@article{MTMT:109827, title = {Paracrine signaling by glial cell-derived triiodothyronine activates neuronal gene expression in the rodent brain and human cells}, url = {https://m2.mtmt.hu/api/publication/109827}, author = {Freitas, BCG and Gereben, Balázs and Castillo, M and Kalló, Imre and Zeöld, Anikó and Egri, Péter and Liposits, Zsolt and Zavacki, AM and Maciel, RMB and Jo, S and Singru, P and Sanchez, E and Lechan, RM and Bianco, AM}, doi = {10.1172/JCI41977}, journal-iso = {J CLIN INVEST}, journal = {JOURNAL OF CLINICAL INVESTIGATION}, volume = {120}, unique-id = {109827}, issn = {0021-9738}, year = {2010}, eissn = {1558-8238}, pages = {2206-2217}, orcid-numbers = {Liposits, Zsolt/0000-0002-3508-2750} } @article{MTMT:1637686, title = {Ontogeny of rapid estrogen-mediated extracellular signal-regulated kinase signaling in the rat cerebellar cortex: Potent nongenomic agonist and endocrine disrupting activity of the xenoestrogen bisphenol A}, url = {https://m2.mtmt.hu/api/publication/1637686}, author = {Zsarnovszky, Attila and Le, HH and Wang, HS and Belcher, SM}, doi = {10.1210/en.2005-0565}, journal-iso = {ENDOCRINOLOGY}, journal = {ENDOCRINOLOGY}, volume = {146}, unique-id = {1637686}, issn = {0013-7227}, abstract = {In addition to regulating estrogen receptor-dependent gene expression, 17 beta-estradiol (E-2) can directly influence intracellular signaling. In primary cultured cerebellar neurons, E-2 was previously shown to regulate growth and oncotic cell death via rapid stimulation of ERK1/2 signaling. Here we show that ERK1/2 signaling in the cerebellum of neonatal and mature rats was rapidly responsive to E-2 and during development to the environmental estrogen bisphenol A (BPA). In vivo dose-response analysis for each estrogenic compound was performed by brief (6-min) intracerebellar injection, followed by rapid fixation and phosphorylation-state-specific immunohistochemistry to quantitatively characterize changes in activated ERK1/2 (pERK) immunopositive cell numbers. Beginning on postnatal d8, E-2 significantly influenced the number of pERK-positive cells in a cell-specific manner that was dependent on concentration and age but not sex. In cerebellar granule cells on postnatal d 10, E-2 or BPA increased pERK-positive cell numbers at low doses (10(-12) to 10(-10) M) and at higher (10(-7) to 10(-6) M) concentrations. Intermediate concentrations of either estrogenic compound did not modify basal ERK signaling. Rapid E-2-induced increases in pERK immunoreactivity were specific to the ERK1/2 pathway as demonstrated by coinjection of the mitogen-activated, ERK-activating kinase (MEK) 1/2 inhibitor U0126. Coadministration of BPA (10(-12) to 10(-10) M) with 10(-10) M E-2 dose-dependently inhibited rapid E-2-induced ERK1/2 activation in developing cerebellar neurons. The ability of BPA to act as a highly potent E-2 mimetic and to also disrupt the rapid actions of E-2 at very low concentrations during cerebellar development highlights the potential low-dose impact of xenoestrogens on the developing brain.}, year = {2005}, eissn = {1945-7170}, pages = {5388-5396} } @article{MTMT:1637684, title = {Estrogen receptor expression in a human primitive neuroectodermal tumor cell line from the cerebral cortex: estrogen stimulates rapid ERK1/2 activation and receptor-dependent cell migration}, url = {https://m2.mtmt.hu/api/publication/1637684}, author = {Kirby, M and Zsarnovszky, Attila and Belcher, SM}, doi = {10.1016/j.bbrc.2004.05.049}, journal-iso = {BIOCHEM BIOPH RES CO}, journal = {BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS}, volume = {319}, unique-id = {1637684}, issn = {0006-291X}, abstract = {Primitive neuroectodermal tumors (PNETs) are the most common form of pediatric brain tumor. Most often these malignant childhood brain tumors arise from neuroepithelial precursor cells in the cerebellum, and less frequently in the cerebral cortex. Because the normal PNET precursor cells from the cerebrum and cerebellum transiently express high levels of estrogen receptors (ERs), we hypothesized that the PNET cells of the cerebrocortical-derived cell line PFSK1 may also express ERs and would be responsive to estrogen. Results of immunoblot studies using ER-specific antiserum indicate that both ERalpha and ERbeta are expressed in PFSK1 cells. The ability of estrogen to rapidly activate MAPK signaling was tested; low physiological concentrations of E-2 stimulated ERK1/2 phosphorylation and nuclear translocation within 15 min of exposure. Exogenously added 17beta-estradiol (E-2) could not stimulate PFSK1 growth, however E-2 significantly increased PFSK1 cell migration, suggesting that rapid actions of E-2 and ER-mediated processes might contribute to the metastatic phenotype of some PNETs. (C) 2004 Elsevier Inc. All rights reserved.}, year = {2004}, eissn = {1090-2104}, pages = {753-758} } @article{MTMT:1617564, title = {Expression and localisation of leptin and leptin receptor in the mammary gland of the dry and lactating non-pregnant cow}, url = {https://m2.mtmt.hu/api/publication/1617564}, author = {Sayed-Ahmed, A and Huszeniczáné Kulcsár, Margit and Rudas, P and Bartha, Tibor}, doi = {10.1556/AVet.52.2004.1.10}, journal-iso = {ACTA VET HUNG}, journal = {ACTA VETERINARIA HUNGARICA}, volume = {52}, unique-id = {1617564}, issn = {0236-6290}, abstract = {Leptin and leptin receptor were studied in the mammary gland of \nnonpregnant dry and lactating cows. Using RT-PCR it was demonstrated \nthat leptin and its short (Ob-Ra) and long (Ob-Rb) receptor isoforms \nare expressed both in the dry and the lactating mammary gland tissue. \nTissue distribution of leptin and its receptor mRNA transcripts were \nexamined by in situ hybridisation, while the leptin protein was \nlocalised by immunohistochemistry. Although in situ hybridisation is \nsemiquantitative, our morphological data suggest that the epithelial \nleptin mRNA expression of the lactating gland is higher than that of \nthe dry gland. To compare the leptin mRNA levels between dry and \nlactating udders competitive PCR was used, which showed no difference \nin leptin expression for the whole mammary tissues. The lack of \ndifference in total leptin mRNA levels is explained by the high adipose \ntissue content of the dry mammary gland. Leptin and its receptor \ntranscripts are expressed mainly in the epithelial cells of lactating \ncows, while in dry mammary tissue the signal is found in the stromal \ntissues as well. The results provide additional evidence that locally \nproduced leptin takes part in the regulation and maintenance of mammary \nepithelial cell activity.}, year = {2004}, eissn = {1588-2705}, pages = {97-111} } @article{MTMT:1637683, title = {Estrogens and ICI182,780 (Faslodex) modulate mitosis and cell death in immature cerebellar neurons via rapid activation of p44/p42 mitogen-activated protein kinase}, url = {https://m2.mtmt.hu/api/publication/1637683}, author = {Wong, JK and Le, HH and Zsarnovszky, Attila and Belcher, SM}, journal-iso = {J NEUROSCI}, journal = {JOURNAL OF NEUROSCIENCE}, volume = {23}, unique-id = {1637683}, issn = {0270-6474}, abstract = {Estrogen influences the development and function of the nervous system through estrogen receptor-dependent changes in gene expression and by rapidly influencing diverse intracellular signaling pathways. We have investigated the influence of estradiol on developing neonatal rat cerebellar neurons in primary culture and found that low concentrations of 17beta-estradiol (17beta-E-2),17alpha-E-2,E- 17beta-E-2-BSA, and ICI182,780 stimulated phosphorylation of the extracellular signal-regulated kinases 1/2 (ERK1/2) mitogen-activated protein kinases (MAPK). Neither testosterone nor progesterone increased ERK1/2 phosphorylation. The effects of the estrogens were specific to the ERK1/2 MAPK pathway and were blocked by U0126, an inhibitor of the ERK1/2 MAPK kinase (MEK1/2). Compared with control cultures, significant MAPK-dependent decreases in viable granule cell numbers were observed in dissociated explant cultures of developing cerebellar neurons 24-96 hr after pulse treatment with 10 pM 17beta-E-2 or 10 nM ICI182,780. In contrast, continuous exposure to 10 pM 17beta-E-2 significantly increased granule cell numbers. Analysis of bromodeoxyuridine incorporation revealed that a 15 min pulsed treatment with 10 pM 17beta-E-2 increased mitogenesis, whereas continuous exposure to the same concentration of 17beta-E-2 was anti-mitotic. Estradiol did not increase caspase activity; however, significant increases in cellular permeability and lysis were observed. Cell lysis and death were independent of the pan-caspase inhibitor zVAD-fmk but were blocked fully by the irreversible calpain inhibitor PD150606. These results indicate that rapid activation of the ERK1/2 MAPK pathway by low concentrations of 17beta-E-2 induces oncotic/necrotic, but not apoptotic, programmed cell death in a subpopulation of developing granule cells and increased mitogenesis of the granule cell neuroblasts refractory to estrogen-induced neurotoxicity.}, year = {2003}, eissn = {1529-2401}, pages = {4984-4995} } @article{MTMT:1637679, title = {Estrogenic actions in the brain: Estrogen, phytoestrogens, and rapid intracellular signaling mechanisms}, url = {https://m2.mtmt.hu/api/publication/1637679}, author = {Belcher, SM and Zsarnovszky, Attila}, journal-iso = {J PHARMACOL EXP THER}, journal = {JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS}, volume = {299}, unique-id = {1637679}, issn = {0022-3565}, abstract = {The endogenous gonadal steroid 17 beta -estradiol (E-2) plays an important role in the development, maturation, and function of a wide variety of reproductive and nonreproductive tissues, including those of the nervous system. The actions of E-2 at target tissues can be divided into 1) long-term "genomic" actions that are mediated by intracellular estrogen receptor-induced changes in gene expression and 2) rapid actions that modulate a diverse array of intracellular signal transduction cascades. Environmental estrogens are compounds present in the environment that can mimic, and in some cases antagonize, the effects of endogenous estrogens. As a result of these actions, there is currently much interest within the scientific community regarding the relative benefits or threats associated with exposure to different environmental estrogens. Within the general public there is considerable acceptance of the benefits associated with increased use of "natural" estrogens as a component of a healthy diet and in postmenopausal women as an alternative to estrogen replacement therapies. First, this review will focus attention on the role of estrogens in the central nervous system by briefly discussing some of the known mechanisms through which estrogen's effects are mediated, focusing on rapid intracellular signaling mechanisms during neurodevelopment. Second, with the hope of bringing attention to an area of study that until recently has received little consideration, we will briefly discuss phytoestrogens and suggest that these compounds have the potential to influence rapid E-2-induced mechanisms in the nervous system in ways that may result in modified brain functions.}, year = {2001}, eissn = {1521-0103}, pages = {408-414} } @article{MTMT:109009, title = {Regional physiological adaptation of the central nervous system deiodinases to iodine deficiency}, url = {https://m2.mtmt.hu/api/publication/109009}, author = {Peeters, R and Fekete, Csaba and Goncalves, C and Legradi, G and Tu, HM and Harney, JW and Bianco, AC and Lechan, RM and Larsen, PR}, journal-iso = {AM J PHYSIOL ENDOC M}, journal = {AMERICAN JOURNAL OF PHYSIOLOGY: ENDOCRINOLOGY AND METABOLISM}, volume = {281}, unique-id = {109009}, issn = {0193-1849}, year = {2001}, eissn = {1522-1555}, pages = {E54-E64} } @article{MTMT:109034, title = {3,3',5-triiodothyronine (T3) uptake and expression of thyroid hormone receptors during the adaptation to hypothyroidism of the brain of chicken}, url = {https://m2.mtmt.hu/api/publication/109034}, author = {Gereben, Balázs and Kollár, Anna and Bartha, T and Buys, N and Decuypere, E and Rudas, P}, journal-iso = {ACTA VET HUNG}, journal = {ACTA VETERINARIA HUNGARICA}, volume = {46}, unique-id = {109034}, issn = {0236-6290}, year = {1998}, eissn = {1588-2705}, pages = {473-485} }