Abstract
Psoriasis is a chronic inflammatory skin disease. Even though scientists predict that abnormalities in lipid metabolism play an important role in the pathogenesis of psoriasis, the actual underlying mechanisms are still unclear. Therefore, understanding the possible relationship between mechanisms of the occurrence of psoriasis and dyslipidemia is an important issue that may lead to the development of effective therapies. Under this principle, we investigated the influences of hyperlipidemia in imiquimod (IMQ)-induced psoriasis-like B6.129S2-Apoetm1Unc/J mice and oxidized low-density lipoprotein (oxLDL) in tumor necrosis factor (TNF)-α-stimulated Hacat cells. In our study, we showed that a high-cholesterol diet aggravated psoriasis-like phenomena in IMQ-treated B6.129S2-Apoetm1Unc/J mice. In vitro analysis showed that oxLDL increased keratinocyte migration and lectin-type oxLDL receptor 1 (LOX-1) expression. Evidence suggested that interleukin (IL)-23 was a main cytokine in the pathogenesis of psoriasis. High-cholesterol diet aggravated IL-23 expression in IMQ-treated B6.129S2-Apoetm1Unc/J mice, and oxLDL induced IL-23 expression mediated by LOX-1 in TNF-α-stimulated Hacat cells. Therefore, it will be interesting to investigate the factors for the oxLDL induction of LOX-1 in psoriasis. LOX-1 receptor expression may be another novel treatment option for psoriasis and might represent the most promising strategy.
Highlights
Psoriasis is a chronic inflammatory skin disease of unknown etiology that is estimated to affect 2–3% of the general population worldwide [1]
After pretreatment of cells with oxidized low-density lipoprotein (oxLDL) for 24 h and scraping for 6 or 18 h, the migratory ability increased with 20 and 60 μg/mL oxLDL in Hacat cells (20 μg/mL oxLDL for 18 h: 200.4 ± 19.8% of the control, 60 μg/mL oxLDL for 6 h: 186.7 ± 11.7% of the control, and 60 μg/mL oxLDL for 18 h: 304.7 ± 25.8% of the control) (Figure 2C). These results indicate that oxLDL potentially increases the migration and lectin-type oxLDL receptor 1 (LOX-1) expression of keratinocytes, which we predict are associated with the expression of LOX-1
The wound healing assay showed that LOX-1 mediated oxLDL-aggravated migration by tumor necrosis factor (TNF)-α-stimulated keratinocytes (Figure 3C). These results suggest that oxLDL induces keratinocyte activity and aggravates TNF-α effects on keratinocytes by mediating LOX-1
Summary
Psoriasis is a chronic inflammatory skin disease of unknown etiology that is estimated to affect 2–3% of the general population worldwide [1]. Even though conventional psoriasis has been thought to be a dermatological disease, current medical literature reports that psoriasis is chronic inflammation [2]. Psoriasis is characterized by patches of abnormal skin that are typically red, itchy, and scaly. Nails, and, sporadically, the joints and is characterized by epidermal hyperproliferation, abnormal differentiation of keratinocytes, and lymphocyte infiltration, which results in the raised plaques that constantly molt scales originating from excessive growth of the epidermal skin layer [3,4]. TNF-α contributes to the hyperproliferation of keratinocytes in the skin and stimulates adhesion molecule expression on vascular endothelial cells [4]
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