Early growth-response factor-1 is involved in cellular injury of transplanted hearts

2005 ◽  
Vol 24 (2) ◽  
pp. S97
Author(s):  
D. Abraham ◽  
S. Aharinejad ◽  
A. Zuckermann ◽  
P. Paulus ◽  
R. Schaefer ◽  
...  
2001 ◽  
Vol 89 (8) ◽  
pp. 670-677 ◽  
Author(s):  
Harry C. Lowe ◽  
Roger G. Fahmy ◽  
Mary M. Kavurma ◽  
Andrew Baker ◽  
Colin N. Chesterman ◽  
...  

1995 ◽  
Vol 270 (12) ◽  
pp. 7004-7010 ◽  
Author(s):  
Edward J. Kilbourne ◽  
Russell Widom ◽  
Douglas C. Harnish ◽  
Sohail Malik ◽  
Sotirios K. Karathanasis

2003 ◽  
Vol 373 (3) ◽  
pp. 739-746 ◽  
Author(s):  
Miguel PIGNATELLI ◽  
Rosario LUNA-MEDINA ◽  
Arturo PÉREZ-RENDÓN ◽  
Angel SANTOS ◽  
Ana PEREZ-CASTILLO

Early growth response factor-1 (EGR-1) is an immediate early gene, which is rapidly activated in quiescent cells by mitogens or in postmitotic neurons after depolarization. EGR-1 has been involved in diverse biological functions such as cell growth, differentiation and apoptosis. Here we report that enforced expression of the EGR-1 gene induces apoptosis, as determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-fluorescein nick-end labelling (TUNEL) analysis, in murine Neuro2A cells. In accordance with this role of EGR-1 in cell death, antisense oligonucleotides increase cell viability in cells cultured in the absence of serum. This apoptotic activity of the EGR-1 appears to be mediated by p73, a member of the p53 family of proteins, since an increase in the amount of p73 is observed in clones stably expressing the EGR-1 protein. We also observed an increase in the transcriptional activity of the mdm2 promoter in cells overexpressing EGR-1, which is paralleled by a marked decrease in the levels of p53 protein, therefore excluding a role of this protein in mediating EGR-1-induced apoptosis. Our results suggest that EGR-1 is an important factor involved in neuronal apoptosis.


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