Artículos de revistas
Proliferative, structural and molecular features of the Mdx mouse prostate
Registro en:
International Journal Of Experimental Pathology. Wiley-blackwell, v. 91, n. 5, n. 408, n. 419, 2010.
0959-9673
WOS:000284319900003
10.1111/j.1365-2613.2010.00722.x
Autor
Pinto, LC
Favaro, WJ
Cagnon, VHA
Institución
Resumen
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) P>The prostate is fundamental to the male reproductive process, and the stroma-epithelium interaction has an important role in prostate maintenance. Studies suggest that dystroglycan (DG) plays a role in cancer development in various organs. Thus, the aims of this work were to characterize morphological and proliferative features of the prostatic stroma and epithelium of mdx mice; to verify the immunolocalization of the alpha and beta DG, IGF-1 and laminin alpha 3 receptors; and to relate those structural and molecular events to prostate pathogenesis and to verify the viability of this experimental model in prostate studies. Thirty male mice (mdx and C57BL10/Uni) were divided into control and mdx groups. Samples from the ventral prostate were collected for immunological, Western Blotting, transmission electron microscopy and morphometric analyses. Oestradiol and testosterone measurements were verified. The results showed diminished testosterone and increased oestradiol levels in the mdx group. Atrophied cells and hypertrophied stroma were seen in the mdx mice. Weak alpha and beta DG and laminin alpha 3 immunolocalization was demonstrated in the mdx group. Intense insulin-like growth factor receptor alpha-1 (IGFR alpha-1) localization was identified in the mdx animals. Thus, mdx animals showed changes in molecular and structural integrity and proliferation signals, leading to glandular homoeostasis imbalance, and compromise of prostate function. Also, the steroid hormone imbalance and the increased IGF-1 receptor level detected in mdx mice could be considered as a crucial factor in the pathogenesis of prostatic disorders. 91 5 408 419 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) FAPESP [07/54689-9, 07/52053-0]