Livin upregulation in keratinocytes of psoriasis patients to promote adhesion molecule expression

Abstract

Background Activation of keratinocytes (KCs) is the main pathological feature of psoriasis.KCs recruit neutrophils by releasing various antimicrobial peptides and chemokines, which is also related to the expression of KC adhesion molecules. However, the regulatory mechanism governing their expression is still unclear. Livin, an inhibitor of the apoptosis protein family member involved in proliferation and metastasis of tumor cells, is significantly increased in psoriatic lesions.Objectives The aim of this study was to investigate the role of Livin in regulating adhesion molecule expression in KCs and release of chemokines that promote the activation and adhesion of neutrophils. MethodsThe expression of Livin in psoriasis patients, imiquimod mouse model, and the combination of IL-17 alpha, IL-22, IL-1 alpha, OSM, and TNF-a (Mix M5)-treated HaCaT cells were detected by immunofluorescence staining, RT-qPCR, and ELISA. Livinoverexpression and knockdown in HaCaT cells transfected with HIV-1-based lentiviral vectors were used to study the function of Livin using RNA-seq. Moreover, differences in the expression of HaCaT cell adhesion molecules after regulation of Livin expression and activation of neutrophils in the co-culture model were verified. Results Livin was upregulated in the KCs of psoriasis patients, imiquimod mouse model and Mix M5-treated HaCaT cells compared with the control groups. Livin in HaCaT cells might regulate the expression of adhesion molecules in KCs. Conclusion Thus, Livin may be a key effector molecule that regulates the expression of adhesion molecules in KCs and promotes the activation and adhesion of neutrophils.

Rehmannioside A Inhibits TRAF6/MAPK Pathway and Improves Psoriasis by Interfering with the Interaction of HaCaT Cells with IL-17A

“…Therefore, Unlike prior research, this study constructed a psoriasis cell model by stimulating HaCaT cells with IL-17A alone. The M5 cytokines, which include IL-1, IL-17A, IL-22, oncostatin M (OSM), and tumor necrosis factor (TNF)-α, have been employed in many recent in vitro psoriasis research [29][30][31] to intervene cells and simulate psoriasis. However, this modeling approach has the disadvantage that it does not allow exploring the effect of candidate drugs on the interaction between keratinocytes and one cytokine alone.…”

Livin is protective in UVB‐induced skin photodamage by regulating keratinocyte activation and inflammatory responses

“…Livin‐knockdown HaCaT cells and Livin‐overexpressing HaCaT cells were derived from our prior experiments; HaCaT refers to a keratinocyte cell line 11 . Negative control (NC‐HaCaT), knockdown HaCaT and overexpression HaCaT cells were produced through the utilization of lentiviral vectors based on HIV‐1.…”

“…Livin-knockdown HaCaT cells and Livin-overexpressing HaCaT cells were derived from our prior experiments; HaCaT refers to a keratinocyte cell line. 11 Negative control (NC-HaCaT), knockdown HaCaT and overexpression HaCaT cells were produced through the utilization of lentiviral vectors based on HIV-1. The three cell types were cultured in RPMI 1640 medium with a 1:100 concentration of penicillin-streptomycin and enriched with 10% FBS.…”

“…A recent investigation has shown that Livin plays a role in KC activation during the inflammatory response to psoriasis. Decreased Livin expression has been linked to the increased release of cytokines in KCs 11 . Nevertheless, there have been limited investigations into the role of Livin in keratinocytes and its impact on the development of UVB‐induced skin photodamage.…”

“…Decreased Livin expression has been linked to the increased release of cytokines in KCs. 11 Nevertheless, there have been limited investigations into the role of Livin in keratinocytes and its impact on the development of UVB-induced skin photodamage.…”