Evaluation of apoptotic genes expression and its protein after treatment of cryptorchid mice.
Cryptorchidism has been proved to cause apoptosis in germ cells in respond to changes in the stimulation levels of specific physiological events. The purpose of this study was to determine whether treatment of bilateral cryptorchidism was associated with alterations in testicular gene expression.



To induce bilateral cryptorchid model, immature mice were anesthetized and a small incision was made in the abdominal skin and peritoneum, then fat pad at the upper end of testis was sutured to the peritoneum. Transcript level of Bax, Bcl-2 proper, p53 and survivin mRNA and protein were determined after performing the two treatment methods: surgical return of testis into scrotum (Exp1) and transplantation of spermatogonial stem cells with later orchidopexy (Exp2), performed 2 and 3 months after heat exposure, respectively.



RT-PCR data showed decreased levels of p53 and Bax expression as well as decreased levels of Bcl-2 mRNA in treatment groups especially after transplantation compared with control group. The expression of survivin 140 was increased significantly after treatment, whereas that of survivin 40 was lower especially in the orchidopexy group. Immunohistochemistry staining showed that the intensity of Bax expression mainly was decreased in treated cryptorchid testis and rates of Bcl-2 were increased significantly, but expression of p53 and survivin proteins did not changed significantly after treatment.



These observations suggest that cell-type-specific and many apoptotic systems control germ cell apoptosis after treatment of cryptorchidism.
Dept. of Anatomical Sciences, School of Medical Sciences, Tarbiat Modarres University, Tehran, Iran.|Dept. of Anatomy, Medical Faculty, Jundishapur University of Medical Sciences, Ahvaz, Iran.
Forouzan
F
Absalan
Dept. of Anatomical Sciences, School of Medical Sciences, Tarbiat Modarres University, Tehran, Iran.
Mansoureh
M
Movahedin
Dept. of Genetics, School of Basic Sciences, Tarbiat Modarres University, Tehran, Iran.
Seyed Javad
SJ
Mowla
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D003456:Cryptorchidism / Q000235:genetics / Q000378:metabolism* / Q000601:surgery*; D051034:Inhibitor of Apoptosis Proteins / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D051379:Mice; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000096:biosynthesis / Q000235:genetics; D013093:Spermatogonia / Q000166:cytology; D013094:Spermatozoa / Q000378:metabolism; D033581:Stem Cell Transplantation; D000077022:Survivin; D013737:Testis / Q000378:metabolism* / Q000601:surgery; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics; D050998:bcl-2 Homologous Antagonist-Killer Protein / Q000096:biosynthesis / Q000235:genetics; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis / Q000235:genetics
C117749:Birc5 protein, mouse; D051034:Inhibitor of Apoptosis Proteins; D012333:RNA, Messenger; D012097:Repressor Proteins; D000077022:Survivin; D016159:Tumor Suppressor Protein p53; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein