Resistin up-regulates fractalkine expression in human endothelial cells: lack of additive effect with TNF-alpha
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Updated: Jun 24, 2026

On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Ileana Manduteanu1, Elena Dragomir, Manuela Calin
1Institute of Cellular Biology and Pathology Nicolae Simionescu, 8 B.P. Hasdeu Street, P.O. Box 35-14, 050568 Bucharest, Romania. ileana.manduteanu@icbp.ro
Abstract:
Resistin is a cytokine and fractalkine (Fk) a cell adhesion molecule and chemokine that contribute to human vascular inflammation by mechanisms not clearly defined. We questioned whether resistin induces Fk expression in human endothelial cells (HEC), compared the effect with that of the pro-inflammatory cytokine, TNF-alpha, and evaluated the consequences of co-stimulating HEC with both activators on Fk induction and on the signalling molecules involved. We found that resistin up-regulated Fk expression at comparable level to that of TNF-alpha by a mechanism involving P38 and JNK MAPK and NF-kappaB. Co-stimulation of cells with resistin and TNF-alpha did not increase Fk expression induced by every single inducer. Moreover resistin reduced the expression induced by TNF-alpha in HEC. The new data uncover Fk as a novel molecular link between resistin and inflammation and show that resistin and TNF-alpha have no additive effect in Fk up-regulation or on the signalling molecules implicated.
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