Mycophenolic acid attenuates the tumour necrosis factor-α-mediated proinflammatory response in endothelial cells by blocking the MAPK/NF-κB and ROS pathways

2013 ◽  
Vol 44 (1) ◽  
pp. 54-64 ◽  
Author(s):  
Wioletta Olejarz ◽  
Dorota Bryk ◽  
Danuta Zapolska-Downar ◽  
Maciej Małecki ◽  
Anna Stachurska ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumour Necrosis Factor ◽  
Mycophenolic Acid ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Proinflammatory Response ◽  
Factor Α ◽  
Necrosis Factor

Ceramide mimics tumour necrosis factor-α in the induction of cell cycle arrest in endothelial cells

2000 ◽  
Vol 267 (14) ◽  
pp. 4325-4333 ◽  
Author(s):  
Rebeca López-Marure ◽  
José L. Ventura ◽  
Luis Sánchez ◽  
Luis F. Montaño ◽  
Alejandro Zentella
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cell Cycle Arrest ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Cycle Arrest ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Activation of RelA homodimers by tumour necrosis factor α: a possible transcriptional activator in human vascular endothelial cells

2005 ◽  
Vol 390 (1) ◽  
pp. 317-324 ◽  
Author(s):  
Nobuyuki Marui ◽  
Russell M. Medford ◽  
Mushtaq Ahmad
Keyword(s):  
Endothelial Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Vascular Endothelial Cells ◽  
Regulation Of Gene Expression ◽  
Simian Virus 40 ◽  
Vascular Endothelial ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

In vascular endothelial cells, cytokines induce genes that are expressed in inflammatory lesions partly through the activation of transcription factor NF-κB (nuclear factor-κB). Among the members of the NF-κB/rel protein family, homodimers of the RelA subunit of NF-κB can also function as strong transactivators when expressed in cells. However, the functional role of endogenous RelA homodimers has not been clearly elucidated. We investigated whether RelA homodimers are induced in cytokine-treated vascular endothelial cells. Gel mobility-shift and supershift assays revealed that a cytokine TNFα (tumour necrosis factor α) activated both NF-κB1/RelA heterodimers and RelA homodimers that bound to a canonical κB sequence, IgκB (immunoglobulin κB), in SV40 (simian virus 40) immortalized HMEC-1 (human dermal microvascular endothelial cell line 1). In HMEC-1 and HUVEC (human umbilical-vein endothelial cells), TNFα also induced RelA homodimers that bound to the sequence 65-2κB, which specifically binds to RelA homodimers but not to NF-κB1/RelA heterodimers in vitro. Deoxycholic acid, a detergent that can dissociate the NF-κB–IκB complex (where IκB stands for inhibitory κB), induced the binding of the RelA homodimers to 65-2κB from the cytosolic fraction of resting HMEC-1. Furthermore, TNFα induced the transcriptional activity of a reporter gene that was driven by 65-2κB in HMEC-1. These results suggest that in addition to NF-κB1/RelA heterodimers, TNFα also induces RelA homodimers that are functionally active. Thus RelA homodimers may actively participate in cytokine regulation of gene expression in human vascular endothelial cells.

Tumour necrosis factor-α gene expression and production in human umbilical arterial endothelial cells

2000 ◽  
Vol 98 (4) ◽  
pp. 461 ◽  
Author(s):  
Thomas NEUHAUS ◽  
Gudrun TOTZKE ◽  
Elisabeth GRUENEWALD ◽  
Hans-Peter JUESTEN ◽  
Agapios SACHINIDIS ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Arterial Endothelial Cells ◽  
Necrosis Factor
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