Journal of pediatric surgery · 2013
Molecular signals governing cremaster muscle development: clues for cryptorchidism.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Szarek Maciej, Li Ruili, Vikraman Jaya, Southwell Bridget, Hutson John M
Аннотация
BACKGROUND/AIM: Cryptorchidism affects 2-4% of newborn boys. Testicular descent requires the gubernaculum to differentiate into cremaster muscle (CM) during androgen-mediated inguino-scrotal descent, but the cellular mechanisms regulating this remodeling remain elusive. β-Catenin, a marker of canonical Wnt signaling, promotes myogenic genes and cellular adhesion. We aimed to determine if androgen receptor (AR) blockade altered β-catenin and its downstream myogenic proteins within the CM.
METHOD: Gubernacula from male rats (n=12) and rats treated with anti-androgen, flutamide (n=12) at E19, D0, D2 were processed for immunohistochemistry. Antibodies against β-catenin, embryonic myosin, and myogenin were visualized by confocal microscopy.
RESULTS: At E19, β-catenin immuno-reactivity (IR) localized to the CM membrane. By D2, cytoplasmic β-catenin-IR was noted with overall β-catenin-IR decreasing. Myogenic proteins resided primarily in cells containing β-catenin on their plasma membrane. Embryonic myosin-IR was high at E19 and then decreased by D2, while myogenin-IR increased. AR blockade increased cytoplasmic β-catenin at D2 and reduced levels of both myogenic proteins.
CONCLUSION: Myogenic proteins are present in CM cells containing β-catenin. AR blockade did not alter cellular adhesion via β-catenin. In contrast, blocking AR prevented β-catenin entering the nucleus and impaired CM myogenesis. Mutations in this pathway may result in idiopathic cryptorchidism.
METHOD: Gubernacula from male rats (n=12) and rats treated with anti-androgen, flutamide (n=12) at E19, D0, D2 were processed for immunohistochemistry. Antibodies against β-catenin, embryonic myosin, and myogenin were visualized by confocal microscopy.
RESULTS: At E19, β-catenin immuno-reactivity (IR) localized to the CM membrane. By D2, cytoplasmic β-catenin-IR was noted with overall β-catenin-IR decreasing. Myogenic proteins resided primarily in cells containing β-catenin on their plasma membrane. Embryonic myosin-IR was high at E19 and then decreased by D2, while myogenin-IR increased. AR blockade increased cytoplasmic β-catenin at D2 and reduced levels of both myogenic proteins.
CONCLUSION: Myogenic proteins are present in CM cells containing β-catenin. AR blockade did not alter cellular adhesion via β-catenin. In contrast, blocking AR prevented β-catenin entering the nucleus and impaired CM myogenesis. Mutations in this pathway may result in idiopathic cryptorchidism.