Increased expression of p53 protein correlates with the extent of myocyte damage in cardiac allograft rejection.
Acute cardiac allograft rejection (ACAR) has been associated with a poor prognosis. The early diagnosis of ACAR necessitates the accurate detection of myocyte damage. Nuclear damage activates p53, a transcription factor that initiates apoptosis and repair. Endomyocardial biopsies (n=25) from 10 cardiac allograft recipients were stained for nuclear p53. The biopsies were divided into rejection groups based on the grading of ACAR: group 1, grade 0; group 2, grade Ia and Ib; group 3, grades II and III. While clinical indices did not correlate with myocyte damage, significantly more myocytes in group 3 stained for nuclear p53 (2.48+/-0.60/mm(2)) compared with group 1 (0.22+/-0.12/mm(2)) and group 2 (0.43+/-0.18/mm(2)). Increased expression of p53 in cardiac myocytes with grade II or grade III rejection provides an objective quantification as an aid in the diagnosis of ACAR.
McLaren
Bernadette K
BK
Department of Pathology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Venkatesh
Prasanna K
PK
Misra
Praphul
P
Zhang
Ping L
PL
Fowler
Marjorie R
MR
D000328:Adult; D017209:Apoptosis; D005260:Female; D006084:Graft Rejection; D016027:Heart Transplantation; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D011379:Prognosis; D012189:Retrospective Studies; D012307:Risk Factors; D013318:Stroke Volume; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000378:metabolism*
D016159:Tumor Suppressor Protein p53