mProX™ Human CXCR2 Stable Cell Line

Hernandez DAZ, et al. "Expression of Transcriptional Factors of T Helper Differentiation (T-bet, GATA-3, ." Current molecular medicine, 2023.
The macrophage migration inhibitory factor (MIF) is a crucial factor in the development of rheumatoid arthritis (RA). Existing research has shown that MIF can induce the production of cytokines associated with T helper (Th)1, Th2, and Th17 responses in peripheral blood mononuclear cells (PBMC) from both RA patients and control subjects (CS). However, the specific molecular mechanisms involved have yet to be fully understood. Therefore, this study sought to investigate the relationship between the expression of MIF receptors (CD44, CD74, CXCR2, 4, 7) and Th differentiation transcription factors (T-bet, GATA-3, RORgammat) in PBMC from CS and RA patients, along with their respective Th1, Th2, and Th17 cytokines. PBMC from both groups were cultured for 24 h, with flow cytometry used to analyze the expression of MIF receptors and transcription factors, and multiplex bead analysis employed to measure cytokine levels in the culture supernatants. Results showed that CD74 expression was significantly increased in T CD4+ lymphocytes from the CS group (p<0.05), while CXCR7 expression was markedly higher in T CD4+ lymphocytes from RA patients (p<0.001). Furthermore, T CD4+ lymphocytes from RA patients exhibited higher levels of GATA3, RORgammat, and FOXP3 expression, as well as increased pro-inflammatory cytokine production, compared to the CS group (p<0.001). These findings demonstrate that CD74 is more highly expressed in PBMC from the CS group, whereas CXCR7 is more prominently expressed in RA patients. It was also observed that FOXP3 may be activated by CD74, while RORgammat may be activated via CXCR7, utilizing the endocytic pathway to promote the secretion of Th17 profile cytokines in RA. In conclusion, this study supports the role of MIF in the development of RA and may help identify potential therapeutic targets for the treatment of this condition.
Pubmed: 37807647   DOI: 10.2174/0115665240260976230925095330

Chabry Y, et al. "Prevention by the CXCR2 antagonist SCH527123 of the calcification of porcine ." Frontiers in cardiovascular medicine, 2023.
Abate et al. (year) highlighted calcification as a leading cause of failure in bioprosthetic heart valves. They further investigated the hypothesis that the inflammation caused by glutaraldehyde (GA) in the fixed cusps of the bioprosthesis plays a crucial role in promoting calcification. To test this, male Sprague Dawley rats were transplanted with GA-fixed or GA-free porcine aortic valve cusps and treated with either 1 mg/kg/day of the C-X-C chemokines receptor 2 (CXCR2) antagonist SCH5217123 or a control for 14 days. Results showed a significant decrease in calcification in rats treated with SCH5217123. Moreover, the treatment also prevented GA-induced infiltration of T-cells and macrophages in the transplanted xenografts. These findings suggest that antagonizing CXCR2 may prevent calcification in GA-fixed bioprosthetic heart valves.
Pubmed: 37781314   DOI: 10.3389/fcvm.2023.1227589