Objective: Psoriasis is often closely related to metabolic syndrome (MS), herein we conducted this study to investigate the clinical characteristics of a large sample of psoriasis patients with MS in Xinjiang, China. Methods:The prevalence of MS, age, height, weight, body mass index (BMI), red blood cell count, white blood cell count, platelet count, aspartate aminotransferase level, alanine aminotransferase level, and other clinical data were analyzed in 2,492 patients with psoriasis. The patients were divided into 2 groups based on the presence of MS and their clinical features were compared. Student t test was used for independent samples, and the chi-square test was used for count data.Results: Among the 2,492 patients, 349 had MS and 1,269 were considered overweight/obese. There were significant differences in sex, age, disease course, age at onset, BMI, systolic blood pressure (SBP), and diastolic blood pressure (DBP) between the patients with MS and those without (all P < 0.05). The red blood cell count (P < 0.001), white blood cell count (P = 0.013), erythrocyte sedimentation rate (P < 0.001), blood urea nitrogen level (P < 0.001), triglyceride level (P < 0.001), total cholesterol level (P < 0.001), and low-density lipoprotein cholesterol level (P = 0.002) were significantly higher in the MS group than in the psoriasis-only group. The high-density lipoprotein cholesterol level was significantly lower in the MS group than in the psoriasis-only group (P < 0.001). The alanine aminotransferase (P = 0.145) and albumin levels (P = 0.192) were not significantly different between the 2 groups (P > 0.05). Binary logistic regression analysis showed that sex, age, BMI, SBP, DBP, and fasting plasma glucose were independent risk factors for MS in patients with psoriasis, and high-density lipoprotein cholesterol was considered a protective factor for these patients. Conclusion:The prevalence of MS in patients with psoriasis is high. Female sex, age, BMI, SBP, DBP, and fasting plasma glucose may be risk factors for psoriasis complicated by MS.

Objectives We investigated the effect and mechanism of miR-21-3p on the biological behavior of keratinocyte HaCaT cells. Methods HaCaT cells were transfected with miR-21-3p mimics and miR-21-3p inhibitor, respectively. Cell proliferation was detected by CCK-8, and apoptosis and cell cycle were analyzed by flow cytometry. The expression changes of Bax and Bcl-2 were measured with immunohistochemistry. The mRNA expressions of IL-17A and STAT3 were detected by real-time fluorescence quantitative PCR. Cytokeratin 17 protein was detected by Western blot. The relationship between miR-21-3p and STAT3 was verified by dual luciferase reporter gene assay. Results The miR-21-3p mimics significantly promoted the proliferation and cell cycle progression of HaCaT cells. However, miR-21-3p mimics significantly inhibited cell apoptosis, decreased Bax expression and increased Bcl-2 expression. Additionally, miR-21-3p mimics significantly increased the expressions of Cytokeratin 17 protein, IL-17A mRNA and STAT3 mRNA. Of note, the miR-21-3p inhibitor exhibited contrary effects to miR-21-3p mimics. Furthermore, STAT3 was a direct target of miR-21-3p. Conclusion miR-21-3p may promote the abnormal proliferation and inhibit apoptosis of HaCaT cells, possibly through regulating JAK/STAT pathway and the expression of Cytokeratin 17.

Cutaneous T-cell lymphomas (CTCLs) are a kind of non-Hodgkin lymphoma that originates from skin, which is difficult to treat with traditional drugs. Human histone deacetylase inhibitors (HDACi) targeted therapy has become a promising treatment strategy in recent years, but some patients can develop resistance to the drug, leading to treatment failure. There are no public reports on whether alternative splicing (AS) and RNA binding proteins (RBP) affect the efficacy of targeted therapy. Using data from the Gene Expression Omnibus (GEO) database, we established a co-change network of AS events and RBP in CTCLs for the first time, and analyzed the potential regulatory effects of RBP on HDACi-related AS events. The dataset GSE132053, which contained the RNA sequence data for 17 HDACi samples, was downloaded and clean reads were aligned to the human GRCh38 genome by hierarchical indexing for spliced alignment of the transcripts, allowing four mismatches. Gene expression levels were evaluated using exons per million fragments mapped for each gene. Student’s t-tests were performed to evaluate the significance of changes in ratios for AS events, and regulated alternative splicing events (RASEs) were defined as events with p values less than 0.05. To sort the differentially expressed genes functional categories, Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways were identified using the KOBAS 2.0 server. The regulatory mechanisms of the RASEs and RBPs were evaluated using Pearson’s correlation coefficient. Seven indirect events of HDACi resistance or sensitivity were identified: NIR_5151_RP11-977G19.10, NIR_4557_IRAG2, NIR_11870_SUMO1, NIR_5347_ING4, NIR_17935_DNAJC2, NIR_17974_CBLL1, and NIR_422_SLC50A1. The potential regulatory relationships between RBPs and HDACi-sensitive RASEs were also analyzed. LEPR and HNRNPAO significantly affected NIR_11870_SUMO1, suggesting a potential regulatory relationship. Additionally, CNN1 may regulate NIR_5347_ING4, CNOT3 may regulate NIR_17935_DNAJC2, and DQX1 and LENG9 may regulate NIR_422_SLC5A1. Overall, our findings establish a theoretical foundation for the precise targeted treatment of CTCLs with HDACi.