Gene transcription of angiotensin II type 2 receptor is repressed by growth factors and glucocorticoids in PC12 cells.
The rat angiotensin II type 2 receptor (AT2-R) expression was markedly downregulated by the mitogenic action of serum, growth factors and dexamethasone. The regulation by serum or growth factors did not affect the AT2-R mRNA half-life (18 h), whereas the AT2-R half-lives of dexamethasone-treated cells and proliferating cells decreased to 10 h and 15 h, respectively. Nuclear run-off assays indicated the mechanism of repression of AT2-R expression by serum, growth factors and dexamethasone or in proliferating cells to be, in large part, transcriptional. These findings indicate that transcription of the AT2-R gene is regulated in a growth state-dependent manner and suggest that this regulation provides a means by which cells can modulate their responsiveness to the actions of angiotensin II mediated through AT2-R.
D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001769:Blood; D015152:Blotting, Northern; D002462:Cell Membrane / Q000378:metabolism; D002467:Cell Nucleus / Q000378:metabolism; D003470:Culture Media; D003513:Cycloheximide / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology*; D004815:Epidermal Growth Factor / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology*; D006133:Growth Substances / Q000494:pharmacology*; D007700:Kinetics; D009414:Nerve Growth Factors / Q000494:pharmacology; D016716:PC12 Cells; D012333:RNA, Messenger / Q000096:biosynthesis / Q000378:metabolism; D051381:Rats; D011945:Receptors, Angiotensin / Q000096:biosynthesis* / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects*
D003470:Culture Media; D005938:Glucocorticoids; D006133:Growth Substances; D009414:Nerve Growth Factors; D012333:RNA, Messenger; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D004815:Epidermal Growth Factor; D003907:Dexamethasone; D003513:Cycloheximide