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Some studies have found that rosiglitazone has a unfavorable effects on three novel inflammatory biomarkers previously shown to independently associate with atherosclerosis (LT[beta]R, PGLYRP-1, and CCL23) and a favorable effect on another novel biomarker (Ling et al., 2015), sRAGE, which previously studies have been shown to be inversely associated with atherosclerosis (Lubrano et al., 2015).
In the GO network, seven genes (C-C motif chemokine ligand 1 [CCL1], CCL23, hemopexin, mucolipin 1, leucine zipper and EF-hand containing transmembrane protein 2, phospholipase A2 group VI [PLA2G6], and protein tyrosine phosphatase, receptor type, C [PTPRC]) were related to cellular metal ion homeostasis in seven major GO terms, and this cluster was the largest in this network.
In addition, cytokine-cytokine receptor interaction signaling pathways were predicted to have strong relationships with the target genes, such as CCL23 ( ENST00000591423 ) , CCR10 ( NM_016602 ), and TNFRSF6B (NM_003823) .
Human CC chemokine CCL23 enhances expression of matrix metalloproteinase-2 and invasion of vascular endothelial cells.
Among them, we found the principal components of major regulatory clusters, involving inflammatory responses (IFNy, IL6, several members of the interleukin 1 pathway, including ILIA, IL1B, IL1RN, and the TNF pathway members TNF, TNFAIP6, TNFSF15, TNFRSF9), angiogenesis (CXCL10, PTGS2), immune regulation (CD80, CD274, CSF3, IL23R), leukocyte chemotaxis (CCL2, CCL3, CCL4, CCL20, CCL23, CCL3L3, CXCL1, CXCL2, CXCL5, CXCL9), transcriptional regulation (EGR1, GATA6, HEY1), proliferation (CDKN2B, FGFR1), adhesion (ITGB8), extracellular matrix remodeling (ADAMTS4), cell-cell communication (GJB2), cell signaling (EDNRB, IRS1, RIN2), ion transmembrane transport (KCNJ2, CLIC4), and response to oxidative stress (SOD2).
Analysis of gene expression in HREC (Figure 4) indicated that high glucose upregulated the transcript levels of interleukin-6 (IL-6) (D), IL-8 (E), IL-10 (F), TNF-[alpha] (G), and C-C motif chemokine ligand 23 (CCL23) (I).
ACKR2 binds most inflammatory CC-chemokines (CCL2, CCL5, CCL3, CCL4, CCL7, CCL8, CCL11, CCL13, CCL17, CCL22, CCL23, and CCL24) leading to their degradation, thereby reducing local levels of inflammatory chemokines.
Potential novel biomarkers of disease activity in rheumatoid arthritis patients: CXCL13, CCL23, transforming growth factor alpha, tumor necrosis factor receptor superfamily member 9, and macrophage colony stimulating factor.
MCP-2 (CCL8), MCP-3 (CCL7), MPIF-1 (CCL23) and 6 Ckine (CCL21) also belongs to the same family as HCC4 (CCL16) [34].
Previous studies involving gene expression analysis have also demonstrated that allergens but not irritants may lead to upregulation of certain genes such as CCL23, CCL4, CYP27A1, HML2, NOTCH3, S100A4, and SLAM in DCs, thus providing the basis for approaches to identify skin-sensitizing chemicals [60].