RESUMEN
La endometriosis es una enfermedad cuya etiología no se conoce y sobre la cual existen diferentes teorías que a la fecha no han sido totalmente demostradas. Está claramente demostrado que las mujeres que presentan dicha enfermedad cursan con infertilidad y que la recurrencia de aparición de los focos endometriósicos es alta, y al parecer no dependientes del estímulo estrogénico. Este fenómeno se ha atribuido a otros factores de crecimiento y algunos oncogenes los cuales son expresados para contrarrestar la falta del estímulo estrogénico. Sin embargo, pocos estudios existen en relación a los oncogenes u otros receptores hormonales, por lo que el presente trabajo tuvo por objetivo el evaluar su expresión tanto en tejido eutópico como en ectópico de mujeres con diagnóstico previo de endometriosis. El análisis de la expresión tanto de c-myc, neu y el receptor de prolactina (PRLr) se realizó por la técnica de RT-PCR. Nuestros resultados demuestran que tanto myc como el PRLr se expresan de manera distinta entre los diferentes tejidos, en tanto que neu se expresa de la misma manera entre los dos tejidos. Con estos datos concluimos que las células que conforman el foco endometriósico presentan un estado diferencial en relación a la expresión de algunos de sus genes, lo cual favorece el desarrollo y mantenimiento de los mismos en un ambiente hormonal diferente al de la cavidad uterina.
Asunto(s)
Humanos , Femenino , Adulto , Persona de Mediana Edad , Endometriosis/fisiopatología , Oncogenes/fisiología , Receptores de Prolactina/análisis , Coristoma/fisiopatología , Estradiol/fisiologíaRESUMEN
OBJECTIVE: To study the effects of 1,25-dihydroxyvitaminD3 (1,25-(OH)2D3) on proliferation and cell death in the rat uterus. MATERIAL AND METHODS: A rat endometrial cell line (Rentro 1) grown in a Dulbecco Minimal Essential Medium (DMEM) supplemented with 1% charcoal stripped serum was used in all experiments in order to eliminate the steroid hormone. Cell monolayer was incubated in the presence and absence of 1,25-(OH)2D3 or 17 beta-estradiol or vehicle. After stimulation, we evaluated cell proliferation and DNA synthesis by trypan blue counting method and flow cytofluorometry, respectively. Finally, the genomic DNA integrity was evaluated by electrophoresis and the bands visualized with ultraviolet light. RESULTS: The cells in medium containing 1% fetal bovine serum free of steroid hormones stimulated the cell growth 85% more than without serum. Supplement with albumin did not allow cell growth. The cells did not respond to 17 beta-estradiol but the presence of 1,25-(OH)2D3 induced cell proliferation. These results confirm that Rentro 1 cells do not express the estrogen receptor and demonstrate their capacity to respond to 1,25-(OH)2D3. Finally, the integrity of DNA was not affected by 1,25(OH)2D3, suggesting that this hormone is not involved in cell death by apoptosis in our cell line, as seen in other cell lines. CONCLUSIONS: 1) 1,25-dihydroxyvitamin D induced cell proliferation in the endometrial cell line Rentro 1 in a dose-dependent fashion and this effect is independent of the presence of an estrogenic stimulus; 2) the increase in cell number was related to DNA synthesis during the cell cycle; and 3) the presence of the hormone in the culture medium was not able to induce cell death.
Asunto(s)
Calcitriol/farmacología , Endometrio/efectos de los fármacos , Animales , Ciclo Celular , Muerte Celular , División Celular/efectos de los fármacos , Línea Celular , Células Cultivadas , ADN/biosíntesis , Endometrio/citología , Femenino , RatasRESUMEN
For several decades it has been known that steroid hormones, estrogen and progesterone, regulate some genes involved in the growth, proliferation and differentiation of the mammary-gland in animals and humans. In the last years, the presence or absence of the nuclear estrogen receptor has been used by clinicians as a marker for tumor malignancy, as a prognostic index or as an important parameter for hormonal therapy with anti-estrogenic compounds of some hormone-dependent breast cancers. This review shows some advances in the knowledge of the structure, function, molecular mechanisms of estrogenic activity, and interaction with proteins like protooncogenes and growth factors. Also, we refer to the role of the estrogen receptor in the physiophatology of breast cancer.
Asunto(s)
Neoplasias de la Mama/fisiopatología , Mama/fisiología , Neoplasias Hormono-Dependientes/fisiopatología , Receptores de Estrógenos , Animales , Mama/fisiopatología , Femenino , Humanos , Glándulas Mamarias Animales/fisiología , Neoplasias Mamarias Animales/fisiopatologíaRESUMEN
OBJECTIVES: It has been suggested that increased matrix metalloproteinases activity promotes the weakening of the amniochorion during normal and premature rupture of membranes. This study was designed to determine whether levels of matrix metalloproteinases and the tissue inhibitor of metalloproteinases-1 in amniotic fluid change in a pattern consistent with this hypothesis. STUDY DESIGN: Gelatinolytic activity, measured by a soluble substrate assay and zymography, and the concentrations of tissue inhibitor of metalloproteinases-1 were estimated in amniotic fluid obtained from (1) normal early gestations, (2) normal term pregnancies with labor, (3) normal term pregnancies without labor, and (4) pregnancies complicated by premature rupture of membranes. The 92 kd type IV collagenase (matrix metalloproteinase-9) was also detected in amniotic fluid by Western blotting. RESULTS: Matrix metalloproteinase activities were higher in amniotic fluid from normal term pregnancies with labor and pregnancies complicated by premature rupture of membranes than from early pregnancies and term gestations without labor. The amniotic fluid from term pregnancies with labor or pregnancies with premature rupture of membranes contained several gelatinases, as revealed by zymography. The major amniotic fluid gelatinolytic activity in premature rupture of membranes and term pregnancies with labor corresponded to matrix metalloproteinase-9. Tissue inhibitor of metalloproteinases-1 concentrations were highest in early-pregnancy amniotic fluid, followed by term gestation with labor, term gestation without labor, and premature rupture of membranes. CONCLUSIONS: Normal labor and premature rupture of membranes are associated with increased levels of matrix metalloproteinases, particularly matrix metalloproteinase-9 in amniotic fluid. Premature rupture of membranes is associated with reduced levels of tissue inhibitor of metalloproteinases-1. The imbalance between matrix metalloproteinases and tissue inhibitor of metalloproteinases-1 in amniotic fluid may reflect a disorder that promotes premature rupture of membranes.
Asunto(s)
Líquido Amniótico/metabolismo , Colagenasas/metabolismo , Rotura Prematura de Membranas Fetales/metabolismo , Glicoproteínas/metabolismo , Western Blotting , Ácido Edético/farmacología , Femenino , Gelatina/metabolismo , Humanos , Técnicas para Inmunoenzimas , Trabajo de Parto , Metaloproteinasa 9 de la Matriz , Embarazo , Inhibidores Tisulares de MetaloproteinasasRESUMEN
Our group has recently described the existence of a chemoattractant factor for spermatozoa contained in the mature follicles fluid. Simultaneously it was possible to develop a new method that permits to evaluate the chemotactic capacity of spermatozoa and that due to its simplicity makes possible the systematic study of CFS features. This study considered CFS molecular characterization from follicular fluid (FF). The FF of women was studied in an Assisted Fertilization Program, that were qualified as mature according to different criteria. The FF were fractioned with different techniques that permitted to separate an active fraction with lipid physicochemical characteristics. The fine layer chromatography showed the presence of different steroids, that were individually assayed for chemotactic activity. Only progesterone showed that activity and its effect showed a dose-response curve within physiological values. Our study permitted to identify progesterone as CFS previously described. This steroid's function is rather new and its action mechanism is being studied in our laboratory.