to significantly increased cell division and angiogenesis – the underlying causes of psoriasis – the team believes this discovery has significant treatment potential.
“We want to examine the ability of psoriasin as a target for therapy. By inhibiting psoriasin, we believe we can reduce vascular formation and thus the proliferation of the disease’s magnitude and intensity,” says Enerbäck, who explains that previous studies in mice have shown that angiogenesis inhibitors reduce neovascularization, inflammation and excessive cell division. Attempts to inhibit VEGF have resulted in unwanted side effects because it exists in normal tissue, where it contributes to wound healing.
“Since psoriasin expresses itself specifically only in the diseased psoriatic skin, we expect that inhibitors against this are highly selective and effective against the disease, and that the risk for side effects is minimal,” says Enerbäck.
To learn more about the study, please click here.
