RESUMEN
The purpose of this study was to determine the effects of ovariectomy and long-term combined sexual hormone replacement on the gap junctional protein, connexin 43 (Cx43) of aortic medial smooth muscle cells in rats. Twenty non-pregnant mature Wistar female rats were divided into five groups (four animals in each group). Group A underwent ovariectomy, Group B underwent ovariectomy and received estradiol propionate, Group C underwent ovariectomy and received medroxyprogesterone acetate and Group D underwent ovariectomy and received both hormones. Group E was sham-operated and used as control. After 15 weeks of treatment, thoracic aortas were removed and immunohistochemistry was carried out using a specific fluorescent antibody against Cx43. Tissue sections were examined by confocal laser scanning microscopy and analysed by the Scion Image program. All five different groups had the same distribution and extent of Cx43 in the aorta. Neither the ovariectomy nor the hormone replacement had any effect on the Cx43 expression of aortic smooth muscle cells in rats as compared to control animals. These results indicate that sexual steroids do not influence the gap junctional protein Cx43 of the medial layer of aorta in rats. They may suggest that the beneficial effects of estrogen are not mediated via gap junctions in the human aorta either.
Asunto(s)
Aorta Torácica/metabolismo , Conexina 43/metabolismo , Estradiol/farmacología , Terapia de Reemplazo de Estrógeno , Acetato de Medroxiprogesterona/farmacología , Músculo Liso Vascular/metabolismo , Ovariectomía , Animales , Aorta Torácica/efectos de los fármacos , Combinación de Medicamentos , Femenino , Técnica del Anticuerpo Fluorescente Indirecta , Procesamiento de Imagen Asistido por Computador , Músculo Liso Vascular/efectos de los fármacos , Ratas , Ratas WistarRESUMEN
BACKGROUND: The association of TN expression, tumour grading and expression of commonly used histopathologic prognostic factors (p53 and estrogen receptor) was examined in 62 cases of invasive ductal carcinoma of the breast. MATERIAL AND METHODS: Following histological grading immunohistochemical reactions were undertaken on routine histopathologic samples and the results semiquantitatively evaluated. RESULTS: Strong TN expression was found in close proximity of the neoplastic epithelial cells in each case, but not in other areas of the stroma. In 10 (16%) cases TN expression was detected to the neoplastic epithelial cells as well. There was no statistically significant difference in the extent of stromal TN immunoreaction between tumours of different grades. A significant difference was found in p53 and estrogen receptor immunoreactions by tumour grade (p = 0.05). TN immunoreaction in the stroma did not correlate with the nuclear expression of p53, Ki-67 and estrogen receptor in the tumour cells. CONCLUSIONS: TN immunoreactivity does not seem to correlate with currently used prognostic factors. The increased expression of stromal TN in invasive breast ductal carcinomas is an other indicator of possible role played by the extracelular matrix components in cancer development.
Asunto(s)
Neoplasias de la Mama/química , Carcinoma Ductal de Mama/química , Tenascina/análisis , Neoplasias de la Mama/patología , Carcinoma Ductal de Mama/patología , Femenino , Humanos , Inmunohistoquímica , Antígeno Ki-67/análisis , Receptores de Estrógenos/análisis , Tenascina/inmunología , Proteína p53 Supresora de Tumor/análisisRESUMEN
The expression and the distribution of tenascin as well as the extent of blood vessel formation (angiogenesis) were investigated in 70 invasive human breast carcinomas. Formalin-fixed, paraffin-embedded specimens were stained with monoclonal antibody against tenascin-C (DAKO and Biogenex). Anti-CD31 antibody (Biogenex), an acknowledged marker of stromal angiogenesis, was used to detect endothelial cells. Tenascin immunostaining was positive in the tumours around the persisting normal ducts, around tumour-cell nests, in the neostroma, in some tumour cells, and it was found in or around vascular channels. Tumour vascularity was assessed by quantitative vascular grading (Chalkley point count) and was related to the localization and intensity of tenascin immunoreactivity. 19 tumours (27.1%) were scored as low, 35 (50%) as medium, and 16 (22.9%) as having a high vascular grade. The positive correlation between the vascular grade and the tenascin immunopositivity in tumour stroma was observed. Our results suggest that tenascin expression may be associated with endothelial cell activation and may play an important role in tumour angiogenesis.