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Gene expression profile comparison in the penile tissue of diabetes and cavernous nerve injury-induced erectile dysfunction rat model

PURPOSE: To investigate the effects of cavernous nerve injury (CNI) on gene expression profiles in the cavernosal tissue of a CNI-induced erectile dysfunction (ED) model and to provide a basis for future investigations to discover potential target genes for ED treatment. MATERIALS AND METHODS: Young...

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Detalles Bibliográficos
Autores principales: Kam, Sung Chul, Lee, Sang Hoon, Jeon, Ju Hong, So, Insuk, Chae, Mee Ree, Park, Jong Kwan, Lee, Sung Won
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Urological Association 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4949699/
https://www.ncbi.nlm.nih.gov/pubmed/27437539
http://dx.doi.org/10.4111/icu.2016.57.4.286
Descripción
Sumario:PURPOSE: To investigate the effects of cavernous nerve injury (CNI) on gene expression profiles in the cavernosal tissue of a CNI-induced erectile dysfunction (ED) model and to provide a basis for future investigations to discover potential target genes for ED treatment. MATERIALS AND METHODS: Young adult rats were divided randomly into 2 groups: sham operation and bilateral CN resection. At 12 weeks after CNI we measured erectile responses and performed microarray experiments and gene set enrichment analysis to reveal gene signatures that were enriched in the CNI-induced ED model. Alterations in gene signatures were compared with those in the diabetes-induced ED model. The diabetic-induced ED data is taken from GSE2457. RESULTS: The mean ratio of intracavernosal pressure/blood pressure for the CNI group (0.54±0.4 cmH(2)O) was significantly lower than that in the sham operation group (0.73±0.8 cmH(2)O, p<0.05). Supervised and unsupervised clustering analysis showed that the diabetes- and CNI-induced ED cavernous tissues had different gene expression profiles from normal cavernous tissues. We identified 46 genes that were upregulated and 77 genes that were downregulated in both the CNI- and diabetes-induced ED models. CONCLUSIONS: Our genome-wide and computational studies provide the groundwork for understanding complex mechanisms and molecular signature changes in ED.