Comparison of apoptotic gene expression profiles between Peyronie's disease plaque and tunica albuginea.
BACKGROUND
The fibrotic plaques of Peyronie/s disease and other localized fibrotic conditions have been considered to be the result of an abnormal wound healing process. The potential role of regulatory disorders of apoptosis in abnormal wound healing may also play a role in the development of Peyronie's disease.


OBJECTIVE
To examine the phenomenon of apoptosis in Peyronie's disease, authors quantified differential levels of gene expression of apoptotic proteins, Fas, Fas Ligand, Bcl-2, p53, Caspase 3 and 8 in Peyronie's plaque and tunica albuginea.


METHODS
Eight patients with Peyronie's disease undergoing surgical correction of the curvature had biopsy specimens taken from both the Peyronie's plaque and normal tunica albuginea. Messenger RNA expression of the apoptotic proteins in the plaque and normal tunica was measured by reverse transcriptase PCR.


RESULTS
Apoptotic gene expression was lower than the housekeeping gene's in half of the tunica albuginea samples and two thirds of the plaque samples. Overall mRNA expressions in the plaque were not significantly different from the normal tunica albuginea.


CONCLUSIONS
The fibrotic plaques of Peyronie's disease and other localized fibrotic conditions have been considered to be the result of an abnormal wound healing process. The potential role of regulatory disorders of apoptosis in abnormal wound healing may also play a role in the development of Peyronie's disease. In this study, the lower expression of apoptotic genes may cause the persistence of collagen producing cells which were up-regulated for unknown reasons and consequently result in plaque formation. Similar expression levels of apoptotic genes in both tunica albuginea and Peyronie's plaques may be due to the generalized physiopathologic alterations in tunica albuginea that lead to plaque formation at a vulnerable region subjected to recurrent traumas.
Department of Urology, Rize University, Rize Medical Faculty, Rize, Turkey. zorbaunal@gmail.com
Orhan U
OU
Zorba
Sema
S
Sirma
Gulay
G
Ozgon
Emre
E
Salabas
Ugur
U
Ozbek
Ates
A
Kadioglu
D017209:Apoptosis / Q000235:genetics*; D001706:Biopsy; D016022:Case-Control Studies; D053148:Caspase 3 / Q000235:genetics; D053181:Caspase 8 / Q000235:genetics; D053222:Fas Ligand Protein / Q000235:genetics; D005355:Fibrosis; D020869:Gene Expression Profiling / Q000379:methods; D005786:Gene Expression Regulation; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D010411:Penile Induration / Q000235:genetics* / Q000473:pathology / Q000601:surgery; D010413:Penis / Q000473:pathology*; D010641:Phenotype; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D014945:Wound Healing / Q000235:genetics; D019014:fas Receptor / Q000235:genetics
C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D019014:fas Receptor; C505407:CASP3 protein, human; C505530:CASP8 protein, human; D053148:Caspase 3; D053181:Caspase 8