CXCL2


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CXCL2

A gene on chromosome 4q13.3 that encodes a chemokine produced by activated monocytes and neutrophils and expressed at sites of inflammation. CXCL2 is thought to have a haematoregulatory role and suppresses haematopoietic progenitor cell proliferation.
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They discovered that curcumin reduces the expression of two pro-inflammatory proteins (cytokines CXCL1 and CXCL2) involved in prostate cancer, and in the mice curcumin caused a reduction in the incidence of metastases.
After endurance racing in horses, CXCL2, also called macrophage inflammatory protein 2-a (MIP2-a), is upregulated in peripheral blood mononuclear cells [4].
Among differentially expressed genes, IL1B, IL17F, IL6R, CXCL2, CCL20 and CCL25 were selected based on their immunological functions and CD8B and CD81 may contribute to variations of blood T lymphocyte subsets.
RNA analysis in ESBC and HNSCC revealed concordant increases in cytokine gene expression, including CXCL2, CCL4, CXCR4, and CXCL12 as well as transcription factors including FOS, ETS1, NF?B, EGR1/2 which are involved in T-cell activation and differentiation.
The researchers confirmed the relationship between deltaNp63 and MDSCs, showing that blocking two signaling molecules, CXCL2 and CCL22, activated by the protein reduced metastasis and blood-vessel growth associated with tumor growth, while increasing levels of these signaling molecules, caused MDSCs to boost the secretion of pro-tumor growth factors.
Chemokines such as CXCL2 and CXCL10 are also detected in endodontic infections.
Among these upregulated proteins, cytokines (TNF-[alpha]) and chemokines (I-309, ICAM-1, MCP-1, M-CSF, CCL3, CXCL12, CXCL2, CXCL9, and CXCL10) were significantly downregulated by MST1 suppression compared with the expression in the negative control animals (Figure 7(d)).
Expression of CXCL12 and CXCl2 was increased when rat MSCs were exposed to a C85 human colorectal cancer cell conditioned medium [56].
Video 1: transient and local vascular leakage during CXCL2 stimulated blood vessel.
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).
Based on the functional categorization of chemokines as described by Zlotnik and Yoshie [30], the elevated chemokines in TS-CONTROL compared to TS-COPD can be classified as follows: Inflammatory (CCL1, 7, and 15; CXCL2 and 9), homeostatic (CCL19, CCL25), and dual function (CCL17).