Search Results

You are looking at 41 - 50 of 475 items for :

  • estrogen and progesterone x
  • Refine by access: All content x
Clear All
Ingrid Segers Follicle Biology Laboratory, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Jette, Belgium

Search for other papers by Ingrid Segers in
Google Scholar
PubMed
Close
,
Tom Adriaenssens Follicle Biology Laboratory, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Jette, Belgium

Search for other papers by Tom Adriaenssens in
Google Scholar
PubMed
Close
,
Sandra Wathlet Follicle Biology Laboratory, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Jette, Belgium

Search for other papers by Sandra Wathlet in
Google Scholar
PubMed
Close
, and
Johan Smitz Follicle Biology Laboratory, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Jette, Belgium

Search for other papers by Johan Smitz in
Google Scholar
PubMed
Close

. Cyp19a1 , converting androgens into estrogens, was again highly expressed in HP-hMG25. Steroid measurements on day 9 corroborated the gene expression patterns, where the E 2 and progesterone content for rFSH25+low-dose LH bioactivity was higher

Free access
José E Sánchez-Criado Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by José E Sánchez-Criado in
Google Scholar
PubMed
Close
,
José C Garrido-Gracia Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by José C Garrido-Gracia in
Google Scholar
PubMed
Close
,
Carmina Bellido Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Carmina Bellido in
Google Scholar
PubMed
Close
,
Rafaela Aguilar Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Rafaela Aguilar in
Google Scholar
PubMed
Close
,
Pedro Guelmes Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Pedro Guelmes in
Google Scholar
PubMed
Close
,
Pedro Abreu Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Pedro Abreu in
Google Scholar
PubMed
Close
,
Rafael Alonso Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Rafael Alonso in
Google Scholar
PubMed
Close
,
Inmaculada Barranco Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Inmaculada Barranco in
Google Scholar
PubMed
Close
,
Yolanda Millán Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Yolanda Millán in
Google Scholar
PubMed
Close
, and
Juana Martín de las Mulas Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain
Department of Physiology, University of La Laguna, La Laguna, Spain
Department of Comparative Pathology, University of Córdoba, Córdoba, Spain

Search for other papers by Juana Martín de las Mulas in
Google Scholar
PubMed
Close

after ovariectomy (OVX) mimicked the endocrine events of pro-oestros through the augmentation of the LHRH-releasing pathway, progesterone (P 4 ) receptor (PR) expression, and PR-dependent LHRH self-priming ( Bellido et al. 2003 , Sánchez-Criado et

Free access
María Andrea Camilletti Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina

Search for other papers by María Andrea Camilletti in
Google Scholar
PubMed
Close
,
Alejandra Abeledo-Machado Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina

Search for other papers by Alejandra Abeledo-Machado in
Google Scholar
PubMed
Close
,
Jimena Ferraris Instituto de Investigaciones Biomédicas, Facultad de Medicina, Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina

Search for other papers by Jimena Ferraris in
Google Scholar
PubMed
Close
,
Pablo A Pérez Centro de Microscopia Electrónica, Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Facultad de Ciencias Medicas, Universidad Nacional de Córdoba, Córdoba, Argentina

Search for other papers by Pablo A Pérez in
Google Scholar
PubMed
Close
,
Erika Y Faraoni Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina

Search for other papers by Erika Y Faraoni in
Google Scholar
PubMed
Close
,
Daniel Pisera Instituto de Investigaciones Biomédicas, Facultad de Medicina, Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina

Search for other papers by Daniel Pisera in
Google Scholar
PubMed
Close
,
Silvina Gutierrez Centro de Microscopia Electrónica, Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Facultad de Ciencias Medicas, Universidad Nacional de Córdoba, Córdoba, Argentina

Search for other papers by Silvina Gutierrez in
Google Scholar
PubMed
Close
, and
Graciela Díaz-Torga Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina

Search for other papers by Graciela Díaz-Torga in
Google Scholar
PubMed
Close

the cell surface through binding to membrane estrogen receptors ( Kelly & Levin 2001 , Levin & Hammes 2016 ). Although it was demonstrated that membrane-initiated signaling could be mediated by the classic receptors ERα and ERβ trafficked to the cell

Free access
Rhone A Mendoza Department of Biomedical Sciences, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Rhone A Mendoza in
Google Scholar
PubMed
Close
,
Marlene I Enriquez Department of Biomedical Sciences, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Marlene I Enriquez in
Google Scholar
PubMed
Close
,
Sylvia M Mejia Department of Biomedical Sciences, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Sylvia M Mejia in
Google Scholar
PubMed
Close
,
Emily E Moody Department of Biomedical Sciences, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Emily E Moody in
Google Scholar
PubMed
Close
, and
Gudmundur Thordarson Department of Biomedical Sciences, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Gudmundur Thordarson in
Google Scholar
PubMed
Close

blot analysis showing expression of the estrogen receptor-α (ERα), the progesterone receptor (PR), and the ERβ in cloned MCF-7 cells stably transfected with a vector producing a small interfering RNA (siRNA) to the insulin-like growth factor-I receptor

Free access
Rhone A Mendoza Department of Biomedical Sciences, Paul L. Foster School of Medicine, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Rhone A Mendoza in
Google Scholar
PubMed
Close
,
Emily E Moody Department of Biomedical Sciences, Paul L. Foster School of Medicine, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Emily E Moody in
Google Scholar
PubMed
Close
,
Marlene I Enriquez Department of Biomedical Sciences, Paul L. Foster School of Medicine, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Marlene I Enriquez in
Google Scholar
PubMed
Close
,
Sylvia M Mejia Department of Biomedical Sciences, Paul L. Foster School of Medicine, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Sylvia M Mejia in
Google Scholar
PubMed
Close
, and
Gudmundur Thordarson Department of Biomedical Sciences, Paul L. Foster School of Medicine, Center of Excellence in Cancer Research, Texas Tech University Health Sciences Center, 5001 El Paso Drive, El Paso, Texas 79905, USA

Search for other papers by Gudmundur Thordarson in
Google Scholar
PubMed
Close

Introduction Estrogen and insulin-like growth factor 1 (IGF-I) are both central to breast development ( Kleinberg & Ruan 2008 ), and evidence indicates that both these hormones affect carcinogenesis of the breast ( Fagan & Yee 2008 ). Although both

Free access
Jyoti Parkash Neurochemistry and Neuroendocrinology Laboratory, Department of Biotechnology, Guru Nanak Dev University, Amritsar-143005, Punjab, India

Search for other papers by Jyoti Parkash in
Google Scholar
PubMed
Close
and
Gurcharan Kaur Neurochemistry and Neuroendocrinology Laboratory, Department of Biotechnology, Guru Nanak Dev University, Amritsar-143005, Punjab, India

Search for other papers by Gurcharan Kaur in
Google Scholar
PubMed
Close

conjunction with cyclic changes in GnRH neuronal terminals. To further test the role of steroid hormones in the cyclic neuronal plasticity of the GnRH neuron, we repeated these experiments in ovariectomized (OVX) and estrogen–progesterone-primed OVX (EBP

Free access
T Engstrom
Search for other papers by T Engstrom in
Google Scholar
PubMed
Close
,
P Bratholm
Search for other papers by P Bratholm in
Google Scholar
PubMed
Close
,
NJ Christensen
Search for other papers by NJ Christensen in
Google Scholar
PubMed
Close
, and
H Vilhardt
Search for other papers by H Vilhardt in
Google Scholar
PubMed
Close

The objective of the present study was to further elucidate our previous observation that beta2-adrenoceptor activation induces oxytocin receptor (OTR) expression in rat myometrium. We wanted to investigate whether the mechanism behind this effect was under the influence of gonadal steroids. Ovariectomized non-pregnant rats were treated with estrogen, progesterone or a combination of both for 3 days. Some rats were concomitantly treated with isoproterenol. Estrogen treatment increased both OTR mRNA production and maximal binding of [3H]-oxytocin to isolated myometrial plasma membranes, but it did not affect contractility of isolated uterine strips challenged with oxytocin. When the estrogen regimen was combined with isoproterenol treatment, an augmented maximal contractile response (Emax) to oxytocin was observed although no further increase in OTR mRNA and binding was seen. Progesterone treatment did not in itself alter OTR mRNA, OTR binding or Emax. However, OTRs were induced at the level of gene expression when progesterone was supplemented with isoproterenol infusion. Finally, progesterone suppressed the effect of estrogen on OTR mRNA production and binding when the two compounds were administered together. However, when isoproterenol treatment was added this effect was abolished and Emax was enhanced more than that seen following treatment with estrogen alone. These data suggest that beta2-adrenoceptor activation represents an important regulator of OTR expression/function in estrogen- and progesterone-dominated rat myometrium.

Free access
AE Calogero
Search for other papers by AE Calogero in
Google Scholar
PubMed
Close
,
N Burrello
Search for other papers by N Burrello in
Google Scholar
PubMed
Close
, and
AM Ossino
Search for other papers by AM Ossino in
Google Scholar
PubMed
Close

Endothelin (ET)-1 and ET-3, two peptides with a potent vasoconstrictive property, produce a variety of biological effects in different tissues by acting through two different receptors, the ET-1 selective ET(A) receptor and the non-selective ETB receptor. An increasing body of literature suggests that ET-1 acts as a paracrine/autocrine regulator of ovarian function. Indeed, ETB receptors have been identified in rat granulosa cells and ET-1 is a potent inhibitor of progesterone production. In contrast, inconsistent data have been reported about the role of ET-1 on estrogen production and the effects of ET-3 are not known. Therefore, the present study was undertaken to evaluate the effects of ET-1 and ET-3 on estrogen and cAMP production, and the receptor type involved. Given that prostanoids modulate ovarian steroidogenesis and that many actions of ETs are mediated by these compounds, we also evaluated whether the effects of ETs on estrogen and cAMP production might be prostanoid-mediated. ET-1, ET-3, and safarotoxin-S6c (SFX-S6c), a selective ETB receptor agonist, inhibited basal estrogen production by granulosa cells obtained from immature, estrogen-primed female rats, in a concentration-dependent manner. All three peptides were also capable of inhibiting the production of estrogen stimulated by a half-maximal (1 mIU/ml) and a maximally stimulatory (3 mIU/ml) concentration of FSH, ET-1 and ET-3 dose-dependently suppressed basal and FSH (1 mIU/ml)-stimulated cAMP production. ET-3 and SFX-S6c were significantly more potent than ET-1 in suppressing estrogen production, suggesting that this effect was not mediated by the ET(A) receptor. Indeed, BQ-123, a selective ET(A) receptor antagonist, did not influence the inhibitory effects of ET-1 and ET-3 on basal and FSH-stimulated estrogen release. To determine a possible involvement of prostanoids, we evaluated the effects of maximally effective concentrations of ET-1 and ET-3 on estrogen and cAMP production in the presence of indomethacin, a prostanoid synthesis inhibitor. This compound did not have any effect on the suppressive effects of ETs on basal or FSH (1 mIU/ml)-stimulated estrogen or cAMP production. In conclusion, ET-1 and ET-3 were able to inhibit estrogen and cAMP production by rat granulosa cells, indicating that the inhibitory effects of ETs on ovarian steroidogenesis are not limited to progesterone biosynthesis. This effect does not appear to be mediated by prostanoids or by the classical ET(A) and ETB receptors, at least under these experimental conditions.

Free access
T Engstrom
Search for other papers by T Engstrom in
Google Scholar
PubMed
Close
,
H Vilhardt
Search for other papers by H Vilhardt in
Google Scholar
PubMed
Close
,
P Bratholm
Search for other papers by P Bratholm in
Google Scholar
PubMed
Close
, and
NJ Christensen
Search for other papers by NJ Christensen in
Google Scholar
PubMed
Close

The effects of in vivo treatment with estrogen and progesterone on isoproterenol-induced uterine relaxation and beta(2)-adrenoceptor (beta(2)AR) mRNA production in non-pregnant rat myometrium were investigated. Whether homologous myometrial desensitization of beta(2)AR function was dependent on or modulated by the two steroids was also examined. Estrogen treatment alone or in combination with progesterone reduced maximal relaxation (E(max)) of isolated uterine strips subsequently challenged with isoproterenol whereas progesterone alone had no effect on this parameter. The reduction was accompanied by an enhanced beta(2)AR mRNA concentration. The concentration of isoproterenol giving half-maximal relaxing response (EC(50)) increased following estrogen treatment and this effect was curbed by progesterone. Isoproterenol had no effect on beta(2)AR transcription irrespective of the steroid regimes employed. E(max) of isolated uterine strips was reduced following prolonged in vivo treatment with isoproterenol but the effect was found only when estrogen alone was administered concomitantly. Finally, in vivo treatment with isoproterenol increased EC(50) of uterine strips subsequently stimulated with isoproterenol in vitro. This effect was independent of steroid treatment. We conclude that homologous desensitization of beta(2)AR function in non-pregnant rat myometrium in terms of sensitivity (EC(50)) is independent of sex steroids but in terms of maximal response (E(max)) occurs only in the presence of estrogen. We speculate whether progesterone withdrawal in connection with the well-known estrogen dominance at rat parturition may strengthen the desensitization induced by beta(2)AR activation and thus contribute to the transformation of the uterus from a quiescent to a highly contractile organ.

Free access
N Fujimoto
Search for other papers by N Fujimoto in
Google Scholar
PubMed
Close
,
N Jinno
Search for other papers by N Jinno in
Google Scholar
PubMed
Close
, and
S Kitamura
Search for other papers by S Kitamura in
Google Scholar
PubMed
Close

Interrelationships between thyroid hormone and estrogen actions have been documented with regard to a variety of physiological functions. Both hormones stimulate transcription of target genes by binding to their nuclear receptors that interact with specific responsive elements (estrogen and thyroid hormone response elements, i.e ERE and TRE, respectively) in the regulatory regions of the gene. In vitro studies have suggested that interplay between the two hormones might be due to cross-talk at hormone responsive elements, with the respective hormone receptors and ligands able to interact, although physiological relevance has yet to be proved. We have proposed a simpler mechanism for thyroid hormone effects on estrogen responses via increase in estrogen receptor alpha (ERalpha) with resultant increase in progesterone receptors, prolactin production and tumor growth. A pituitary cell line, GH3, has been widely used to investigate the function of mammo-somatotropic cells, especially regarding regulation of GH and prolactin production. In the present study, an ERE-luc reporter was transfected into GH3 cells and the responses to endogenous ERalpha were examined. We demonstrated that: (1)l -3,5,3'-triiodothyronine (T3) induces mRNA expression of ERalpha; (2) T3 alone is able to induce ERE-luc activity and this is inhibited by OH-tamoxifen; (3) T3 synergistically acts on estradiol (E2)-induced ERE responses; and (4) ERE-luc activity is enchanted by co-transfection of an ERalpha expression vector. These results support the hypothesis that estrogen responses are potentiated by T3 through up-regulation of ERalpha levels.

Free access