Psoriasin (S100A7) promotes stress-induced angiogenesis

Abstract

SummaryBackground Vascular modifications occur early in the development of psoriasis, and angiogenesis is one of the key features in the pathogenesis of the disease. Objectives To identify the role of the S100 protein psoriasin in psoriasis-associated angiogenesis. Methods The role of psoriasin in mediating angiogenesis was investigated by silencing psoriasin with small interfering RNA (siRNA) and measuring psoriasisassociated angiogenic factors in human epidermal keratinocytes. The secretion of psoriasin and the effect of psoriasin on general regulators of angiogenesis in keratinocytes, and on endothelial cell migration, proliferation, tube formation and production of angiogenic mediators, was evaluated. Results Reactive oxygen species (ROS) and hypoxia induced the expression of psoriasin. Downregulation of psoriasin in keratinocytes using siRNA altered the ROSinduced expression of the psoriasis-associated angiogenic factors vascular endothelial growth factor (VEGF), heparin-binding epidermal growth factor-like growth factor, matrix metalloproteinase 1 and thrombospondin 1. Overexpression of psoriasin altered several regulators of angiogenesis and led to the secretion of psoriasin. Treatment with extracellular psoriasin induced proliferation, migration and tube formation in dermal-derived endothelial cells to a similar extent as VEGF and interleukin-17, and induced the expression and release of proangiogenic mediators. These effects were suggested to be mediated by the PI3K and nuclear factor kappa B pathways. Conclusions These findings suggest that psoriasin expression is promoted by oxidative stress in keratinocytes and amplifies the ROS-induced expression of angiogenic factors relevant to psoriasis. Moreover, extracellularly secreted psoriasin may act on dermal endothelial cells to contribute to key features angiogenesis.

East Indian Sandalwood Oil (EISO) Alleviates Inflammatory and Proliferative Pathologies of Psoriasis

“…Elevated expression of psoriasin in psoriatic plaques (Morizane and Gallo, 2012), as well as in other hyper-angiogenic conditions, has validated it as a marker to assess in the context of psoriasis (Vegfors et al, 2016). Additionally, psoriasin is a chemotactic for CD4+ T cells and neutrophils (Jinquan et al, 1996), and is induced by psoriasis-associated inflammatory cytokines that include IL-1β, IL-17, IL-22, and TNF-α (Liang et al, 2006).…”

Psoriasin (S100A7): a novel mediator of angiogenesis

“…In this issue of the BJD , Vegfors et al . found that stress signals, such as hypoxia and reactive oxygen species (ROS) induce S100A7 expression in keratinocytes.…”

“…Vegfors et al . also showed that hypoxia and ROS can increase the expression of S100A7 in keratinocytes, but it is not clear how a hypoxic and inflammatory microenvironment induces angiogenesis.…”

The study of the specific pharmacological activity of Dermabin on the model of the experimental contact dermatitis in rats

“…CCL20, CCL27 and monokine induced by γ-interferon (MIG) participate in involvement of T-cells to the psoriatic rash zone [14,15,21]. Moreover, in psoriasis the release of angiogenic factors and pro-inflammatory cytokines intensifies, and the level of anti-inflammatory cytokines decreases [9,22].…”