Expression of p53 family in scars.
BACKGROUND
There have been some reports on the relationship between p53 and keloid formation. However, there have been no studies comparing the p53 expression among scars in various stages of maturity. However, p63 and p73 have been identified as p53-related genes and have been found to be similar to p53 in their structures and functions and these proteins have also been suggested to relate to scar formation.


OBJECTIVE
We investigate the expression of three proteins of the p53 family in scars with various clinical manifestations and discuss the shared features and differences of these proteins.


METHODS
Forty untreated scar lesions consisting of keloids, hypertrophic scars, and atrophic scars were prepared for investigation. We detected the expression of p53, p63 and p73 proteins using Western blot analysis and histopathological study in each sample.


RESULTS
The 40 lesions were divided into four groups according to their clinical manifestations: keloid (Group A), red hypertrophic scar (Group B), white and hard hypertrophic scar (Group C), atrophic white scar (Group D). In Groups A and B, the histopathological findings demonstrated increased fibroblasts, capillary vessels and infiltration of inflammatory cells. In Group C, most of these changes decreased but proliferation of collagen fibers was evident. In Group D, the degree of proliferation of collagen fibers was much less and capillary vessels and infiltration of inflammatory cells were not evident. The levels of p53 protein elevated in Groups A, B and C and were higher in order of Groups A, B and C. In Group D, the level of p53 was almost the same as that of the control. The level of p63 protein was almost the same as that of the control in all groups. The level of p73 protein was elevated only in Group C.


CONCLUSIONS
The p53 family members behave in a different manner in various scar tissues. It is suggested that these proteins play different roles in scar formation and the development of unfavorable scars.
Tanaka
Aya
A
Division of Plastic Surgery, Nara Medical University, Kashihara, Shijocho 840, Kashihara, Nara 634-0813, Japan. atanaka@nmu-gw.naramed-u.ac.jp
Hatoko
Mitsuo
M
Tada
Hideyuki
H
Iioka
Hiroshi
H
Niitsuma
Katsunori
K
Miyagawa
Sachiko
S
D000293:Adolescent; D000328:Adult; D001284:Atrophy; D015153:Blotting, Western; D002648:Child; D002675:Child, Preschool; D004268:DNA-Binding Proteins / Q000378:metabolism*; D016147:Genes, Tumor Suppressor; D006801:Humans; D006984:Hypertrophy; D007223:Infant; D007627:Keloid / Q000378:metabolism* / Q000473:pathology; D008875:Middle Aged; D009687:Nuclear Proteins / Q000378:metabolism*; D010750:Phosphoproteins / Q000378:metabolism*; D015534:Trans-Activators / Q000378:metabolism*; D014157:Transcription Factors; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D025521:Tumor Suppressor Proteins
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D010750:Phosphoproteins; C115051:TP63 protein, human; C000606460:TP73 protein, human; D015534:Trans-Activators; D014157:Transcription Factors; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins