Regulation of Angiogenesis in Psoriasis by Dermal Mscs-Derived-EDIL3 via the Integrin Pathway

Abstract

One of the earliest events in the development of psoriatic lesion is a vascular network expansion. The abnormal vascular network is associated with increased endothelial cells (ECs) survival, proliferation, adhesion, migration, angiogenesis and permeability in psoriatic lesion. Recently, researchers found that the dermal mesenchymal stem cells (DMSCs) in psoriatic lesion involved in course of psoriasis. Our prior study demonstrated the mRNA and protein expression of the epidermal growth factor (EGF)-like repeats and discoidin I-like domains 3 (EDIL3) which is an important angiogenic and anti-inflammatory mediator in DMSCs was significantly upregulated in psoriasis. So, this study aimed to explore the association between DMSCs-derived-EDIL3 and psoriasis-associated angiogenesis in vivo and in vitro. In the present study, we confirmed that in vitro DMSCs-derived-EDIL3 involved in the adhesion, migration and tube formation of ECs via integrin-FAK/MEK/ERK signaling. In vivo, this research found that after injected recombination EDIL3 protein, the epidermis thickness and microvessel density were both elevated in the IMQ-induced psoriasis-like mouse model. Based on these results, we suggested that the modification of DMSCs, EDIL3 and integrin signal pathway might be a novel therapeutic strategy for psoriasis.