Abstract:
:The mechanism by which p53 activates apoptosis in various cell systems is unknown. In the absence of an external death stimulus, p53 and p53-dependent genes, bcl-2 and bax, cannot trigger apoptosis. However, p53 may enhance not only transcription of bax and repress bcl-2, but also may upregulate the local renin-angiotensin system, inducing the formation and secretion of angiotensin II from the cells. To test this hypothesis, adult rat ventricular myocytes were infected with AdCMV.p53, which resulted in downregulation of Bcl-2, upregulation of Bax, and death of 34% of the cells. Gel retardation assays demonstrated p53 binding in the promoters of angiotensinogen and angiotensin II AT1 receptor subtype. Angiotensinogen and AT1 mRNAs increased in AdCMV.p53 cells and this phenomenon was associated with a 14-fold increase in the secretion of angiotensin II. The AT1 receptor blocker losartan and angiotensin II antibody prevented p53-induced apoptosis. Thus, p53 enhances the myocyte renin-angiotensin-system and decreases the Bcl-2/Bax ratio in the cells, triggering apoptosis. The identification of this new pathway in p53-mediated apoptosis may be critical in the alterations of myocardial function in the pathologic heart.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Pierzchalski P,Reiss K,Cheng W,Cirielli C,Kajstura J,Nitahara JA,Rizk M,Capogrossi MC,Anversa Pdoi
10.1006/excr.1997.3604subject
Has Abstractpub_date
1997-07-10 00:00:00pages
57-65issue
1eissn
0014-4827issn
1090-2422pii
S0014-4827(97)93604-1journal_volume
234pub_type
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