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Journal articles on the topic 'Adrenergic and thyroid signalling'

Author: Grafiati

Published: 28 June 2021

Last updated: 29 July 2025

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1

Gachkar, Sogol, Sebastian Nock, Cathleen Geissler, et al. "Aortic effects of thyroid hormone in male mice." Journal of Molecular Endocrinology 62, no. 3 (2019): 91–99. http://dx.doi.org/10.1530/jme-18-0217.

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It is well established that thyroid hormones are required for cardiovascular functions; however, the molecular mechanisms remain incompletely understood, especially the individual contributions of genomic and non-genomic signalling pathways. In this study, we dissected how thyroid hormones modulate aortic contractility. To test the immediate effects of thyroid hormones on vasocontractility, we used a wire myograph to record the contractile response of dissected mouse aortas to the adrenergic agonist phenylephrine in the presence of different doses of T3 (3,3′,5-triiodothyronine). Interestingly

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2

Zarain-Herzberg, Angel. "Regulation of the sarcoplasmic reticulum Ca2+-ATPase expression in the hypertrophic and failing heartThis paper is part of a series in the Journal's “Made in Canada” section. The paper has undergone peer review." Canadian Journal of Physiology and Pharmacology 84, no. 5 (2006): 509–21. http://dx.doi.org/10.1139/y06-023.

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The sarcoplasmic reticulum (SR) plays a central role in the contraction and relaxation coupling in the myocardium. The SR Ca2+-ATPase (SERCA2) transports Ca2+ inside the SR lumen during relaxation of the cardiac myocyte. It is well known that diminished contractility of the hypertrophic cardiac myocyte is the main factor of ventricular dysfunction in the failing heart. A key feature of the failing heart is a decreased content and activity of SERCA2, which is the cause of some of the physiological defects observed in the hypertrophic cardiomyocyte performance that are important during transitio

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3

Pantos, Constantinos, Iordanis Mourouzis, Christodoulos Xinaris та ін. "Time-dependent changes in the expression of thyroid hormone receptor α1 in the myocardium after acute myocardial infarction: possible implications in cardiac remodelling". European Journal of Endocrinology 156, № 4 (2007): 415–24. http://dx.doi.org/10.1530/eje-06-0707.

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The present study investigated whether changes in thyroid hormone (TH) signalling can occur after acute myocardial infarction (AMI) with possible physiological consequences on myocardial performance. TH may regulate several genes encoding important structural and regulatory proteins particularly through the TRα1 receptor which is predominant in the myocardium. AMI was induced in rats by ligating the left coronary artery while sham-operated animals served as controls. This resulted in impaired cardiac function in AMI animals after 2 and 13 weeks accompanied by a shift in myosin isoforms express

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4

DAZA, Francisco J., Roberto PARRILLA та Angeles MARTÍN-REQUERO. "3,5,3′-Tri-iodo-l-thyronine acutely regulates a protein kinase C-sensitive, Ca2+-independent, branch of the hepatic α1-adrenoreceptor signalling pathway". Biochemical Journal 331, № 1 (1998): 89–97. http://dx.doi.org/10.1042/bj3310089.

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This work aimed to investigate the acute effect of the thyroid hormone 3,5,3´-tri-iodo-l-thyronine (T3) in regulating the hepatic metabolism either directly or by controlling the responsiveness to Ca2+-mobilizing agonists. We did not detect any acute metabolic effect of T3 either in perfused liver or in isolated liver cells. However, T3 exerted a powerful inhibitory effect on the α1-adrenoreceptor-mediated responses. The promptness of this T3 effect rules out that it was the result of rate changes in gene(s) transcription. T3 inhibited the α1-adrenoreceptor-mediated sustained stimulation of re

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5

Shimegi, S., F. Okajima, and Y. Kondo. "Permissive stimulation of Ca(2+)-induced phospholipase A2 by an adenosine receptor agonist in a pertussis toxin-sensitive manner in FRTL-5 thyroid cells: a new ‘cross-talk’ mechanism in Ca2+ signalling." Biochemical Journal 299, no. 3 (1994): 845–51. http://dx.doi.org/10.1042/bj2990845.

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We have described the pertussis toxin (PTX)-sensitive potentiation of P2-purinergic agonist-induced phospholipase C activation, Ca2+ mobilization and arachidonic acid release by an adenosine receptor agonist, N6-(L-2-phenylisopropyl)adenosine (PIA), which alone cannot influence any of these cellular activities [Okajima, Sato, Nazarea, Sho and Kondo (1989) J. Biol. Chem. 264, 13029-13037]. In the present study we have found that arachidonic acid release was associated with lysophosphatidylcholine production, and conclude that arachidonic acid is produced by phospholipase A2 in FRTL-5 thyroid ce

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6

Sohn, Rebecca, Gundula Rösch, Marius Junker, Andrea Meurer, Frank Zaucke, and Zsuzsa Jenei-Lanzl. "Adrenergic signalling in osteoarthritis." Cellular Signalling 82 (June 2021): 109948. http://dx.doi.org/10.1016/j.cellsig.2021.109948.

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7

McMacken, Grace, and Hanns Lochmuller. "ADRENERGIC SIGNALLING AND CONGENITAL MYASTHENIC SYNDROMES." Journal of Neurology, Neurosurgery & Psychiatry 87, no. 12 (2016): e1.77-e1. http://dx.doi.org/10.1136/jnnp-2016-315106.168.

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8

Kanagy, Nancy L. "α2-Adrenergic receptor signalling in hypertension". Clinical Science 109, № 5 (2005): 431–37. http://dx.doi.org/10.1042/cs20050101.

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Cardiovascular regulation by the sympathetic nervous system is mediated by activation of one or more of the nine known subtypes of the adrenergic receptor family; α1A-, α1B-, α1D-, α2A-, α2B-, α2C-, β1-, β2- and β3-ARs (adrenoceptors). The role of the α2-AR family has long been known to include presynaptic inhibition of neurotransmitter release, diminished sympathetic efferent traffic, vasodilation and vasoconstriction. This complex response is mediated by one of three subtypes which all uniquely affect blood pressure and blood flow. All three subtypes are present in the brain, kidney, heart a

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9

Suddle, A., and S. Klimach. "Lactate and adrenergic signalling in trauma." Annals of The Royal College of Surgeons of England 98, no. 03 (2016): 238–39. http://dx.doi.org/10.1308/rcsann.2016.0097.

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10

McMacken, Grace, Sally Spendiff, Rachel Howarth, et al. "PO167 Adrenergic signalling and congenital myasthenic syndromes." Journal of Neurology, Neurosurgery & Psychiatry 88, Suppl 1 (2017): A56.3—A56. http://dx.doi.org/10.1136/jnnp-2017-abn.194.

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11

Herness, Scott, Fang‐li Zhao, Namik Kaya, Shao‐gang Lu, Tiansheng Shen, and Xiao‐Dong Sun. "Adrenergic signalling between rat taste receptor cells." Journal of Physiology 543, no. 2 (2002): 601–14. http://dx.doi.org/10.1113/jphysiol.2002.020438.

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12

Wu, Yuanjun, Yu Zhao, Xiaojie Ma, Yunjuan Zhu, Jaimin Patel та Zhongzhen Nie. "The Arf GAP AGAP2 interacts with β-arrestin2 and regulates β2-adrenergic receptor recycling and ERK activation". Biochemical Journal 452, № 3 (2013): 411–21. http://dx.doi.org/10.1042/bj20121004.

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AGAP2 [Arf (ADP-ribosylation factor) GAP (GTPase-activating protein) with GTP-binding-protein-like, ankyrin repeat and PH (pleckstrin homology) domains] is a multidomain Arf GAP that was shown to promote the fast recycling of transferrin receptors. In the present study we tested the hypothesis that AGAP2 regulates the trafficking of β2-adrenergic receptors. We found that AGAP2 formed a complex with β-arrestin1 and β-arrestin2, proteins that are known to regulate β2-adrenergic receptor signalling and trafficking. AGAP2 co-localized with β-arrestin2 on the plasma membrane, and knockdown of AGAP2

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13

García-Jiménez, Custodia, and Pilar Santisteban. "TSH signalling and cancer." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 5 (2007): 654–71. http://dx.doi.org/10.1590/s0004-27302007000500003.

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Thyroid cancers are the most frequent endocrine neoplasms and mutations in the thyrotropin receptor (TSHR) are unusually frequent. Here we present the state-of-the-art concerning the role of TSHR in thyroid cancer and discuss it in light of the cancer stem cell theory or the classical view. We briefly review the gene and protein structure updating the cancer related TSHR mutations database. Intriguingly, hyperfunctioning TSHR mutants characterise differentiated cancers in contrast to undifferentiated thyroid cancers which very often bear silenced TSHR. It remains unclear whether TSHR alteratio

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14

Kubota, K., and S. H. Ingbar. "Influences of thyroid status and sympathoadrenal system on extrarenal potassium disposal." American Journal of Physiology-Endocrinology and Metabolism 258, no. 3 (1990): E428—E435. http://dx.doi.org/10.1152/ajpendo.1990.258.3.e428.

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Effects of hyper- and hypothyroidism on the ability of rats to transfer acute intravenous loads of potassium from the extracellular to the intracellular milieu (extrarenal potassium disposal, ERPD) were studied. We also examined the effects of the sympathoadrenal system on ERPD, as well as the manner in which it interacts with thyroid status. Experiments were performed in thyroidectomized (hypothyroid), sham-operated (euthyroid), or 3,5,3'-triiodo-L-thyronine-treated (thyrotoxic) rats. In anesthetized, acutely nephrectomized animals given a constant infusion of KCl over a 90-min period, ERPD w

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15

Brandi, Maria Luisa, Carlo M. Rotella, Roberto Zonefrati, Roberto Toccafondi, and Salvatore M. Aloj. "Loss of adrenergic regulation of cAMP production in the FRTL-5 cell line." Acta Endocrinologica 111, no. 1 (1986): 54–61. http://dx.doi.org/10.1530/acta.0.1110054.

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Abstract. Rat thyroid cells in primary culture augment cAMP production when challenged with β-adrenergic agonists; at 10−5m the potency is isoproterenol > nor-epinephrine > epinephrine. In analogy with human thyroid cells, rat thyroid primary cultures display α-adrenergic-stimulated cGMP production which inhibits TSH and norepinephrine stimulation of cAMP. Adrenergic regulation of cyclic nucelotide production is lost in the cloned thyroid cell line of rat origin known as FRTL-5. Also the potentiating effect of phentolamine on TSH stimulation of cAMP production in thyroid primary cultures

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16

Yamashita, Kamejiro, Yuji Aiyoshi, Nobuaki Kuzuya, and Yoshinobu Koide. "Alterations of adrenergic systems in thyroid slices from patients with Graves' disease." Acta Endocrinologica 110, no. 3 (1985): 360–65. http://dx.doi.org/10.1530/acta.0.1100360.

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Abstract. The responses to TSH of tissue cAMP levels in thyroid slices from patients with Graves' disease were significantly lower than those in normal thyroid slices. Conversely, tissue cAMP levels in thyroid slices from these patients were greatly increased by β-adrenergic agonists, either isoproterenol or norepinephrine compared with those in normal thyroid slices. The elevation of cAMP levels induced by TSH in normal thyroid slices was significantly reduced by norepinephrine via α-adrenergic action as reported previously in canine thyroid slices, while such an elevation by TSH of cAMP leve

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17

Chhatar, Sushanta, and Girdhari Lal. "Role of adrenergic receptor signalling in neuroimmune communication." Current Research in Immunology 2 (2021): 202–17. http://dx.doi.org/10.1016/j.crimmu.2021.11.001.

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18

Cotecchia, S., A. L. Lattion, D. Diviani та A. Cavalli. "Signalling and regulation of the α1B-adrenergic receptor". Biochemical Society Transactions 23, № 1 (1995): 121–25. http://dx.doi.org/10.1042/bst0230121.

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19

Zholobenko, Aleksey, Eva Gabrielová, Jiří Nečas, and Martin Modrianský. "Modulation of Adrenergic Signalling by Flavonoids in Cardioprotection." Biophysical Journal 106, no. 2 (2014): 304a—305a. http://dx.doi.org/10.1016/j.bpj.2013.11.1768.

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20

Joiner, Mei-ling A., Marie-France Lisé, Eunice Y. Yuen та ін. "Assembly of a β2-adrenergic receptor—GluR1 signalling complex for localized cAMP signalling". EMBO Journal 29, № 2 (2009): 482–95. http://dx.doi.org/10.1038/emboj.2009.344.

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21

Lauby, Samantha C., and Patrick O. McGowan. "Early life variations in temperature exposure affect the epigenetic regulation of the paraventricular nucleus in female rat pups." Proceedings of the Royal Society B: Biological Sciences 287, no. 1937 (2020): 20201991. http://dx.doi.org/10.1098/rspb.2020.1991.

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Early life maternal care received has a profound effect on later-life behaviour in adult offspring, and previous studies have suggested epigenetic mechanisms are involved. Changes in thyroid hormone receptor signalling may be related to differences in maternal care received and DNA methylation modifications. We investigated the effects of variations in temperature exposure (a proxy of maternal contact) and licking-like tactile stimulation on these processes in week-old female rat pups. We assessed thyroid hormone receptor signalling by measuring circulating triiodothyronine and transcript abun

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22

Mondragón-Terán, Paul, Luz Berenice López-Hernández, José Gutiérrez-Salinas, Juan Antonio Suárez-Cuenca, Rosa Isela Luna-Ceballos, and Aura Erazo Valle-Solís. "Intracellular signalling mechanisms in thyroid cancer." Cirugía y Cirujanos (English Edition) 84, no. 5 (2016): 434–43. http://dx.doi.org/10.1016/j.circen.2016.08.011.

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23

Yeh, L. F., S. P. Baker, and M. J. Katovich. "Thyroxine, renal beta-adrenergic receptors, and dipsogenesis in food-deprived rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 1 (1988): R33—R39. http://dx.doi.org/10.1152/ajpregu.1988.254.1.r33.

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The effect of thyroxine (T4) replacement on the increased renal beta-adrenergic receptor number and the increased beta-adrenergic dipsogenic responsiveness of fasted rats was studied in male Sprague-Dawley rats. Food deprivation significantly decreased serum thyroxine (T4) and triiodothyronine (T3) levels, increased the dipsogenic response to isoproterenol, and elevated renal beta-adrenergic receptor concentration. Daily administration of T4 (40 micrograms/kg) to food-deprived rats restored serum thyroid levels to normal. Thyroxine replacement also reduced the increased beta-adrenergic dipsoge

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24

Cordeiro, Aline, Luana Lopes Souza, Marcelo Einicker-Lamas, and Carmen Cabanelas Pazos-Moura. "Non-classic thyroid hormone signalling involved in hepatic lipid metabolism." Journal of Endocrinology 216, no. 3 (2013): R47—R57. http://dx.doi.org/10.1530/joe-12-0542.

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Thyroid hormones are important modulators of lipid metabolism because the liver is a primary hormonal target. The hypolipidaemic effects of thyroid hormones result from the balance between direct and indirect actions resulting in stimulation of lipid synthesis and lipid oxidation, which favours degradation pathways. Originally, it was believed that thyroid hormone activity was only transduced by alteration of gene transcription mediated by the nuclear receptor thyroid hormone receptors, comprising the classic action of thyroid hormone. However, the discovery of other effects independent of thi

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25

Zi, Min, Sukhpal Prehar, Elizabeth J. Cartwright, Michael Emerson та Ludwig Neyses. "The sarcolemmal calcium pump modulates β-adrenergic hypertrophic signalling". Journal of Molecular and Cellular Cardiology 40, № 6 (2006): 1003–4. http://dx.doi.org/10.1016/j.yjmcc.2006.03.244.

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26

Davidson, M. J., and W. J. Koch. "Genetic manipulation of b-adrenergic signalling in heart failure." Acta Physiologica Scandinavica 173, no. 1 (2001): 145–50. http://dx.doi.org/10.1046/j.1365-201x.2001.00900.x.

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27

Jönsson, Cecilia, Ana P. Castor Batista, Preben Kjølhede та Peter Strålfors. "Insulin and β-adrenergic receptors mediate lipolytic and anti-lipolytic signalling that is not altered by type 2 diabetes in human adipocytes". Biochemical Journal 476, № 19 (2019): 2883–908. http://dx.doi.org/10.1042/bcj20190594.

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Abstract Control of fatty acid storage and release in adipose tissue is fundamental in energy homeostasis and the development of obesity and type 2 diabetes. We here take the whole signalling network into account to identify how insulin and β-adrenergic stimulation in concert controls lipolysis in mature subcutaneous adipocytes obtained from non-diabetic and, in parallel, type 2 diabetic women. We report that, and show how, the anti-lipolytic effect of insulin can be fully explained by protein kinase B (PKB/Akt)-dependent activation of the phosphodiesterase PDE3B. Through the same PKB-dependen

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28

Kim, Brian, Suzy D. Carvalho-Bianco, and P. Reed Larsen. "Thyroid hormone and adrenergic signaling in the heart." Arquivos Brasileiros de Endocrinologia & Metabologia 48, no. 1 (2004): 171–75. http://dx.doi.org/10.1590/s0004-27302004000100019.

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Thyroid hormone action has profound consequences for the heart, ranging from atrial fibrillation to hemodynamic collapse. It has long been known that the cardiovascular signs and symptoms seen in thyrotoxicosis resemble those seen in states of catecholamine excess. However, measured concentrations of serum catecholamines in patients with thyrotoxicosis are typically normal or even low, suggesting an increase in the adrenergic responsiveness of the thyrotoxic heart. In spite of several decades of work, the question of whether thyroid hormone increases cardiac adrenergic responsiveness is still

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Larsson, Malin, Nils Rudqvist, Johan Spetz, et al. "Long-term transcriptomic and proteomic effects in Sprague Dawley rat thyroid and plasma after internal low dose 131I exposure." PLOS ONE 15, no. 12 (2020): e0244098. http://dx.doi.org/10.1371/journal.pone.0244098.

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Background Radioiodide (131I) is commonly used to treat thyroid cancer and hyperthyroidis.131I released during nuclear accidents, have resulted in increased incidence of thyroid cancer in children. Therefore, a better understanding of underlying cellular mechanisms behind 131I exposure is of great clinical and radiation protection interest. The aim of this work was to study the long-term dose-related effects of 131I exposure in thyroid tissue and plasma in young rats and identify potential biomarkers. Materials and methods Male Sprague Dawley rats (5-week-old) were i.v. injected with 0.5, 5.0,

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30

Silva, J. Enrique, and Suzy D. C. Bianco. "Thyroid–Adrenergic Interactions: Physiological and Clinical Implications." Thyroid 18, no. 2 (2008): 157–65. http://dx.doi.org/10.1089/thy.2007.0252.

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31

Nilsson, Ove R., and Bengt E. Karlberg. "Thyroid hormones and the adrenergic nervous system." Acta Medica Scandinavica 213, S672 (2009): 27–32. http://dx.doi.org/10.1111/j.0954-6820.1983.tb01610.x.

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32

Burrows, Natalie, Muhammad Babur, Julia Resch, Kaye J. Williams, and Georg Brabant. "Hypoxia-Inducible Factor in Thyroid Carcinoma." Journal of Thyroid Research 2011 (2011): 1–17. http://dx.doi.org/10.4061/2011/762905.

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Intratumoural hypoxia (low oxygen tension) is associated with aggressive disease and poor prognosis. Hypoxia-inducible factor-1 is a transcription factor activated by hypoxia that regulates the expression of genes that promote tumour cell survival, progression, metastasis, and resistance to chemo/radiotherapy. In addition to hypoxia, HIF-1 can be activated by growth factor-signalling pathways such as the mitogen-activated protein kinases- (MAPK-) and phosphatidylinositol-3-OH kinases- (PI3K-) signalling cascades. Mutations in these pathways are common in thyroid carcinoma and lead to enhanced

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33

Grassby, Paul F., and John H. McNeill. "Sensitivity changes to inotropic agents in rabbit atria after chronic experimental diabetes." Canadian Journal of Physiology and Pharmacology 66, no. 12 (1988): 1475–80. http://dx.doi.org/10.1139/y88-241.

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The effect of experimental diabetes on the sensitivity of isolated left atrial strips to inotropic agents was investigated in rabbits made diabetic with alloxan. After 4 weeks of diabetes no change in sensitivity was detected in response to isoproterenol or ouabain. In contrast, 15 weeks of diabetes induced a decreased sensitivity to β-adrenergic stimulation, exhibited as a shift to the right in concentration–response curves obtained in response to isoproterenol and noradrenaline. In addition, after 15 weeks of diabetes the inotropic response to ouabain was depressed, and a small decrease in s

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34

Rupp, H., and R. Wahl. "Influence of thyroid hormones and catecholamines on myosin of swim-exercised rats." Journal of Applied Physiology 68, no. 3 (1990): 973–78. http://dx.doi.org/10.1152/jappl.1990.68.3.973.

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To define the physiological signals involved in the redirection of myosin expression in the swim-exercised rat, the relative influence of thyroid hormones and beta-adrenergic blockade was determined. Swimming exercise resulted in an increased proportion of myosin V1 (60.9 +/- 9.7 vs. 38.0 +/- 4.1% of sedentary rats fed ad libitum) but did not increase serum concentrations of total and free thyroxine or triiodothyronine determined either 17-21 h or immediately after swimming. The proportion of V1 increased, although intermittently food-deprived rats with the body weight of swimming rats exhibit

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35

Yang, Hua-Qian, Peng Zhou, Li-Peng Wang та ін. "Compartmentalized β1-adrenergic signalling synchronizes excitation–contraction coupling without modulating individual Ca2+ sparks in healthy and hypertrophied cardiomyocytes". Cardiovascular Research 116, № 13 (2020): 2069–80. http://dx.doi.org/10.1093/cvr/cvaa013.

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Abstract Aims β-adrenergic receptors (βARs) play pivotal roles in regulating cardiac excitation–contraction (E-C) coupling. Global signalling of β1ARs up-regulates both the influx of Ca2+ through sarcolemmal L-type Ca2+ channels (LCCs) and the release of Ca2+ from the sarcoplasmic reticulum (SR) through the ryanodine receptors (RyRs). However, we recently found that β2AR stimulation meditates ‘offside compartmentalization’, confining β1AR signalling into subsarcolemmal nanodomains without reaching SR proteins. In the present study, we aim to investigate the new question, whether and how compar

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36

Mantzouratou, Polyxeni, Angelo Michele Lavecchia, and Christodoulos Xinaris. "Thyroid Hormone Signalling in Human Evolution and Disease: A Novel Hypothesis." Journal of Clinical Medicine 11, no. 1 (2021): 43. http://dx.doi.org/10.3390/jcm11010043.

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Thyroid hormone (TH) signalling is a universally conserved pathway with pleiotropic actions that is able to control the development, metabolism, and homeostasis of organisms. Using evidence from paleoecology/palaeoanthropology and data from the physiology of modern humans, we try to assess the natural history of TH signalling and its role in human evolution. Our net thesis is that TH signalling has likely played a critical role in human evolution by facilitating the adaptive responses of early hominids to unprecedently challenging and continuously changing environments. These ancient roles hav

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Sysa-Shah, Polina, Carlo G. Tocchetti, Manveen Gupta та ін. "Bidirectional cross-regulation between ErbB2 and β-adrenergic signalling pathways". Cardiovascular Research 109, № 3 (2015): 358–73. http://dx.doi.org/10.1093/cvr/cvv274.

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Ji, Xian-Fei, Shuo Wang, Lin Yang та Chun-Sheng Li. "Impaired β-adrenergic receptor signalling in post-resuscitation myocardial dysfunction". Resuscitation 83, № 5 (2012): 640–44. http://dx.doi.org/10.1016/j.resuscitation.2011.11.014.

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Sato, Shoko, Naoki Sato, Raymond K. Kudej та ін. "β-Adrenergic Receptor Signalling in Stunned Myocardium of Conscious Pigs". Journal of Molecular and Cellular Cardiology 29, № 5 (1997): 1387–400. http://dx.doi.org/10.1006/jmcc.1997.0377.

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Zhang, Biqin, Cheukyau Luk, Joyce Valadares, Christos Aronis та Lazaros C. Foukas. "Dominant Role of PI3K p110α over p110β in Insulin and β-Adrenergic Receptor Signalling". International Journal of Molecular Sciences 22, № 23 (2021): 12813. http://dx.doi.org/10.3390/ijms222312813.

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Attribution of specific roles to the two ubiquitously expressed PI 3-kinase (PI3K) isoforms p110α and p110β in biological functions they have been implicated, such as in insulin signalling, has been challenging. While p110α has been demonstrated to be the principal isoform activated downstream of the insulin receptor, several studies have provided evidence for a role of p110β. Here we have used isoform-selective inhibitors to estimate the relative contribution of each of these isoforms in insulin signalling in adipocytes, which are a cell type with essential roles in regulation of metabolism a

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41

Maloyan, Alina, та Michal Horowitz. "β-Adrenergic signaling and thyroid hormones affect HSP72 expression during heat acclimation". Journal of Applied Physiology 93, № 1 (2002): 107–15. http://dx.doi.org/10.1152/japplphysiol.01122.2001.

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Heat acclimation upregulates 72-kDa heat shock protein (HSP72) and predisposes to faster activation of the heat shock response (HSR). This study investigates the role played by β-adrenergic signaling and/or plasma thyroxine level in eliciting these features by using rats undergoing 1) heat acclimation (AC; 34°C, 2 and 30 days); 2) AC with β-adrenergic blockade; 3) AC-maintained euthyroid; 4) hypothyroid; 5) hyperthyroid; and 6) controls. The hsp72 mRNA (RT-PCR) and HSP72 levels (Western blot) were measured before and after heat stress (2 h, 41°C, rectal temperature monitored). β-Adrenergic blo

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Hemmings, Susan J., and Kenneth B. Storey. "Alterations in hepatic adrenergic receptor status in Rana sylvatica in response to freezing and thawing: implications to the freeze-induced glycemic response." Canadian Journal of Physiology and Pharmacology 72, no. 12 (1994): 1552–60. http://dx.doi.org/10.1139/y94-223.

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In Rana sylvatica, freeze-induced liberation of glucose from hepatic glycogen stores plays a critical role in conferring freeze tolerance. To determine whether an alteration in hepatic adrenergic receptor status, which dictates catecholamine-directed hepatic glycogenolytic responses, is involved in the glycemic response to freezing, hepatic α1 α2, and β2 adrenergic receptors and calcium transport were characterized by radioligand and radioisotopic techniques, respectively, in plasma membranes isolated from the livers of control, −2.5 °C-exposed, and frozen–thawed frogs. The three adrenergic re

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Masterson, Caleb, Scott McClintick, and Paul Durham. "Abstract #1151: Nociceptive Signalling in Medullary Thyroid Carcinoma." Endocrine Practice 22 (May 2016): 276. http://dx.doi.org/10.1016/s1530-891x(20)44796-2.

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Daza, Francisco J., Roberto Parrilla та Angeles Martín-Requero. "Influence of thyroid status on hepatic α1-adrenoreceptor responsiveness". American Journal of Physiology-Endocrinology and Metabolism 273, № 6 (1997): E1065—E1072. http://dx.doi.org/10.1152/ajpendo.1997.273.6.e1065.

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The present work aimed to elucidate the influence of thyroid functional status on the α1-adrenoreceptor-induced activation of hepatic metabolic functions. The experiments were performed in either a nonrecirculating liver perfusion system featuring continuous monitoring of portal pressure,[Formula: see text], pCa, and pH, or isolated hepatocytes from euthyroid, hyperthyroid, and hypothyroid rats. Hypothyroidism decreased the α1-adrenergic stimulation of respiration, glycogen breakdown, and gluconeogenesis. These effects were accompanied by a decreased intracellular Ca2+ mobilization corroborati

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Sheikh, Abid Ali, Mudassir Jan Makhdoomi, Abid Hussain Rather, Tasleem Arif Lone, and Nisar Ahmad Syed. "Papillary thyroid cancer and its gene polymorphism; A molecular mechanistic perspective." Indian Journal of Pharmacy and Pharmacology 11, no. 1 (2024): 3–9. http://dx.doi.org/10.18231/j.ijpp.2024.002.

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Thyroid cancer stands as the predominant malignancy within the endocrine system, comprising about 1% of newly identified cancer instances. Papillary Thyroid Cancer (PTC) is the predominant form of thyroid cancer, representing 80% or more of thyroid malignancies. Thyroid carcinoma harbours assorted genetic alterations which are highly prevalent, several of these characteristics are unique to this form of cancer. The conventional oncogenic genetic modifications frequently observed in thyroid carcinoma encompass RAS mutations RET/PTC rearrangements and PAX8-peroxisome proliferator-activated recep

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Mughal, Bilal B., Jean-Baptiste Fini, and Barbara A. Demeneix. "Thyroid-disrupting chemicals and brain development: an update." Endocrine Connections 7, no. 4 (2018): R160—R186. http://dx.doi.org/10.1530/ec-18-0029.

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This review covers recent findings on the main categories of thyroid hormone–disrupting chemicals and their effects on brain development. We draw mostly on epidemiological and experimental data published in the last decade. For each chemical class considered, we deal with not only the thyroid hormone–disrupting effects but also briefly mention the main mechanisms by which the same chemicals could modify estrogen and/or androgen signalling, thereby exacerbating adverse effects on endocrine-dependent developmental programmes. Further, we emphasize recent data showing how maternal thyroid hormone

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Schöfl, C., A. Sanchez-Bueno, G. Brabant, P. H. Cobbold, and K. S. R. Cuthbertson. "Frequency and amplitude enhancement of calcium transients by cyclic AMP in hepatocytes." Biochemical Journal 273, no. 3 (1991): 799–802. http://dx.doi.org/10.1042/bj2730799.

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Interactions between signalling pathways such as the cyclic AMP and the Ca2+/phosphatidylinositol pathway may occur and be of major relevance in the regulation of cell function. We demonstrate here that cyclic-AMP-dependent mechanisms cause a marked increase in frequency and peak free Ca2+ of alpha 1-receptor-induced Ca2+ transients in single hepatocytes and lower the threshold for alpha 1-receptor agonists. Adrenaline at low physiological concentrations generates alpha 1-receptor-induced Ca2+ transients, which requires activation of the beta 2-receptor signalling pathway. We conclude that an

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Samita, Kundu, Roy Sumedha, Biswas Angshuman, and K. Ray Arun. "Evaluating the role of Adrenergic compounds on Synaptosomal Na+-K+-ATPase and Ca2+/Mg2+-ATPase during Central Thyroid Hormone Homeostasis." International Journal of Life Sciences Research 10, no. 2 (2022): 33–40. https://doi.org/10.5281/zenodo.6598548.

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<strong>Abstract:</strong> Hypothyroidism is associated with significant symptoms and an adverse effect on the quality of life. There exists a central homeostatic mechanism in the adult mammalian brain to defer these adverse neuropsychological manifestations, for some days. Thyroid hormone is known to affect the activities of some enzymes involved in neurotransmission. In this study, a reflection of the physiological consequences of ‘central thyroid hormone homeostasis’ has been addressed with the study of the activities of the synaptosomal membrane Na+-K+-ATPase and Ca2+/Mg2+-ATPa

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Balligand, Jean-Luc. "Phosphatase regulatory subunits in beta-adrenergic signalling: a delicate balancing act." Cardiovascular Research 115, no. 3 (2018): 477–78. http://dx.doi.org/10.1093/cvr/cvy275.

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Zhang, Jin, Christopher J. Hupfeld, Susan S. Taylor, Jerrold M. Olefsky та Roger Y. Tsien. "Insulin disrupts β-adrenergic signalling to protein kinase A in adipocytes". Nature 437, № 7058 (2005): 569–73. http://dx.doi.org/10.1038/nature04140.

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