Increased Apoptosis of Spermatogenic Cells in Cryptorchidism Rat Model and Its Correlation With Transforming Growth Factor Beta Type II Receptor
Objectives To investigate the role played by transforming growth factor beta receptor II (TGFβRII) in cryptorchidism-induced spermatocyte apoptosis. Methods A unilateral cryptorchidism rat model was surgically established in 20-day-old male SD rats. Testis samples were collected 0, 4, 7, 14, and 21...
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Published in | Urology (Ridgewood, N.J.) Vol. 75; no. 4; pp. 992 - 998 |
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Abstract | Objectives To investigate the role played by transforming growth factor beta receptor II (TGFβRII) in cryptorchidism-induced spermatocyte apoptosis. Methods A unilateral cryptorchidism rat model was surgically established in 20-day-old male SD rats. Testis samples were collected 0, 4, 7, 14, and 21 days after surgery. Histologic changes, apoptosis, TGFβRII/smad, and TGFβRII/mitogen-activated protein kinase activation were explored by hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and western blot analysis, respectively. TGFβRII was knocked down in GC-2 spg cells and the cells were then treated with hyperthermia. Western blot analysis was performed to detect TGFβRII, the phosphorylation status of smad2, smad3, and p38 and the cleavage status of caspase-3. Results Surgically induced cryptorchidism significantly impaired testis growth and spermatogenesis in unilateral undescended testes (UUTs) compared with contralateral descended testes 7, 14, and 21 days after surgery. The mean apoptotic index was significantly higher in UUTs than in contralateral descended testes. Western blot analysis showed that TGFβRII and smad2 expression increased. Phosphorylation of smad2, smad3, and p38 and cleavage of caspase-3 increased in UUTs. TGFβRII knockdown in GC-2 spg cells reduced hyperthermia-induced apoptosis by inhibiting smad2, smad3, and p38 phosphorylation as well as downstream caspase-3 cleavage. Conclusions Cryptorchidism lowered the growth rate of testes by inducing apoptosis, via a mechanism involving the activation of the TGFβR/smad and TGFβR/mitogen-activated protein kinase pathways. |
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AbstractList | OBJECTIVESTo investigate the role played by transforming growth factor beta receptor II (TGFbetaRII) in cryptorchidism-induced spermatocyte apoptosis.METHODSA unilateral cryptorchidism rat model was surgically established in 20-day-old male SD rats. Testis samples were collected 0, 4, 7, 14, and 21 days after surgery. Histologic changes, apoptosis, TGFbetaRII/smad, and TGFbetaRII/mitogen-activated protein kinase activation were explored by hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and western blot analysis, respectively. TGFbetaRII was knocked down in GC-2 spg cells and the cells were then treated with hyperthermia. Western blot analysis was performed to detect TGFbetaRII, the phosphorylation status of smad2, smad3, and p38 and the cleavage status of caspase-3.RESULTSSurgically induced cryptorchidism significantly impaired testis growth and spermatogenesis in unilateral undescended testes (UUTs) compared with contralateral descended testes 7, 14, and 21 days after surgery. The mean apoptotic index was significantly higher in UUTs than in contralateral descended testes. Western blot analysis showed that TGFbetaRII and smad2 expression increased. Phosphorylation of smad2, smad3, and p38 and cleavage of caspase-3 increased in UUTs. TGFbetaRII knockdown in GC-2 spg cells reduced hyperthermia-induced apoptosis by inhibiting smad2, smad3, and p38 phosphorylation as well as downstream caspase-3 cleavage.CONCLUSIONSCryptorchidism lowered the growth rate of testes by inducing apoptosis, via a mechanism involving the activation of the TGFbetaR/smad and TGFbetaR/mitogen-activated protein kinase pathways. To investigate the role played by transforming growth factor beta receptor II (TGFbetaRII) in cryptorchidism-induced spermatocyte apoptosis. A unilateral cryptorchidism rat model was surgically established in 20-day-old male SD rats. Testis samples were collected 0, 4, 7, 14, and 21 days after surgery. Histologic changes, apoptosis, TGFbetaRII/smad, and TGFbetaRII/mitogen-activated protein kinase activation were explored by hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and western blot analysis, respectively. TGFbetaRII was knocked down in GC-2 spg cells and the cells were then treated with hyperthermia. Western blot analysis was performed to detect TGFbetaRII, the phosphorylation status of smad2, smad3, and p38 and the cleavage status of caspase-3. Surgically induced cryptorchidism significantly impaired testis growth and spermatogenesis in unilateral undescended testes (UUTs) compared with contralateral descended testes 7, 14, and 21 days after surgery. The mean apoptotic index was significantly higher in UUTs than in contralateral descended testes. Western blot analysis showed that TGFbetaRII and smad2 expression increased. Phosphorylation of smad2, smad3, and p38 and cleavage of caspase-3 increased in UUTs. TGFbetaRII knockdown in GC-2 spg cells reduced hyperthermia-induced apoptosis by inhibiting smad2, smad3, and p38 phosphorylation as well as downstream caspase-3 cleavage. Cryptorchidism lowered the growth rate of testes by inducing apoptosis, via a mechanism involving the activation of the TGFbetaR/smad and TGFbetaR/mitogen-activated protein kinase pathways. To investigate the role played by transforming growth factor beta receptor II (TGFβRII) in cryptorchidism-induced spermatocyte apoptosis. A unilateral cryptorchidism rat model was surgically established in 20-day-old male SD rats. Testis samples were collected 0, 4, 7, 14, and 21 days after surgery. Histologic changes, apoptosis, TGFβRII/smad, and TGFβRII/mitogen-activated protein kinase activation were explored by hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and western blot analysis, respectively. TGFβRII was knocked down in GC-2 spg cells and the cells were then treated with hyperthermia. Western blot analysis was performed to detect TGFβRII, the phosphorylation status of smad2, smad3, and p38 and the cleavage status of caspase-3. Surgically induced cryptorchidism significantly impaired testis growth and spermatogenesis in unilateral undescended testes (UUTs) compared with contralateral descended testes 7, 14, and 21 days after surgery. The mean apoptotic index was significantly higher in UUTs than in contralateral descended testes. Western blot analysis showed that TGFβRII and smad2 expression increased. Phosphorylation of smad2, smad3, and p38 and cleavage of caspase-3 increased in UUTs. TGFβRII knockdown in GC-2 spg cells reduced hyperthermia-induced apoptosis by inhibiting smad2, smad3, and p38 phosphorylation as well as downstream caspase-3 cleavage. Cryptorchidism lowered the growth rate of testes by inducing apoptosis, via a mechanism involving the activation of the TGFβR/smad and TGFβR/mitogen-activated protein kinase pathways. Objectives To investigate the role played by transforming growth factor beta receptor II (TGFβRII) in cryptorchidism-induced spermatocyte apoptosis. Methods A unilateral cryptorchidism rat model was surgically established in 20-day-old male SD rats. Testis samples were collected 0, 4, 7, 14, and 21 days after surgery. Histologic changes, apoptosis, TGFβRII/smad, and TGFβRII/mitogen-activated protein kinase activation were explored by hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and western blot analysis, respectively. TGFβRII was knocked down in GC-2 spg cells and the cells were then treated with hyperthermia. Western blot analysis was performed to detect TGFβRII, the phosphorylation status of smad2, smad3, and p38 and the cleavage status of caspase-3. Results Surgically induced cryptorchidism significantly impaired testis growth and spermatogenesis in unilateral undescended testes (UUTs) compared with contralateral descended testes 7, 14, and 21 days after surgery. The mean apoptotic index was significantly higher in UUTs than in contralateral descended testes. Western blot analysis showed that TGFβRII and smad2 expression increased. Phosphorylation of smad2, smad3, and p38 and cleavage of caspase-3 increased in UUTs. TGFβRII knockdown in GC-2 spg cells reduced hyperthermia-induced apoptosis by inhibiting smad2, smad3, and p38 phosphorylation as well as downstream caspase-3 cleavage. Conclusions Cryptorchidism lowered the growth rate of testes by inducing apoptosis, via a mechanism involving the activation of the TGFβR/smad and TGFβR/mitogen-activated protein kinase pathways. |
Author | Yuan, Jian-Lin Zhang, Yun-Tao Wang, Yong |
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CitedBy_id | crossref_primary_10_1111_andr_12923 crossref_primary_10_1016_j_gene_2016_02_007 crossref_primary_10_1186_s12917_020_02591_1 crossref_primary_10_1071_RD18469 crossref_primary_10_1155_2022_6891897 |
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Snippet | Objectives To investigate the role played by transforming growth factor beta receptor II (TGFβRII) in cryptorchidism-induced spermatocyte apoptosis. Methods A... To investigate the role played by transforming growth factor beta receptor II (TGFβRII) in cryptorchidism-induced spermatocyte apoptosis. A unilateral... To investigate the role played by transforming growth factor beta receptor II (TGFbetaRII) in cryptorchidism-induced spermatocyte apoptosis. A unilateral... OBJECTIVESTo investigate the role played by transforming growth factor beta receptor II (TGFbetaRII) in cryptorchidism-induced spermatocyte apoptosis.METHODSA... |
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SubjectTerms | Animals Apoptosis Cryptorchidism - metabolism Cryptorchidism - pathology Disease Models, Animal Male p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Protein-Serine-Threonine Kinases - physiology Rats Receptors, Transforming Growth Factor beta - physiology Smad Proteins - metabolism Spermatocytes - pathology Urology |
Title | Increased Apoptosis of Spermatogenic Cells in Cryptorchidism Rat Model and Its Correlation With Transforming Growth Factor Beta Type II Receptor |
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