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Journal articles on the topic 'Adrenergic and thyroid signalling'

Author: Grafiati

Published: 28 June 2021

Last updated: 5 February 2022

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1

Gachkar, Sogol, Sebastian Nock, Cathleen Geissler, Rebecca Oelkrug, Kornelia Johann, Julia Resch, Awahan Rahman, Anders Arner, Henriette Kirchner, and Jens Mittag. "Aortic effects of thyroid hormone in male mice." Journal of Molecular Endocrinology 62, no. 3 (April 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, we observed reduced vasoconstriction under low and high T3 concentrations, indicating an inversed U-shaped curve with maximal constrictive capacity at euthyroid conditions. We then tested for possible genomic actions of thyroid hormones on vasocontractility by treating mice for 4 days with 1 mg/L thyroxine in drinking water. The study revealed that in contrast to the non-genomic actions the aortas of these animals were hyperresponsive to the contractile stimulus, an effect not observed in endogenously hyperthyroid TRβ knockout mice. To identify targets of genomic thyroid hormone action, we analysed aortic gene expression by microarray, revealing several altered genes including the well-known thyroid hormone target gene hairless. Taken together, the findings demonstrate that thyroid hormones regulate aortic tone through genomic and non-genomic actions, although genomic actions seem to prevail in vivo. Moreover, we identified several novel thyroid hormone target genes that could provide a better understanding of the molecular changes occurring in the hyperthyroid aorta.

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2

Pantos, Constantinos, Iordanis Mourouzis, Christodoulos Xinaris, Alexandros D. Kokkinos, Konstantinos Markakis, Antonios Dimopoulos, Matthew Panagiotou, Theodosios Saranteas, Georgia Kostopanagiotou, and Dennis V. Cokkinos. "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, no. 4 (April 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 expression towards a fetal phenotype in the non-infarcted area. Cardiac hypertrophy was evident in AMI hearts after 13 weeks but not at 2 weeks. This response was associated with a differential pattern of TH changes at 2 and 13 weeks; T3 and T4 levels in plasma were not changed at 2 weeks but T3 was significantly lower and T4 remained unchanged at 13 weeks. A twofold increase in TRα1 expression was observed after 13 weeks in the non-infarcted area, P<0.05 versus sham operated, while TRα1 expression remained unchanged at 2 weeks. A 2.2-fold decrease in TRβ1 expression was found in the non-infarcted area at 13 weeks, P<0.05, while no change in TRβ1 expression was seen at 2 weeks. Parallel studies with neonatal cardiomyocytes showed that phenylephrine (PE) administration resulted in 4.5-fold increase in the expression of TRα1 and 1.6-fold decrease in TRβ1 expression versus untreated, P<0.05. In conclusion, cardiac dysfunction which occurs at late stages after AMI is associated with increased expression of TRα1 receptor and lower circulating tri-iodothyronine levels. Thus, apo-TRα1 receptor state may prevail contributing to cardiac fetal phenotype. Furthermore, down-regulation of TRβ1 also contributes to fetal phenotypic changes. α1-adrenergic signalling is, at least in part, involved in this response.

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3

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 (May 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 transition of compensated hypertrophy to heart failure. In this review different possible mechanisms responsible for decreased transcriptional regulation of the SERCA2 gene are examined, which appear to be the primary cause for decreased SERCA2 expression in heart failure. The experimental evidence suggests that several signalling pathways are involved in the downregulation of SERCA2 expression in the hypertrophic and failing cardiomyocyte. Therapeutic upregulation of SERCA2 expression using replication deficient adenoviral expression vectors, pharmacological interventions using thyroid hormone analogues, β-adrenergic receptor antagonists, and novel metabolically active compounds are currently under investigation for the treatment of uncompensated cardiac hypertrophy and heart failure.

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4

DAZA, Francisco J., Roberto PARRILLA, and 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, no. 1 (April 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 respiration and release of Ca2+ and H+, but not the glycogenolytic or gluconeogenic responses, in perfused liver. In isolated liver cells, T3 enhanced the α1-agonist-induced increase in cytosolic free Ca2+ and impeded the intracellular alkalinization. Since T3 also prevented the α1-adrenoreceptor-mediated activation of protein kinase C, its effects on pH seem to be the result of a lack of activation of the Na+/H+ exchanger. The failure of T3 to prevent the α1-adrenergic stimulation of gluconeogenesis despite the inhibition of protein kinase C activation indicates that the elevation of cytosolic free Ca2+ is a sufficient signal to elicit that response. T3 also impaired some of the angiotensin-II-mediated responses, but did not alter the effects of PMA on hepatic metabolism, indicating, therefore, that some postreceptor event is the target for T3 actions. The differential effect of T3 in enhancing the α1-adrenoreceptor-mediated increase in cytosolic free Ca2+ and preventing the activation of protein kinase C, provides a unique tool for further investigating the role of each branch of the signalling pathway in controlling the hepatic functions. Moreover, the low effective concentrations of T3 (⩽ 10 nM) in perturbing the α1-adrenoreceptor-mediated response suggests its physiological significance.

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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 (May 1, 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 cells. This led us to assume that PIA augments P2-purinergic arachidonic acid release by increasing [Ca2+]i which, in turn, activates Ca(2+)-sensitive phospholipase A2. The arachidonic acid-releasing response to PIA was, however, always considerably higher (3.1-fold increase) than the Ca2+ response (1.3-fold increase) to the adenosine derivative. In addition, arachidonic acid release induced by the [Ca2+]i increase caused by thapsigargin, an endoplasmic-reticulum Ca(2+)-ATPase inhibitor, or calcium ionophores was also potentiated by PIA without any effect on [Ca2+]i and phospholipase C activity. This action of PIA was also PTX-sensitive, but not affected by the forskolin- or cholera toxin-induced increase in the cellular cyclic AMP (cAMP), suggesting that a PTX-sensitive G-protein(s) and not cAMP mediates the PIA-induced potentiation of Ca(2+)-generated phospholipase A2 activation. Although acute phorbol ester activation of protein kinase C induced arachidonic acid release, P2-purinergic and alpha 1-adrenergic stimulation of arachidonic acid release was markedly increased by the protein kinase C down-regulation caused by the phorbol ester. This suggests a suppressive role for protein kinase C in the agonist-induced activation of arachidonic acid release. We conclude that PIA (and perhaps any of the G1-activating agonists) augments an agonist (maybe any of the Ca(2+)-mobilizing agents)-induced arachidonic acid release by activation of Ca(2+)-dependent phospholipase A2 in addition to enhancement of agonist-induced phospholipase C followed by an increase in [Ca2+]i.

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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

Kanagy, Nancy L. "α2-Adrenergic receptor signalling in hypertension." Clinical Science 109, no. 5 (October 24, 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 and vasculature. However, each differentially influences blood pressure and sympathetic transmission. Activation of α2A-ARs in cardiovascular control centres of the brain lowers blood pressure and decreases plasma noradrenaline (norepinephrine), activation of peripheral α2B-ARs causes sodium retention and vasoconstriction, whereas activation of peripheral α2C-ARs causes cold-induced vasoconstriction. In addition, non-selective agonists elicit endothelium-dependent vasodilation and presynaptic inhibition of noradrenaline release. The evidence that each of these receptor subtypes uniquely participates in cardiovascular control is discussed in this review.

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8

McMacken, Grace, and Hanns Lochmuller. "ADRENERGIC SIGNALLING AND CONGENITAL MYASTHENIC SYNDROMES." Journal of Neurology, Neurosurgery & Psychiatry 87, no. 12 (November 15, 2016): e1.77-e1. http://dx.doi.org/10.1136/jnnp-2016-315106.168.

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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 (March 2016): 238–39. http://dx.doi.org/10.1308/rcsann.2016.0097.

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10

McMacken, Grace, Sally Spendiff, Rachel Howarth, Dan Cox, Clarke Slater, Andreas Roos, Roger Whittaker, and Hanns Lochmuller. "PO167 Adrenergic signalling and congenital myasthenic syndromes." Journal of Neurology, Neurosurgery & Psychiatry 88, Suppl 1 (December 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 (September 2002): 601–14. http://dx.doi.org/10.1113/jphysiol.2002.020438.

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12

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

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13

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

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14

Joiner, Mei-ling A., Marie-France Lisé, Eunice Y. Yuen, Angel Y. F. Kam, Mingxu Zhang, Duane D. Hall, Zulfiqar A. Malik, et al. "Assembly of a β2-adrenergic receptor—GluR1 signalling complex for localized cAMP signalling." EMBO Journal 29, no. 2 (November 26, 2009): 482–95. http://dx.doi.org/10.1038/emboj.2009.344.

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15

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 (September 2016): 434–43. http://dx.doi.org/10.1016/j.circen.2016.08.011.

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16

García-Jiménez, Custodia, and Pilar Santisteban. "TSH signalling and cancer." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 5 (July 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 alterations in thyroid cancers play a role in the onset or they appear as a consequence of genetic instability during evolution, but the presence of functional TSHR is exploited in therapy. We outline the signalling network build up in the thyrocyte between TSHR/PKA and other proliferative pathways such as Wnt, PI3K and MAPK. This network’s integrity surely plays a role in the onset/evolution of thyroid cancer and needs further research. Lastly, future investigation of epigenetic events occurring at the TSHR and other loci may give better clues for molecular based therapy of undifferentiated thyroid carcinomas. Targeted demethylating agents, histone deacetylase inhibitors combined with retinoids and specific RNAis may help treatment in the future.

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17

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

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18

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

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19

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

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20

Nilsson, Ove R., and Bengt E. Karlberg. "Thyroid hormones and the adrenergic nervous system." Acta Medica Scandinavica 213, S672 (April 24, 2009): 27–32. http://dx.doi.org/10.1111/j.0954-6820.1983.tb01610.x.

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21

Wu, Yuanjun, Yu Zhao, Xiaojie Ma, Yunjuan Zhu, Jaimin Patel, and Zhongzhen Nie. "The Arf GAP AGAP2 interacts with β-arrestin2 and regulates β2-adrenergic receptor recycling and ERK activation." Biochemical Journal 452, no. 3 (May 31, 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 expression reduced plasma membrane association of β-arrestin2 upon β2-adrenergic receptor activation. AGAP2 also co-localized with internalized β2-adrenergic receptors on endosomes, and overexpression of AGAP2 slowed accumulation of β2-adrenergic receptor in the perinuclear recycling endosomes. In contrast, knockdown of AGAP2 expression prevented the recycling of the β2-adrenergic receptor back to the plasma membrane. In addition, AGAP2 formed a complex with endogenous ERK (extracellular-signal-regulated kinase) and overexpression of AGAP2 potentiated ERK phosphorylation induced by β2-adrenergic receptors. Taken together, these results support the hypothesis that AGAP2 plays a role in the signalling and recycling of β2-adrenergic receptors.

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22

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

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23

Sysa-Shah, Polina, Carlo G. Tocchetti, Manveen Gupta, Peter P. Rainer, Xiaoxu Shen, Byung-Hak Kang, Frances Belmonte, et al. "Bidirectional cross-regulation between ErbB2 and β-adrenergic signalling pathways." Cardiovascular Research 109, no. 3 (December 21, 2015): 358–73. http://dx.doi.org/10.1093/cvr/cvv274.

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24

Sato, Shoko, Naoki Sato, Raymond K. Kudej, Masami Uechi, Kuniya Asai, You-Tang Shen, Yoshihiro Ishikawa, Stephen F. Vatner, and Dorothy E. Vatner. "β-Adrenergic Receptor Signalling in Stunned Myocardium of Conscious Pigs." Journal of Molecular and Cellular Cardiology 29, no. 5 (May 1997): 1387–400. http://dx.doi.org/10.1006/jmcc.1997.0377.

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25

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 (March 1, 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 was assessed as an inverse function of the increase in plasma potassium concentration. Some animals were subjected to chemical sympathectomy, adrenalectomy, the administration of adrenergic antagonists, or the infusion of adrenergic agonists. The effects of these treatments in various combinations on ERPD in animals of differing thyroid status were determined and the following conclusions could be drawn: 1) beta 2-adrenergic influences increase ERPD; 2) alpha 1- and alpha 2-adrenergic influences decrease ERPD; 3) these influences of the sympathoadrenal system on ERPD are qualitatively independent of thyroid status, and in all three thyroid states, beta-adrenergic enhancement predominates over alpha-adrenergic inhibition; 4) thyrotoxicosis increases and hypothyroidism decreases ERPD, and these effects are qualitatively independent of the presence of sympathoadrenal activity; 5) the intrinsic effect of thyroid hormone insufficiency and increased alpha-adrenergic tone and/or responsiveness together account for the decreased ERPD observed in hypothyroid animals; and 6) the intrinsic effect of thyroid hormone excess and increased beta-adrenergic tone and/or responsiveness, as well as decreased alpha-adrenergic tone and/or responsiveness, together account for the increased ERPD found in thyrotoxic animals.

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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 (February 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 controversial. In this brief review, we consider the reasons underlying this controversy, focusing on the complexity of the adrenergic signaling cascade.

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27

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 HIF-1 expression and activity. Here, we summarise current data that highlights the potential role of both hypoxia and MAPK/PI3K-induced HIF-1 signalling in thyroid carcinoma progression, metastatic characteristics, and the potential role of HIF-1 in thyroid carcinoma response to radiotherapy. Direct or indirect targeting of HIF-1 using an MAPK or PI3K inhibitor in combination with radiotherapy may be a new potential therapeutic target to improve the therapeutic response of thyroid carcinoma to radiotherapy and reduce metastatic burden.

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28

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 (January 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 becomes an inhibitory one in the FRTL-5 cells. Neither 'soluble factors' nor contamination of other cell populations could account for the different behaviour of the primary culture and the cell line toward adrenergic regulation. The reported activation by norepinephrine of iodide efflux in FRTL-5 cells rules out the loss of specific adrenergic receptors in the FRTL-5 cells. It is proposed that the cloning of FRTL-5 cells from primary cultures causes an 'alteration' in the coupling of adrenergic receptors to the adenylate cyclase system. This alteration does not affect those mechansism of message transduction that do not involve cAMP as the signal.

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29

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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30

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 (November 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 levels in slices of Graves' disease thyroids was not inhibited, or rather increased by norepinephrine. These results indicate that, in addition to low responses to TSH, α- and β-adrenergic systems were functionally altered in thyroid tissues of patients with Graves' disease.

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31

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 (October 28, 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 abundance of thyroid hormone receptors and the thyroid hormone-responsive genes DNA methyltransferase 3a and oxytocin in the paraventricular nucleus of the hypothalamus. DNA methylation of the oxytocin promoter was assessed in relation to changes in thyroid hormone receptor binding. Repeated room temperature exposure was associated with a decrease in thyroid hormone receptor signalling measures relative to nest temperature exposure, while acute room temperature exposure was associated with an increase. Repeated room temperature exposure also increased thyroid hormone receptor binding and DNA methylation at the oxytocin promoter. These findings suggest that repeated room temperature exposure may affect DNA methylation levels as a consequence of alterations in thyroid hormone receptor signalling.

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32

Carlberg, Carsten. "Mechanisms of Nuclear Signalling by Vitamin D3. Interplay with Retinoid and Thyroid Hormone Signalling." European Journal of Biochemistry 231, no. 3 (August 1995): 517–27. http://dx.doi.org/10.1111/j.1432-1033.1995.tb20727.x.

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Iacovelli, Luisa, Luisa Di Menna, Daniel Peterlik, Christina Stangl, Rosamaria Orlando, Gemma Molinaro, Antonio De Blasi, et al. "Type-7 metabotropic glutamate receptors negatively regulate α1-adrenergic receptor signalling." Neuropharmacology 113 (February 2017): 343–53. http://dx.doi.org/10.1016/j.neuropharm.2016.10.018.

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Balligand, Jean-Luc. "Phosphatase regulatory subunits in beta-adrenergic signalling: a delicate balancing act." Cardiovascular Research 115, no. 3 (December 5, 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, and Roger Y. Tsien. "Insulin disrupts β-adrenergic signalling to protein kinase A in adipocytes." Nature 437, no. 7058 (September 2005): 569–73. http://dx.doi.org/10.1038/nature04140.

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Pavoine, Catherine, and Nicole Defer. "The cardiac β2-adrenergic signalling a new role for the cPLA2." Cellular Signalling 17, no. 2 (February 2005): 141–52. http://dx.doi.org/10.1016/j.cellsig.2004.09.001.

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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 (January 7, 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 this classic mechanism characterised a new model of thyroid hormone action, the non-classic mechanism that involves other signalling pathways. To date, this mechanism and its relevance have been intensively described. Considering the increasing evidence for non-classic signalling of thyroid hormones and the major influence of these hormones in the regulation of lipid metabolism, we reviewed the role of thyroid hormone in cytosolic signalling cascades, focusing on the regulation of second messengers, and the activity of effector proteins and the implication of these mechanisms on the control of hepatic lipid metabolism.

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Yang, Hua-Qian, Peng Zhou, Li-Peng Wang, Yan-Ting Zhao, Yu-Jie Ren, Yun-Bo Guo, Ming Xu, and Shi-Qiang Wang. "Compartmentalized β1-adrenergic signalling synchronizes excitation–contraction coupling without modulating individual Ca2+ sparks in healthy and hypertrophied cardiomyocytes." Cardiovascular Research 116, no. 13 (February 7, 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 compartmentalized β1AR signalling regulates cardiac E-C coupling. Methods and results By combining confocal Ca2+ imaging and patch-clamp techniques, we investigated the effects of compartmentalized βAR signalling on E-C coupling at both cellular and molecular levels. We found that simultaneous activation of β2 and β1ARs, in contrast to global signalling of β1ARs, modulated neither the amplitude and spatiotemporal properties of Ca2+ sparks nor the kinetics of the RyR response to LCC Ca2+ sparklets. Nevertheless, by up-regulating LCC current, compartmentalized β1AR signalling synchronized RyR Ca2+ release and increased the functional reserve (stability margin) of E-C coupling. In circumstances of briefer excitation durations or lower RyR responsivity, compartmentalized βAR signalling, by increasing the intensity of Ca2+ triggers, helped stabilize the performance of E-C coupling and enhanced the Ca2+ transient amplitude in failing heart cells. Conclusion Given that compartmentalized βAR signalling can be induced by stress-associated levels of catecholamines, our results revealed an important, yet unappreciated, heart regulation mechanism that is autoadaptive to varied stress conditions.

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Hinterseher, Ulrike, Annette Wunderlich, Silvia Roth, Annette Ramaswamy, Detlef K. Bartsch, Stefan Hauptmann, Brandon H. Greene, Volker Fendrich, and Sebastian Hoffmann. "Expression of hedgehog signalling pathway in anaplastic thyroid cancer." Endocrine 45, no. 3 (July 17, 2013): 439–47. http://dx.doi.org/10.1007/s12020-013-0015-y.

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Jacquemin, C. "Glycosyl phosphatidylinositol in thyroid: cell signalling or protein anchor?" Biochimie 73, no. 1 (January 1991): 37–40. http://dx.doi.org/10.1016/0300-9084(91)90071-8.

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Geven, Edwin J. W., and Peter H. M. Klaren. "The teleost head kidney: Integrating thyroid and immune signalling." Developmental & Comparative Immunology 66 (January 2017): 73–83. http://dx.doi.org/10.1016/j.dci.2016.06.025.

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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 (January 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 dipsogenic responsiveness in the food-deprived rats to control levels. In addition, daily administration of thyroxine reduced the beta-adrenergic receptor concentration in renal cortices to that observed in controls. Thyroid treatment tended to decrease the isoproterenol-induced renin release in food-deprived rats and increase the response in the control rats. These results suggest that the relative hypothyroid state observed in the food-deprived rat may be responsible for the increased concentration of renal beta-receptors and the associated activation of the renin-angiotensin system, which may be partially responsible for the observed increased dipsogenic response induced by isoproterenol. Collectively, the data reaffirm the interaction of thyroid hormone and beta-adrenergic responsiveness, although it is of interest that, in regard to renal beta-receptors, the concentrations are decreased to normal by thyroid treatment, whereas previous studies in hypothyroid rats demonstrate an increase to normal of cardiac beta-receptors. This would suggest thyroid hormone may normalize a response in an opposite direction depending on the direction of the disturbance.

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Jönsson, Cecilia, Ana P. Castor Batista, Preben Kjølhede, and 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, no. 19 (October 11, 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-dependent pathway β-adrenergic receptor signalling, via cAMP and PI3Kα, is anti-lipolytic and inhibits its own stimulation of lipolysis by 50%. Through this pathway both insulin and β-adrenergic signalling control phosphorylation of FOXO1. The dose–response of lipolysis is bell-shaped, such that insulin is anti-lipolytic at low concentrations, but at higher concentrations of insulin lipolysis was increasingly restored due to inhibition of PDE3B. The control of lipolysis was not altered in adipocytes from diabetic individuals. However, the release of fatty acids was increased by 50% in diabetes due to reduced reesterification of lipolytically liberated fatty acids. In conclusion, our results reveal mechanisms of control by insulin and β-adrenergic stimulation — in human adipocytes — that define a network of checks and balances ensuring robust control to secure uninterrupted supply of fatty acids without reaching concentrations that put cellular integrity at risk. Moreover, our results define how selective insulin resistance leave lipolytic control by insulin unaltered in diabetes, while the fatty acid release is substantially increased.

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Maloyan, Alina, and Michal Horowitz. "β-Adrenergic signaling and thyroid hormones affect HSP72 expression during heat acclimation." Journal of Applied Physiology 93, no. 1 (July 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 blockade during AC abolished HSP72 accumulation, without disrupting HSR. Low thyroxine blunted the HSR at posttranscriptional level, whereas thyroxine administration in hyperthyroid and AC-maintained euthyroid rats arrested heat stress-evoked hsp72transcription. We conclude that β-adrenergic signaling contributes to the high HSP72 level characterizing the AC state. Thyroxine has two opposing effects: 1) direct repressive on rapid hsp72 transcription after heat stress; and 2) indirect stimulatory via β-adrenergic signaling. Low thyroxine could account for diminished HSP72 synthesis via lower heat production and thermoregulatory set point.

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Larsson, Malin, Nils Rudqvist, Johan Spetz, Emman Shubbar, Toshima Z. Parris, Britta Langen, Khalil Helou, and Eva Forssell-Aronsson. "Long-term transcriptomic and proteomic effects in Sprague Dawley rat thyroid and plasma after internal low dose 131I exposure." PLOS ONE 15, no. 12 (December 31, 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, 50 or 500 kBq 131I (Dthyroid ca 1–1000 mGy), and killed after nine months at which time the thyroid and blood samples were collected. Gene expression microarray analysis (thyroid samples) and LC-MS/MS analysis (thyroid and plasma samples) were performed to assess differential gene and protein expression profiles in treated and corresponding untreated control samples. Bioinformatics analyses were performed using the DAVID functional annotation tool and Ingenuity Pathway Analysis (IPA). The gene expression microarray data and LC-MS/MS data were validated using qRT-PCR and ELISA, respectively. Results Nine 131I exposure-related candidate biomarkers (transcripts: Afp and RT1-Bb, and proteins: ARF3, DLD, IKBKB, NONO, RAB6A, RPN2, and SLC25A5) were identified in thyroid tissue. Two dose-related protein candidate biomarkers were identified in thyroid (APRT and LDHA) and two in plasma (DSG4 and TGM3). Candidate biomarkers for thyroid function included the ACADL and SORBS2 (all activities), TPO and TG proteins (low activities). 131I exposure was shown to have a profound effect on metabolism, immune system, apoptosis and cell death. Furthermore, several signalling pathways essential for normal cellular function (actin cytoskeleton signalling, HGF signalling, NRF2-mediated oxidative stress, integrin signalling, calcium signalling) were also significantly regulated. Conclusion Exposure-related and dose-related effects on gene and protein expression generated few expression patterns useful as biomarkers for thyroid function and cancer.

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Huynh, Karina. "Novel gut microbiota-derived metabolite promotes platelet thrombosis via adrenergic receptor signalling." Nature Reviews Cardiology 17, no. 5 (March 24, 2020): 265. http://dx.doi.org/10.1038/s41569-020-0367-y.

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Najafi, Aref, Vasco Sequeira, Diederik W. D. Kuster, and Jolanda van der Velden. "β-adrenergic receptor signalling and its functional consequences in the diseased heart." European Journal of Clinical Investigation 46, no. 4 (February 19, 2016): 362–74. http://dx.doi.org/10.1111/eci.12598.

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Isidori, Andrea M., Marisa Cornacchione, Federica Barbagallo, Antonio Di Grazia, Florencia Barrios, Lorenzo Fassina, Lucia Monaco, et al. "Inhibition of type 5 phosphodiesterase counteracts β2-adrenergic signalling in beating cardiomyocytes." Cardiovascular Research 106, no. 3 (April 7, 2015): 408–20. http://dx.doi.org/10.1093/cvr/cvv123.

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Goodloe, Adele H., Jared M. Evans, Sumit Middha, Abhiram Prasad, and Timothy M. Olson. "Characterizing genetic variation of adrenergic signalling pathways in Takotsubo (stress) cardiomyopathy exomes." European Journal of Heart Failure 16, no. 9 (August 8, 2014): 942–49. http://dx.doi.org/10.1002/ejhf.145.

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Daza, Francisco J., Roberto Parrilla, and Angeles Martín-Requero. "Influence of thyroid status on hepatic α1-adrenoreceptor responsiveness." American Journal of Physiology-Endocrinology and Metabolism 273, no. 6 (December 1, 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 corroborating that those processes are regulated by the Ca2+-dependent branch of the α1-adrenoreceptor signaling pathway. Moreover, in hyperthyroid rats the α1-adrenergic-induced increase in cytosolic Ca2+ was enhanced, and glucose synthesis or mobilization was not altered. The thyroid status influenced neither the α1-adrenergic stimulation of vascular smooth muscle contraction nor the α1-agonist-induced intracellular alkalinization and protein kinase C (PKC) activation. Thus the distinct impairment of the Ca2+-dependent branch of the α1-adrenoreceptor signaling pathway by thyroid status provides a useful tool to investigate the role played by each signaling pathway, Ca2+ or PKC, in controlling hepatic functions.

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