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Regulation of ankyrin repeat and suppressor of cytokine signalling box protein 4 expression in the immortalized murine endothelial cell lines MS1 and SVR: a role for tumour necrosis factor alpha and oxygen
Author(s) -
Bode Michael,
Wu Yaxu,
Pi Xinchun,
Lockyer Pamela,
Dechyapirom Weeranun,
Portbury Andrea L.,
Patterson Cam
Publication year - 2011
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1755
Subject(s) - biology , microbiology and biotechnology , tumor necrosis factor alpha , cytokine , downregulation and upregulation , transcription factor , endothelial stem cell , angiogenesis , nfkb1 , oxygen tension , immunology , cancer research , chemistry , genetics , in vitro , gene , organic chemistry , oxygen
During vascular development, endothelial cells are exposed to a variety of rapidly changing factors, including fluctuating oxygen levels. We have previously shown that ankyrin repeat and suppressor of cytokine signalling box protein 4 (ASB4) is the most highly differentially expressed gene in the vascular lineage during early differentiation and is expressed in the embryonic vasculature at a time when oxygen tension is rising because of the onset of placental blood flow. To further our understanding of the regulation of ASB4 expression in endothelial cells, we tested the effect of various stressors for their ability to alter ASB4 expression in the immortalized murine endothelial cell lines MS1 and SVR. ASB4 expression is decreased during hypoxic insult and shear stress, whereas it is increased in response to tumour necrosis factor alpha (TNF‐ α ). Further investigation indicated that nuclear factor kappa B (NF‐ κ B) is the responsible transcription factor involved in the TNF‐ α ‐induced upregulation of ASB4, placing ASB4 downstream of NF‐ κ B in the TNF‐ α signalling cascade and identifying it as a potential regulator for TNF‐ α 's numerous functions associated with inflammation, angiogenesis and apoptosis. Copyright © 2011 John Wiley & Sons, Ltd.