The journal of sexual medicine · 2010
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its death receptor (DR5) in Peyronie's disease. A biomolecular study of apoptosis activation.
СтатьяНазвание и аннотация: Перевод в очереди
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Loreto Carla, Barbagli Guido, Djinovic Rados, Vespasiani Giuseppe, Carnazza Maria Luisa, Miano Roberto, Musumeci Giuseppe, Sansalone Salvatore
Аннотация
INTRODUCTION: Peyronie's disease (PD) is a connective tissue disorder of tunica albuginea (TA), a thick fibrous sheath surrounding the corpora cavernosa of the penis. Relatively, little is known about the disease itself.
AIM: To investigate whether the apoptosis cascade in degenerated and macroscopically deformed TA from men with PD is activated through the extrinsic pathway, by assessing the immunoexpression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its death receptor, DR5.
METHODS: TA plaques from 15 men with PD and from four unaffected men were processed for TRAIL and DR5 immunohistochemistry and Western blot analysis.
MAIN OUTCOME MEASURES: A greater understanding of the pathophysiology of PD through a molecular approach, to gain insights that may lead to novel forms of treatment.
RESULTS: Activation of the apoptosis mechanisms through the extrinsic pathway was demonstrated by TRAIL and DR5 overexpression in fibroblasts and myofibroblasts from affected TA.
CONCLUSION: The finding that apoptosis activation in TA plaques occurs, at least in part, via the extrinsic pathway may help devise novel therapeutic options for these patients.
AIM: To investigate whether the apoptosis cascade in degenerated and macroscopically deformed TA from men with PD is activated through the extrinsic pathway, by assessing the immunoexpression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its death receptor, DR5.
METHODS: TA plaques from 15 men with PD and from four unaffected men were processed for TRAIL and DR5 immunohistochemistry and Western blot analysis.
MAIN OUTCOME MEASURES: A greater understanding of the pathophysiology of PD through a molecular approach, to gain insights that may lead to novel forms of treatment.
RESULTS: Activation of the apoptosis mechanisms through the extrinsic pathway was demonstrated by TRAIL and DR5 overexpression in fibroblasts and myofibroblasts from affected TA.
CONCLUSION: The finding that apoptosis activation in TA plaques occurs, at least in part, via the extrinsic pathway may help devise novel therapeutic options for these patients.