Inhibition of VCAM-1 expression by CORM-3: the role of the ubiquitin proteasome system, p38 and mitochondrial respiration

ABSTRACT: Carbon monoxide (CO) abrogates TNF-alpha mediated inflammatory responses in endothelial cells, yet, the underlying mechanism hereof is still elusive. We sought to explore potential mechanisms by which CO down-regulates VCAM-1 expression on TNF-alpha stimulated human umbilical vein endothelial cells (HUVEC). By genome-wide gene expression profiling and pathway analysis we studied the relevance of particular pathways for the anti-inflammatory effect of CO. In CO-releasing molecules-3 (CORM-3) stimulated HUVEC, significant changes in gene expression were found for genes implicated in the proteasome and porphyrine pathways. Although proteasome activities were increased by CORM-3, proteasome inhibitors did not abolish CORM-3‘s effect. Likewise, HO-1 inhibitors did not abrogate the ability of

ORGANISM(S): Homo sapiens

SUBMITTER: Benito Yard 

PROVIDER: E-GEOD-22175 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress