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Lipopolysaccharide increases monocyte binding to mesangial cells through fractalkine and its receptor

Title
Lipopolysaccharide increases monocyte binding to mesangial cells through fractalkine and its receptor
Authors
Park J.Song K.H.Ha H.
Ewha Authors
하헌주
SCOPUS Author ID
하헌주scopus
Issue Date
2012
Journal Title
Transplantation Proceedings
ISSN
0041-1345JCR Link
Citation
vol. 44, no. 4, pp. 1029 - 1031
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Fractalkine (CX3CL1) is a unique chemokine that functions not only as a chemokine but also as an adhesion molecule. Fractalkine plays an important role in the recruitment of macrophages into the kidneys by binding to its specific receptor CX3CR1, and renal fractalkine expression was shown to be increased in chronic renal allograft rejection. Considering that microcapillary inflammation is a key feature of chronic renal allograft rejection, the present study examined whether monocytes bind to mesangial cells cultured in the presence of lipopolysaccharide (LPS) through fractalkine/CX3CR1 in order to understand their regulation with respect to inflammation-induced renal allograft dysfunction. Mouse mesangial cells were stimulated with LPS in the presence or absence of fractalkine or CX3CR1 siRNA. Calcein-AM-labeled monocytes were used to evaluate monocyte binding. Fractalkine and CX3CR1 mRNA and protein expression were measured by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. LPS at 100 ng/mL significantly increased monocyte binding to mesangial cells. Each siRNA against fractalkine or CX3CR1 effectively inhibited LPS-induced monocyte-mesangial cell binding. Fractalkine and CX3CR1 mRNA expression were enhanced in mesangial cells stimulated with LPS. Fractalkine protein synthesis in media and lysate of mesangial cells were also induced by LPS. These results demonstrated that LPS induces monocyte-mesangial cell binding through the fractalkine/CX3CR1 system and suggested that fractalkine/CX3CR1 system may contribute to renal inflammation leading to chronic renal allograft rejection. © 2012 Elsevier Inc.
DOI
10.1016/j.transproceed.2012.03.046
Appears in Collections:
약학대학 > 약학과 > Journal papers
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