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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00978.2001
Submitted on November 7, 2001
Accepted on March 21, 2002
B
1 Res. Center, Pavillon HDQ, Centre Hospitalier Universitaire de Quebec, Quebec City, PQ, Canada
2 Angiogene Inc., Montreal, PQ, Canada
* To whom correspondence should be addressed. E-mail: francois.marceau{at}crhdq.ulaval.ca.
Kinin B1 receptor (B1R) expression and the importance of the transcription factor NF-B in this process has been evaluated in models based on the rabbit aorta : the freshly isolated tissue (post-isolation induction) and cultured smooth muscle cells (SMCs). A 3 h incubation of freshly isolated tissues determined a sharp B1R mRNA increase (RT-PCR). Co-incubation of tissues with a stimulus (interleukin-1ß, fetal bovine serum, epidermal growth factor or cycloheximide) further increased mRNA levels. Cultured SMCs possessed a basal population of surface B1Rs ([3H]Lys-des-Arg9-BK binding) that was upregulated by treatments with the same set of stimuli (binding, mRNA, nuclear run-on). Pharmacological inhibitors of NF-B (MG 132, Bay 11-7082, dexamethasone) or actinomycin D reduced the post-isolation induction of B1Rs in fresh aortic tissue (contractility or mRNA) and cytokine effect on cells (mRNA, binding). NF-B may be a common mediator of various stimuli that increase B1R gene transcription in the rabbit aorta, including tissue isolation, but cycloheximide also stabilizes B1R mRNA. The SMC model faithfully mimic the in vivo situation with regard to B1R regulation.
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