Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10771459 | Biochemical and Biophysical Research Communications | 2005 | 7 Pages |
Abstract
We recently reported that vasohibin is a negative feedback regulator of angiogenesis, and it is specifically expressed in endothelial cells. Here, we characterize the regulation of vasohibin expression. Two possible splicing variants were found, and the longer isoform was preferentially expressed. VEGF induced the expression of vasohibin, and this induction was abrogated by anti-VEGFR2 mAb but not by anti-VEGFR1 mAb. Pharmacological analysis revealed that the downstream targets of VEGFR2 were PKCs, especially PKCδ. Actinomycin D did not alter the kinetics of vasohibin mRNA induction upon VEGF treatment, whereas cycloheximide completely abolished its induction. We tested the effect of various inflammatory cytokines on vasohibin expression. TNFα, IL1 and IFNγ decreased VEGF-stimulated vasohibin expression. Actinomycin D did not alter the kinetics of vasohibin mRNA induction upon TNFα treatment. These results indicate that the expression of vasohibin in endothelial cells is regulated either positively or negatively by certain factors at the transcriptional level.
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Authors
Kazue Shimizu, Kazuhide Watanabe, Hiroshi Yamashita, Mayumi Abe, Hironobu Yoshimatsu, Hideki Ohta, Hikaru Sonoda, Yasufumi Sato,