Search Results
You are looking at 1 - 6 of 6 items for
- Author: Fernanda Parborell x
- Refine by access: All content x
Search for other papers by Dalhia Abramovich in
Google Scholar
PubMed
Search for other papers by Alejandra Rodriguez Celin in
Google Scholar
PubMed
Search for other papers by Fátima Hernandez in
Google Scholar
PubMed
Instituto de Biología y Medicina Experimental (IBYME)-CONICET, Departamento de Química Biológica, Obligado 2490, 1428 Buenos Aires, Argentina
Search for other papers by Marta Tesone in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
This study investigated the protein expression and cellular localization of ANGPT1, ANGPT2, and their receptor TEK, as well as vascular endothelial growth factor A (VEGFA) and its receptor KDR (VEGFR2) during folliculogenesis. To obtain follicles at different stages for immunochemistry and western analyses, we used prepubertal untreated, diethylstilbestrol- and equine chorionic gonadotropin-treated rats. To confirm that these hormonal treatments reflect physiological change, we used non-treated adult rats. No expression of ANGPT1 was observed in granulosa cells (Gc) from immature hormone-treated and non-treated rats at any follicular stage. By contrast, ANGPT1 expression in theca cells (Tc) increased with follicular maturation. ANGPT2 protein was either absent or weakly expressed in Gc at all follicular stages. In Tc, minimal expression of ANGPT2 protein was detected in the preantral follicle (PF), whereas it was stronger in the early antral follicle (EAF) and preovulatory follicle (POF). TEK staining was absent in Gc but was intense in Tc at every follicular stage. Staining for VEGFA was either absent or weakly present in Gc and Tc in PF and EAF, although in POF it was stronger in Gc and Tc. Staining for KDR was absent in Gc and very low in Tc from PF. Gc and Tc of EAF showed positive staining for KDR and in POF the staining was stronger. These results were confirmed by western immunoblot. A similar pattern of expression of these proteins was observed in cycling rats. In conclusion, we observed that the protein expression of ANGPT1, ANGPT2, VEGFA and their receptors increased during follicular development in rats.
Search for other papers by Mariana Di Pietro in
Google Scholar
PubMed
Search for other papers by Natalia Pascuali in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Dalhia Abramovich in
Google Scholar
PubMed
Polycystic ovary syndrome (PCOS) is the most prevalent endocrine pathology among women in reproductive age. Its main symptoms are oligo or amenorrhea, hyperandrogenism and the presence of ovarian cysts. It is also associated with infertility, obesity and insulin resistance. Mainly due to its heterogeneity, PCOS treatments are directed to manage its symptoms and to prevent associated diseases. The correct formation and regression of blood vessels during each ovarian cycle is indispensable for proper follicular development, ovulation and corpus luteum formation. The importance of these processes opened a new and promising field: ovarian angiogenesis. Vascular alterations characterize numerous pathologies, either with increased, decreased or abnormal angiogenesis. In the last years, several anomalies of ovarian angiogenesis have been described in women with PCOS. Therefore, it has been suggested that these alterations may be associated with the decreased – or lack of – ovulation rates and for the formation of cysts in the PCOS ovaries. Restoration of a proper vessel formation in the ovaries may lead to improved follicular development and ovulation in these patients. In the present review, we attempt to summarize the alterations in ovarian angiogenesis that have been described in women with PCOS. We also discuss the therapeutic approaches aimed to correct these alterations and their beneficial effects on the treatment of infertility in PCOS.
Search for other papers by Ianina Ferder in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Victoria Sundblad in
Google Scholar
PubMed
Search for other papers by Violeta Chiauzzi in
Google Scholar
PubMed
Search for other papers by Karina Gómez in
Google Scholar
PubMed
Search for other papers by Eduardo H Charreau in
Google Scholar
PubMed
Instituto de Biología y Medicina Experimental (IByME)- CONICET, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI)- CONICET, Departamento de Química Biológica, Centro Nacional de Genética Médica, Vuelta de Obligado 2490, C1428ADN Ciudad de Buenos Aires, Argentina
Search for other papers by Marta Tesone in
Google Scholar
PubMed
Instituto de Biología y Medicina Experimental (IByME)- CONICET, Instituto de Investigaciones en Ingeniería Genética y Biología Molecular (INGEBI)- CONICET, Departamento de Química Biológica, Centro Nacional de Genética Médica, Vuelta de Obligado 2490, C1428ADN Ciudad de Buenos Aires, Argentina
Search for other papers by Liliana Dain in
Google Scholar
PubMed
Fragile X mental retardation protein (FMRP) belongs to a small family of RNA-binding proteins. Its absence or inactivity is responsible for fragile X syndrome, the most common cause of inherited mental retardation. Despite its ubiquitous expression, FMRP function and expression remain almost understudied in non-neuronal tissues, though previous studies on germline development during oogenesis may suggest a special function of this protein also in ovarian tissue. In addition, the well-documented association of FMR1 premutation state with fragile X-related premature ovarian insufficiency adds interest to the role of FMRP in ovarian physiology. The aim of the present work was to investigate the expression of Fmr1 mRNA and its protein, FMRP, at different stages of rat follicular development. By immunohistochemical studies we demonstrated FMRP expression in granulosa, theca and germ cells in all stages of follicular development. In addition, changes in Fmr1 expression, both at the protein and mRNA levels, were observed. FMRP levels increased upon follicular development while preantral and early antral follicles presented similar levels of Fmr1 transcripts with decreased expression in preovulatory follicles. These observations suggest that Fmr1 expression in the ovary is regulated at different and perhaps independent levels. In addition, our results show expression of at least four different isoforms of FMRP during all stages of follicular growth with expression patterns that differ from those observed in brain and testis. Our study shows a regulated expression of Fmr1, both at mRNA and protein levels, during rat follicular development.
Search for other papers by Laura Tatiana Pelegrina in
Google Scholar
PubMed
Search for other papers by Antonella Rosario Ramona Cáceres in
Google Scholar
PubMed
Search for other papers by Fernando Alfredo Giuliani in
Google Scholar
PubMed
Search for other papers by Joana Antonella Asensio in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Myriam Raquel Laconi in
Google Scholar
PubMed
Search for other papers by Laura Tatiana Pelegrina in
Google Scholar
PubMed
Search for other papers by Antonella Rosario Ramona Cáceres in
Google Scholar
PubMed
Search for other papers by Fernando Alfredo Giuliani in
Google Scholar
PubMed
Search for other papers by Joana Antonella Asensio in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Myriam Raquel Laconi in
Google Scholar
PubMed
Allopregnanolone, a progesterone metabolite, is one of the best characterized neurosteroids. In a dose that mimics serum levels during stress, allopregnanolone inhibits sexual receptivity and ovulation and induces a decrease in luteinizing hormone levels. The aim of this work was to examine the effect of an intracerebroventricular administration of allopregnanolone on ovarian morphophysiology; serum and tissue levels of progesterone and estrogen; and enzymatic activity of 3β-hydroxysteroid dehydrogenase, 20α-hydroxysteroid dehydrogenase and 3α-hydroxysteroid oxido-reductase in the ovary and in the medial basal hypothalamus on the morning of estrus. Ovarian morphology was analyzed under light microscopy. The hormone assays were performed by radioimmunoassay. The enzymatic activities were measured by spectrophotometric analysis. The morphometric analysis revealed that, in allopregnanolone-treated animals, the number of secondary and Graafian follicles was decreased, whereas that of atretic follicles and cysts was significantly increased. Some cysts showed luteinized unruptured follicles. There were no differences in the number of tertiary follicles or corpora lutea in comparison with the corresponding control groups. In allopregnanolone-treated animals, progesterone serum levels were increased, whereas ovarian progesterone levels were decreased. Moreover, 3β-HSD and 3α-HSOR enzymatic activities were increased in the medial basal hypothalamus, whereas ovarian levels were decreased. The enzyme 20α-hydroxysteroid dehydrogenase showed the opposite profile. The results of this study showed that allopregnanolone interferes on ovarian steroidogenesis and ovarian morphophysiology in rats, providing a clear evidence for the role of this neurosteroid in the control of reproductive function under stress situations.
Free Spanish abstract: A Spanish translation of this abstract is freely available at http://www.reproduction-online.org/content/153/1/75/suppl/DC1.
Search for other papers by Candela Velazquez in
Google Scholar
PubMed
Search for other papers by Mayra Bordaquievich in
Google Scholar
PubMed
Search for other papers by Yamila Herrero in
Google Scholar
PubMed
Search for other papers by Débora Juana Cohen in
Google Scholar
PubMed
Search for other papers by María Silvia Bianchi in
Google Scholar
PubMed
Search for other papers by Patricia Cuasnicu in
Google Scholar
PubMed
Search for other papers by Katherine Prost in
Google Scholar
PubMed
Department of Pathology, College of Medicine, University of Illinois at Chicago (UIC), Chicago, Illinois, USA
Search for other papers by Natalia Pascuali in
Google Scholar
PubMed
Search for other papers by Fernanda Parborell in
Google Scholar
PubMed
Search for other papers by Dalhia Abramovich in
Google Scholar
PubMed
In brief
The hypoglycemic drug metformin has shown reproductive effects in women, although its mechanism of action is not fully understood. In this study, we demonstrate the direct effects of metformin on the ovary of healthy mice, with no alterations in fertility.
Abstract
Metformin is a hypoglycemic drug widely used in type-2 diabetes (T2D) patients. In recent years, this drug has been suggested as a treatment for gestational diabetes and recommended to women with ovarian hyperstimulation syndrome (PCOS) to increase the chances of pregnancy or avoid early miscarriages. However, the exact effects of metformin on the female reproductive tract in general, and on the ovary in particular, are still not completely understood. In this study, we analyzed the effect of metformin on fertility and ovarian physiology in healthy female mice. We found that this drug altered the estrous cycle, early follicular development, serum estradiol and progesterone levels, and ovarian steroidogenic enzyme expression. Moreover, ovarian angiogenesis was lower in metformin-treated animals compared with untreated ones, whereas natural or gonadotropin-induced fertilization rates remained unchanged. However, offspring of metformin-treated animals displayed decreased body weight at birth. In this work, we unraveled the main effects of metformin on the ovary, isolated from other conditions such as hyperglycemia and hyperandrogenism, which is essential for a better understanding of metformin’s mechanisms of action on reproduction and fertility.
