Requirement of caspases and p38 MAPK for TRAIL-mediated ICAM-1 expression by human astroglial cells.

Abstract:

:Among tumor necrosis factor (TNF) superfamily, TNF-related apoptosis inducing ligand (TRAIL) along with TNF-alpha and FasL is known as death ligand due to its selective cytotoxicity against transformed tumor cells. TRAIL can also induce alternative angiogenic and/or proinflammatory signals other than apoptosis, however, the molecular mechanisms responsible for the alternative signals have not been detailed yet. Intercellular adhesion molecule-1 (ICAM-1) is thought to be involved in the processes of metastasis and angiogenesis in various tumors. We investigated the molecular mechanisms responsible for ICAM-1 expression by death ligands in human astroglial cells to delineate the alternative signals of these ligands. Here, we demonstrate that (1) death ligands induced expression of ICAM-1 at the mRNA and protein levels in human astroglial cells; (2) pre-treatment of z-VAD-fmk and/or SB202190 suppressed death ligand-induced ICAM-1 expression and subsequent adhesion of activated monocytic cells; and (3) inhibition of caspase suppressed death ligand-induced phosphorylation of p38 MAPK and IKK. These findings suggest biological function of death receptors other than apoptosis in human astroglial cells, and the involvement of caspase and/or p38 MAPK in alternative signaling through death receptors.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Choi K,Song S,Choi C

doi

10.1016/j.imlet.2008.01.010

subject

Has Abstract

pub_date

2008-05-15 00:00:00

pages

168-73

issue

2

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(08)00038-2

journal_volume

117

pub_type

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