Acitretin Promotes the Differentiation of Myeloid-Derived Suppressor Cells in the Treatment of Psoriasis

Li, Panpan; Peng, Cong; Chen, Xiang; Wu, Lisha; Yin, Mingzhu; Li, Jie; Qin, Qian; Kuang, Yehong; Zhu, Wu

doi:10.3389/fmed.2021.625130

Cited by 8 publications

(11 citation statements)

References 57 publications

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“…However, this study highlights acitretin, one of the biologics annotated here as being effective against STAT3. Its mode of action, which can decrease the myeloid form of cancer in the psoriasis model, is summarized ( Table 11 ) [ 84 ].…”

Section: Discussionmentioning

confidence: 99%

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Anand

2022

Cells

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Psoriasis is a persistent T-cell-supported inflammatory cutaneous disorder, which is defined by a significant expansion of basal cells in the epidermis. Cell cycle and STAT genes that control cell cycle progression and viral infection have been revealed to be comorbid with the development of certain cancers and other disorders, due to their abnormal or scanty expression. The purpose of this study is to evaluate the expression of certain cell cycle and STAT1/3 genes in psoriasis patients and to determine the types of comorbidities associated with these genes. To do so, we opted to adopt the in silico methodology, since it is a quick and easy way to discover any potential comorbidity risks that may exist in psoriasis patients. With the genes collected from early research groups, protein networks were created in this work using the NetworkAnalyst program. The crucial hub genes were identified by setting the degree parameter, and they were then used in gene ontology and pathway assessments. The transcription factors that control the hub genes were detected by exploring TRRUST, and DGIdb was probed for remedies that target transcription factors and hubs. Using the degree filter, the first protein subnetwork produced seven hub genes, including STAT3, CCNB1, STAT1, CCND1, CDC20, HSPA4, and MAD2L1. The hub genes were shown to be implicated in cell cycle pathways by the gene ontology and Reactome annotations. The former four hubs were found in signaling pathways, including prolactin, FoxO, JAK/STAT, and p53, according to the KEGG annotation. Furthermore, they enhanced several malignancies, including pancreatic cancer, Kaposi’s sarcoma, non-small cell lung cancer, and acute myeloid leukemia. Viral infections, including measles, hepatitis C, Epstein–Barr virus, and HTLV-1 and viral carcinogenesis were among the other susceptible diseases. Diabetes and inflammatory bowel disease were conjointly annotated. In total, 129 medicines were discovered in DGIdb to be effective against the transcription factors BRCA1, RELA, TP53, and MYC, as opposed to 10 medications against the hubs, STAT3 and CCND1, in tandem with 8 common medicines. The study suggests that the annotated medications should be tested in suitable psoriatic cell lines and animal models to optimize the drugs used based on the kind, severity, and related comorbidities of psoriasis. Furthermore, a personalized medicine protocol must be designed for each psoriasis patient that displays different comorbidities.

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Section: Discussionmentioning

confidence: 99%

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Anand

2022

Cells

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“…The comparative Ct method was used to quantify target gene (IL‐8, IL‐6, and TNF‐α) expression. The relative mRNA expression of IL‐8, IL‐6, and TNF‐α was normalized to β‐actin (internal control) using the 2 −ΔΔCt method 38 . ΔΔCt = (Ct target gene— Ct internal control ) experimental group —(Ct target gene —Ct internal control ) normal control group .…”

Section: Methodsmentioning

confidence: 99%

Etanercept ameliorates psoriasis progression through regulating high mobility group box 1 pathway

et al. 2023

Skin Research and Technology

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Background As a common skin disease, psoriasis is related to inflammation and immune response. Due to the frequent recurrence of psoriasis, the treatment of psoriasis remains a clinical challenge. As an effective tumor necrosis factor‐alpha (TNF‐α) inhibitor, etanercept has been used for the treatment of psoriasis. However, some patients with psoriasis have no response to etanercept or discontinue treatment. To improve the therapeutic effect of etanercept, searching the potential biomarkers and investigating the related mechanisms of etanercept in the treatment of psoriasis are vital. Materials and methods We stimulated HaCaT cells with lipopolysaccharide (LPS) to generate cellular psoriatic changes and established an imiquimod (IMQ)‐induced psoriasis‐like mouse model, and then used an etanercept to treat cell and mouse model. Results Etanercept alleviated IMQ‐induced pathological changes and inflammation, and it also decreased the protein expression of high mobility group box 1 (HMGB1), receptor for advanced glycation end‐products, and toll‐like receptor 4. Moreover, the results of in vitro experiments showed that etanercept inhibited proliferation and inflammation, and promoted cell cycle arrest and apoptosis in LPS‐treated HaCaT cells. Knockdown of HMGB1 further enhanced the inhibitory effects of etanercept on LPS‐treated HaCaT cell viability and inflammation, while overexpression of HMGB1 notably reversed the inhibitory effects of etanercept on LPS‐induced HaCaT cell viability and inflammation. Conclusion Etanercept inhibited proliferation and inflammation and promoted cell cycle arrest and apoptosis in LPS‐induced HaCaT cells, and etanercept ameliorated inflammation in a psoriasis‐like mouse model.

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“…Myeloid-derived suppressor cells (MDSCs) have been demonstrated involved in the progress of psoriasis. GSH synthesis in MDSCs isolated from the bone marrow of IMQ-induced psoriatic mice model with ROS accumulation was reduced, resulting in interruption of MDSCs differentiation into CD11c + MHC II + dendritic cells and CD206 + M2 macrophages to exacerbate skin inflammation [ 65 ]. In murine macrophages, LPS/IMQ could induce ROS/RNS-NF-κB/ERK/JNK signaling pathway and decrease the expression of NRF2, increasing iNOS and other inflammatory cytokines to exacerbate psoriasiform skin inflammation [ 66 ].…”

Section: Oxidative Stress and Its Roles In Different Cell Types Dysfu...mentioning

confidence: 99%

Advances in the modulation of ROS and transdermal administration for anti-psoriatic nanotherapies

Chen

Qian

et al. 2022

J Nanobiotechnol

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Reactive oxygen species (ROS) at supraphysiological concentration have a determinate role in contributing to immuno-metabolic disorders in the epithelial immune microenvironment (EIME) of psoriatic lesions. With an exclusive focus on the gene-oxidative stress environment interaction in the EIME, a comprehensive strategy based on ROS-regulating nanomedicines is greatly anticipated to become the mainstay of anti-psoriasis treatment. This potential therapeutic modality could inhibit the acceleration of psoriasis via remodeling the redox equilibrium and reshaping the EIME. Herein, we present a marked overview of the current progress in the pathomechanisms of psoriasis, with particular concerns on the potential pathogenic role of ROS, which significantly dysregulates redox metabolism of keratinocytes (KCs) and skin-resident or -infiltrating cells. Meanwhile, the emergence of versatile nanomaterial-guided evolution for transdermal drug delivery has been attractive for the percutaneous administration of antipsoriatic therapies in recent years. We emphasize the underlying molecular mechanism of ROS-based nanoreactors for improved therapeutic outcomes against psoriasis and summarize up-to-date progress relating to the advantages and limitations of nanotherapeutic application for transdermal administration, as well as update an insight into potential future directions for nanotherapies in ROS-related skin diseases. Graphical Abstract

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Acitretin Promotes the Differentiation of Myeloid-Derived Suppressor Cells in the Treatment of Psoriasis

Cited by 8 publications

References 57 publications

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Etanercept ameliorates psoriasis progression through regulating high mobility group box 1 pathway

Advances in the modulation of ROS and transdermal administration for anti-psoriatic nanotherapies

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