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Lipopolysaccharide‐induced expression of VCAM‐1 in human renal mesangial cells
Author(s) -
Chen JungTsan,
Yang ChuenMao
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.963.1
Subject(s) - vcam 1 , p38 mitogen activated protein kinases , mapk/erk pathway , cell adhesion molecule , microbiology and biotechnology , western blot , lipopolysaccharide , nf κb , phosphorylation , flow cytometry , cell adhesion , chemistry , signal transduction , icam 1 , cancer research , biology , immunology , cell , biochemistry , gene
Several factors have been shown to trigger the pathologenesis of renal inflammatory diseases. Vascular cell adhesion molecule‐1 (VCAM‐1) is one kind of adhesion molecule participating in the process of polymorphonuclear cells (PMNs) transmigration, which recruit and adhesion to the renal glomerular mesangial cells. Thus, up‐regulation of VCAM‐1 may play a pivotal role in inflammatory responses of kidney. However, the mechanisms underlying LPS‐induced VCAM‐1 expression in HRMCs remains unknown. Western blot, real‐time PCR, promoter luciferase assay and monocytes adhesion analyses showed that in HRMCs, LPS‐induced VCAM‐1 mRNA and protein expression, and promoter activity was attenuated by the inhibitors of p42/p44 MAPK (U0126), p38 MAPK (SB202190) and NF‐κB (Bay11‐7082). In addition, LPS stimulated phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK which was attenuated by the inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), and JNK (SP600125). Besides, we also investigate that ROS is involved in LPS‐induced VCAM‐1 expression, determined by flow cytometry and H 2 DCFDA assays. These results suggested that in HRMCs, LPS‐induced VCAM‐1 expression was mediated through phosphorylation of MAPKs and NF‐κB pathways, and contributed to leukocyte/HRMCs interaction and promote inflammatory responses.