anti-PR-3 (C-ANCA) IgG ELISA Kit

Aims: All-trans retinoic acid (ATRA) is used to treat patients with acute promyelocytic leukemia (APL) due to its ability to resume the differentiation of APL cells. Recently, clinical trials have been started to evaluate ATRA plus arsenic trioxide (ATO) as a combination treatment for APL patients. However, little is known about the detailed mechanisms underlying its efficacy. We therefore investigated the effects of this combination on the differentiation and differentiation-related gene expression. Main methods: Human leukemia HL-60 cells differentiation was examined using nitro blue tetrazolium and CD11b. The levels of mRNA and protein were determined by RT-qPCR, microarray, western blot and ELISA, respectively. The promoter activity was assessed by luciferase activity. The arsenic concentration was determined by ICP-MS. Key findings: ATRA-induced HL-60 differentiation was augmented by co-treatment with ATO. A microarray analysis showed that ATRA plus ATO treatment markedly down-regulated the expression of proteinase 3 (PRTN3), which is involved in the differentiation arrest of leukemia cells, compared with treatment with ATRA alone. The PRTN3 mRNA level was suppressed by treatment with ATRA alone, and then further suppressed by co-treatment with ATO, accompanied by a concomitant increase in Sp1 protein, which is known to facilitate differentiation. The expression levels of azurocidin, telomerase reverse transcriptase, ferritin, and interleukin-1 beta were also altered by co-treatment with ATO. Significance: Co-treatment with ATO enhances ATRA-induced HL-60 differentiation by altering the expression of genes involved in cell differentiation, providing the molecular basis for a combination therapy using ATO plus ATRA to treat leukemia patients. (C) 2016 Elsevier Inc. All rights reserved.

The purpose of this study was to detect the differentially expressed genes between ossified herniated discs and herniated discs without ossification. In addition, we sought to identify a few candidate genes and pathways by using bioinformatics analysis. We analyzed 6 samples each of ossified herniated discs (experimental group) and herniated discs without ossification (control group). Purified mRNA and cDNA extracted from the samples were subjected to sequencing. The NOISeq method was used to statistically identify the differentially expressed genes (DEGs) between the 2 groups. An in-depth analysis using bioinformatics tools based on the DEGs was performed using Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, and protein-protein interaction network analysis. The top 6 DEGs were verified using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A total of 132 DEGs was detected. A total of 129 genes in the ossified group were upregulated and 3 genes were found to be downregulated as compared to the control group. The top 3 cellular components in GO ontologies analysis were extracellular matrix components. GO functions were mainly related to the glycoprotein in the cell membrane and extracellular matrix. The GO process was related to completing response to stimulus, immune reflex and defense. The top 5 KEGG enrichment pathways were associated with infection and inflammation. Three of the top 20 DEGs [sclerostin (SOST), WNT inhibitory factor 1 (WIF1) and secreted frizzled related protein 4 (SFRP4)] were related to the inhibition of the Wnt pathway. The ossified discs exhibited a higher expression of the top 6 DEGs [SOST, joining chain of multimeric IgA and IgM (IGJ; also known as JCHAIN), defensin alpha 4 (DEFA4), SFRP4, proteinase 3 (PRTN3) and cathepsin G (CTSG)], with the associated P-values of 0.045, 0.000, 0.008, 0.010, 0.015 and 0.002, respectively, as calculated by the independent sample t-test. The gene expression profiling of the 2 groups revealed differential gene expression. Thus, our data suggest that Wnt pathway abnormality and local inflammation may be related to disc ossification.