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[Regulative effect of nuclear factor kappa B on the expression of intercellular adhesion molecular-1 in human
Insights
Nuclear factor kappa B (NF-kappa B) regulates intercellular adhesion molecule-1 (ICAM-1) expression in human mesangial cells stimulated by interleukin-1 beta (IL-1 beta). This signaling pathway is involved in glomerular immune-inflammatory processes.
Area of Science:
- Molecular Biology
- Immunology
- Cell Biology
Context:
- Interleukin-1 beta (IL-1 beta) is a key inflammatory cytokine.
- Intercellular Adhesion Molecule-1 (ICAM-1) plays a role in immune cell adhesion and inflammation.
- Human Mesangial Cells (HMC) are crucial components of the glomerulus.
Purpose:
- To investigate the role of nuclear factor kappa B (NF-kappa B) in mediating IL-1 beta-induced ICAM-1 expression in HMC.
- To elucidate the signaling pathway involved in glomerular inflammation.
Summary:
- Interleukin-1 beta (IL-1 beta) rapidly activates nuclear factor kappa B (NF-kappa B) and upregulates ICAM-1 expression at both mRNA and protein levels in HMC.
- Inhibition of NF-kappa B activation using TPCK significantly blocked IL-1 beta-induced ICAM-1 expression.
- Electrophoresis mobility shift assay (EMSA), Northern Blot, and Cell ELISA were used to measure NF-kappa B activation and ICAM-1 expression.
Impact:
- NF-kappa B acts as a signaling factor for IL-1 beta-stimulated ICAM-1 expression in HMC.
- This finding suggests a mechanism by which NF-kappa B modulates immune-inflammatory processes in glomerular diseases.
Objective:
To study the regulative effect of nuclear factor kappa B (NF-kappa B) on the expression of intercellular adhesion molecular-1(ICAM-1) in human mesangial cells (HMC) by interleukin I-1 beta (IL-1 beta).
Methods:
Activation of NF-kappa B was measured by electrophoresis mobility shift assay (EMSA). ICAM-1 expression was detected by Northern Blot and Cell ELISA.
Results:
rhIL-1 beta (10 ng/ml) could rapidly stimulate activation and translocation of NF-kappa B, and also could enhance the expression of ICAM-1 in mRNA (0.14 vs 0.35) and protein (0.92 +/- 0.10 vs 1.35 +/- 0.11, P < 0.01) level. After pretreatment with 100 mumol/L L-1-chlor-3-(4-tosylamido)-4-phenyl-2 butanon (TPCK), an inhibitor of NF-kappa B, both ICAM-1 levels of mRNA and protein stimulated by rhIL-1 beta were blocked by about 50% in these cells (0.46 +/- 0.05 vs 1.29 +/- 0.12, P < 0.01) compared with the rhIL-1 beta-stimulated group.
Conclusion:
These results suggest that NF-kappa B is one of the signaling factors for IL-1-stimulated ICAM-1 expression in HMC. It may modulate the immune-inflammatory process in glomerular diseases.
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