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Stimulation of tissue-type plasminogen activator expression by retinoic
acid in human endothelial cells requires retinoic acid receptor beta 2
induction
M Lansink and T Kooistra
Gaubius Laboratory, Leiden, The Netherlands.
We previously showed the involvement of retinoic acid receptor alpha (RAR
alpha) in the induction of tissue-type plasminogen activator (t- PA)
synthesis by RA in human umbilical vein endothelial cells (HUVECs).
However, the rather slow onset of this induction of t-PA synthesis
suggested an indirect role of RAR alpha. Here, we show that the protein
synthesis inhibitor, cycloheximide completely blocks the induction of t- PA
by RA, which points to the need of an intermediary protein in t-PA
stimulation. This intermediary protein is likely to be RAR beta 2 on the
basis of the following findings: (1) the induction of RAR beta by RA
exactly precedes that of t-PA; (2) HUVECs with elevated RAR beta mRNA
levels show an undelayed t-PA induction on stimulation with RA, and this
response can be almost completely inhibited with an RAR antagonist; and (3)
an antisense oligodeoxynucleotide against the translation initiation site
of RAR beta 2 mRNA greatly reduces the t-PA induction by RA. Thus,
induction of t-PA by RA in HUVECs involves a 2- step mechanism requiring
induction of RAR beta 2 via RAR alpha, followed by induction of t-PA
synthesis via RAR beta 2. Each of these steps is shown to have a different
activation profile with RA and 9 cis RA.
Volume 88,
Issue 2,
pp. 531-541,
07/15/1996
Copyright © 1996 by The American Society of Hematology
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