scholarly journals Premature senescence of highly proliferative endothelial progenitor cells is induced by tumor necrosis factor‐α via the p38 mitogen‐activated protein kinase pathway

2009 ◽  
Vol 23 (5) ◽  
pp. 1358-1365 ◽  
Author(s):  
Yanmin Zhang ◽  
Brittney‐Shea Herbert ◽  
Gangaraju Rajashekhar ◽  
David A. Ingram ◽  
Mervin C. Yoder ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mitogen Activated Protein Kinase ◽  
Premature Senescence ◽  
Mitogen Activated Protein ◽  
Factor Α ◽  
Kinase Pathway ◽  
Necrosis Factor

Graft Expression of p38 and Tumor Necrosis Factor-α in Heart Transplantation in Rats

2002 ◽  
Vol 12 (4) ◽  
pp. 309-313
Author(s):  
Xiaopeng Zhang ◽  
Yuemin Cao ◽  
Aihong Meng ◽  
Yushan Bai
Keyword(s):  
Protein Kinase ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mitogen Activated Protein Kinase ◽  
Brown Norway ◽  
Lewis Rat ◽  
Mitogen Activated Protein ◽  
Factor Α ◽  
Necrosis Factor

Objectives To investigate the expression of p38 mitogen-activated protein kinase and its relationship with myocardial apoptosis and tumor necrosis factor-α during acute cardiac allograft rejection and to study the effects of tacrolimus on the expression of the kinase. Methods Rats were divided into 3 groups: isograft (Lewis heart to Lewis rat; control group), allograft (Brown Norway heart to Lewis rat), and tacrolimus-treated allograft (Brown Norway heart to tacrolimus-treated Lewis rat). Grafts were collected 1, 3, 5, and 7 days after transplantation for determination of histopathological features, apoptosis of cardiac cells (by terminal deoxynucleotidyl transferase–mediated dUTP-biotin nick labeling), number of cells positive for both p38 and CD8 (by laser scanning confocal imaging), and expression of the kinase (by Western immunoblotting) and tumor necrosis factor-α (by reverse-transcriptase polymerase chain reaction). Results Compared with isografts from the control group, grafts from the untreated allograft group had significantly more apoptotic cells, greater expression of tumor necrosis factor-α and p38 mitogen-activated protein kinase, and more CD8-p38 double-positive cells at 5 and 7 days ( P<.05). The increases were prevented by treatment with tacrolimus. Conclusions The findings that the number of apoptotic cells, the number of CD8-p38 double-positive cells, the expression of tumor necrosis factor-α and p38 mitogen-activated protein kinase all increased during the same period in the allografts in nonimmunosuppressed recipients suggests that intragraft expression of p38 would be associated with the rejection in acute cardiac allograft rejection. Tacrolimus may alleviate rejection partly by inhibiting p38 mitogen-activated protein kinase.

Sign in / Sign up

Export Citation Format

Share Document