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Journal articles on the topic 'Non genomic effects'

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Author: Grafiati

Published: 10 December 2022

Last updated: 21 February 2023

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1

Verhovez, Andrea, Tracy A. Williams, Silvia Monticone, Valentina Crudo, Jacopo Burrello, Maddalena Galmozzi, Michele Covella, Franco Veglio, and Paolo Mulatero. "Genomic and Non-genomic Effects of Aldosterone." Current Signal Transduction Therapy 7, no. 2 (May 1, 2012): 132–41. http://dx.doi.org/10.2174/157436212800376708.

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Kowalik, M. K., D. Slonina, and J. Kotwica. "Genomic and non-genomic effects of progesterone and pregnenolone on the function of bovine endometrial cells." Veterinární Medicína 54, No. 5 (June 1, 2009): 205–14. http://dx.doi.org/10.17221/58/2009-vetmed.

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Progesterone (P<sub4</sub>) decreases oxytocin (OT)-stimulated prostaglandin (PG)F<sub>2α</sub>, but not PGE<sub>2</sub> secretion from bovine endometrial cells and this effect is partly elicited via a non-genomic route. The aim of this study was to determine whether P<sub>4</sub> and pregnenolone (P<sub>5</sub>), in the presence or absence of OT, influence: (a) the gene expression of enzymes responsible for PG<sub>s</sub> synthesis: cyclooxygenase-2 (COX-2), synthase of PGF<sub>2α</sub> (PGFS) and PGE=sub>2</sub> (PGES), (b) protein expression of COX-2, PGFS and PGES, and (c) P<sub>4</sub> receptor membrane component 1 (PGRMC1) gene expression in bovine endometrial cells. The epithelial endometrial cells (2.5 × 10<sup>5</sup>/ml) from Days 14–16 of the oestrous cycle were incubated for 72–96 h to attach the cells to the bottom of a well. Next, the cells were preincubated for 30 min with P<sub>4</sub> and P<sub>5</sub> (10<sup>–5</sup>M each) and incubated for 4 h and 6 h alone or with OT (10<sup>–7</sup>M). Thereafter, the medium was collected for PGE<sub>2</sub> and PGFM determination, while cells were harvested for gene and protein expression analysis. The used steroids: (a) inhibited OT-stimulated PGF<sub>2α</sub>, but not PGE<sub>2</sub> secretion from endometrial cells, (b) did not affect the expression of mRNA for COX-2, PGFS, PGES and PGRMC1 in endometrial cells after 4 and 6 h, (c) they decreased OT-stimulated COX-2 mRNA expression only after 6 h incubation, and (d) did not influence COX-2, PGFS and PGES protein expression after 6 h. These results indicate that P<sub>4</sub> and P<sub>5</sub> inhibit OT-stimulated secretion/production of luteolytic PGF<sub>2α</sub> by a transcription-independent mechanism and partly by down-regulation of COX-2 mRNA.

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Ordóñez-Morán, Paloma, and Alberto Muñoz. "Nuclear receptors: Genomic and non-genomic effects converge." Cell Cycle 8, no. 11 (June 2009): 1675–80. http://dx.doi.org/10.4161/cc.8.11.8579.

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4

Viñas, René, Yow-Jiun Jeng, and Cheryl S. Watson. "Non-Genomic Effects of Xenoestrogen Mixtures." International Journal of Environmental Research and Public Health 9, no. 8 (July 31, 2012): 2694–714. http://dx.doi.org/10.3390/ijerph9082694.

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5

Jia, Wan-Yu, and Jian-Jiang Zhang. "Effects of glucocorticoids on leukocytes: Genomic and non-genomic mechanisms." World Journal of Clinical Cases 10, no. 21 (July 26, 2022): 7187–94. http://dx.doi.org/10.12998/wjcc.v10.i21.7187.

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6

McEwen, Bruce S. "Non-genomic and genomic effects of steroids on neural activity." Trends in Pharmacological Sciences 12 (January 1991): 141–47. http://dx.doi.org/10.1016/0165-6147(91)90531-v.

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7

Weiss, Daniel J., and Erlio Gurpide. "Non-genomic effects of estrogens and antiestrogens." Journal of Steroid Biochemistry 31, no. 4 (October 1988): 671–76. http://dx.doi.org/10.1016/0022-4731(88)90017-9.

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8

SIMONCINI, T. "Genomic and non-genomic effects of estrogens on endothelial cells*1." Steroids 69, no. 8-9 (August 2004): 537–42. http://dx.doi.org/10.1016/j.steroids.2004.05.009.

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9

Lecoq, L., P. Vincent, A. Lavoie-Lamoureux, and J. P. Lavoie. "Genomic and non-genomic effects of dexamethasone on equine peripheral blood neutrophils." Veterinary Immunology and Immunopathology 128, no. 1-3 (March 2009): 126–31. http://dx.doi.org/10.1016/j.vetimm.2008.10.303.

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10

Bruscoli, Stefano, Rosa Di Virgilio, Valerio Donato, Enrico Velardi, Monia Baldoni, Cristina Marchetti, Graziella Migliorati, and Carlo Riccardi. "Genomic and non-genomic effects of different glucocorticoids on mouse thymocyte apoptosis." European Journal of Pharmacology 529, no. 1-3 (January 2006): 63–70. http://dx.doi.org/10.1016/j.ejphar.2005.10.053.

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11

Straltsova, Darya Y., Maryia A. Charnysh, Palina V. Hryvusevich, and Vadim V. Demidchik. "Non-genomic effects of steroid hormones: role of ion channels." Journal of the Belarusian State University. Biology, no. 3 (October 31, 2019): 3–12. http://dx.doi.org/10.33581/2521-1722-2019-3-3-12.

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In animals, steroid hormones can act using genomic and non-genomic mechanisms. Plant steroid hormones, brassinosteroids, are capable of inducing the expression of some gene ensembles, however their non-genomic pathways for triggering the physiological effects are still unclear. In this paper, we propose the hypothesis on existence of brassinosteroid non-genomic effects in plant cells. This non-genomic pathway could due to modulation of ion channel activities and modification of membrane receptors.

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12

Pi, Min, Abby L. Parrill, and L. Darryl Quarles. "GPRC6A Mediates the Non-genomic Effects of Steroids." Journal of Biological Chemistry 285, no. 51 (October 13, 2010): 39953–64. http://dx.doi.org/10.1074/jbc.m110.158063.

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13

Panettieri, Reynold A., Dedmer Schaafsma, Yassine Amrani, Cynthia Koziol-White, Rennolds Ostrom, and Omar Tliba. "Non-genomic Effects of Glucocorticoids: An Updated View." Trends in Pharmacological Sciences 40, no. 1 (January 2019): 38–49. http://dx.doi.org/10.1016/j.tips.2018.11.002.

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14

Stratton, Rebecca C., Charlotte Poile, and Nina M. Storey. "Non-Genomic Effects of 17beta-Estradiol on Cardiomyocytes." Biophysical Journal 100, no. 3 (February 2011): 574a. http://dx.doi.org/10.1016/j.bpj.2010.12.3322.

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15

Azuma, Kotaro, and Satoshi Inoue. "Genomic and non-genomic actions of estrogen: recent developments." BioMolecular Concepts 3, no. 4 (August 1, 2012): 365–70. http://dx.doi.org/10.1515/bmc-2012-0002.

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AbstractEstrogen affects transcriptional status by activating its corresponding nuclear receptor, the estrogen receptor (ER). It can also induce rapid cellular reactions within a few minutes, and this feature cannot be explained by the transcription-mediated effects of estrogen. The latter mechanisms are called ‘non-genomic actions’ of estrogen. In contrast, the former classic modes of action came to be called ‘genomic actions’. One of the recent developments of research on estrogen was the substantiation of the non-genomic actions of estrogen; these were initially observed and reported as intriguing phenomena more than 40 years ago. The interacting molecules as well as the biological significance of non-genomic actions have now been shown. In the field of genomic actions, invention and spread of new technologies, including high-throughput sequencers, promoted a comprehensive view of estrogen-mediated transcriptional regulation.

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Mir, Negar, Shannon A. Chin, Michael C. Riddell, and Jacqueline L. Beaudry. "Genomic and Non-Genomic Actions of Glucocorticoids on Adipose Tissue Lipid Metabolism." International Journal of Molecular Sciences 22, no. 16 (August 7, 2021): 8503. http://dx.doi.org/10.3390/ijms22168503.

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Glucocorticoids (GCs) are hormones that aid the body under stress by regulating glucose and free fatty acids. GCs maintain energy homeostasis in multiple tissues, including those in the liver and skeletal muscle, white adipose tissue (WAT), and brown adipose tissue (BAT). WAT stores energy as triglycerides, while BAT uses fatty acids for heat generation. The multiple genomic and non-genomic pathways in GC signaling vary with exposure duration, location (adipose tissue depot), and species. Genomic effects occur directly through the cytosolic GC receptor (GR), regulating the expression of proteins related to lipid metabolism, such as ATGL and HSL. Non-genomic effects act through mechanisms often independent of the cytosolic GR and happen shortly after GC exposure. Studying the effects of GCs on adipose tissue breakdown and generation (lipolysis and adipogenesis) leads to insights for treatment of adipose-related diseases, such as obesity, coronary disease, and cancer, but has led to controversy among researchers, largely due to the complexity of the process. This paper reviews the recent literature on the genomic and non-genomic effects of GCs on WAT and BAT lipolysis and proposes research to address the many gaps in knowledge related to GC activity and its effects on disease.

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17

Lucas-Herald, Angela K., Rheure Alves-Lopes, Augusto C. Montezano, S. Faisal Ahmed, and Rhian M. Touyz. "Genomic and non-genomic effects of androgens in the cardiovascular system: clinical implications." Clinical Science 131, no. 13 (June 23, 2017): 1405–18. http://dx.doi.org/10.1042/cs20170090.

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The principle steroidal androgens are testosterone and its metabolite 5α-dihydrotestosterone (DHT), which is converted from testosterone by the enzyme 5α-reductase. Through the classic pathway with androgens crossing the plasma membrane and binding to the androgen receptor (AR) or via mechanisms independent of the ligand-dependent transactivation function of nuclear receptors, testosterone induces genomic and non-genomic effects respectively. AR is widely distributed in several tissues, including vascular endothelial and smooth muscle cells. Androgens are essential for many developmental and physiological processes, especially in male reproductive tissues. It is now clear that androgens have multiple actions besides sex differentiation and sexual maturation and that many physiological systems are influenced by androgens, including regulation of cardiovascular function [nitric oxide (NO) release, Ca2+ mobilization, vascular apoptosis, hypertrophy, calcification, senescence and reactive oxygen species (ROS) generation]. This review focuses on evidence indicating that interplay between genomic and non-genomic actions of testosterone may influence cardiovascular function.

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18

Mikics, Éva, Menno R. Kruk, and József Haller. "Genomic and non-genomic effects of glucocorticoids on aggressive behavior in male rats." Psychoneuroendocrinology 29, no. 5 (June 2004): 618–35. http://dx.doi.org/10.1016/s0306-4530(03)00090-8.

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19

Kusaka, Eriko, Mayu Sugiyama, Norie Senoo, Atsuki Yamamoto, and Yukio Sugimoto. "Genomic and non-genomic effects of glucocorticoids on allergic rhinitis model in mice." International Immunopharmacology 16, no. 2 (June 2013): 279–87. http://dx.doi.org/10.1016/j.intimp.2013.03.030.

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20

Herve, J. "Non-genomic Effects of Steroid Hormones on Membrane Channels." Mini-Reviews in Medicinal Chemistry 2, no. 4 (August 1, 2002): 411–17. http://dx.doi.org/10.2174/1389557023405981.

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21

Blomberg Jensen, Martin, and Steen Dissing. "Non-genomic effects of vitamin D in human spermatozoa." Steroids 77, no. 10 (August 2012): 903–9. http://dx.doi.org/10.1016/j.steroids.2012.02.020.

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22

Wehling, Martin, and Ralf Lösel. "Non-genomic steroid hormone effects: Membrane or intracellular receptors?" Journal of Steroid Biochemistry and Molecular Biology 102, no. 1-5 (December 2006): 180–83. http://dx.doi.org/10.1016/j.jsbmb.2006.09.016.

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23

Makara, Gábor B., and József Haller. "Non-genomic effects of glucocorticoids in the neural system." Progress in Neurobiology 65, no. 4 (November 2001): 367–90. http://dx.doi.org/10.1016/s0301-0082(01)00012-0.

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24

Chun, Tae-Yon, and J. Howard Pratt. "Non-genomic effects of aldosterone: new actions and questions." Trends in Endocrinology & Metabolism 15, no. 8 (October 2004): 353–54. http://dx.doi.org/10.1016/j.tem.2004.08.002.

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25

Farhat, Michel Y., Sylvie Abi-Younes, and Peter W. Ramwell. "Non-genomic effects of estrogen and the vessel wall." Biochemical Pharmacology 51, no. 5 (March 1996): 571–76. http://dx.doi.org/10.1016/s0006-2952(95)02159-0.

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26

CHUN, T., and J. PRATT. "Non-genomic effects of aldosterone: new actions and questions." Trends in Endocrinology and Metabolism 15, no. 8 (October 2004): 353–54. http://dx.doi.org/10.1016/s1043-2760(04)00183-3.

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27

Gutiérrez, M., V. Martínez, B. Cantabrana, and A. Hidalgo. "Genomic and non-genomic effects of steroidal drugs on smooth muscle contraction in vitro." Life Sciences 55, no. 6 (January 1994): 437–43. http://dx.doi.org/10.1016/0024-3205(94)90055-8.

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28

Yadav, Seema, Xianming Wei, Priya Joyce, Felicity Atkin, Emily Deomano, Yue Sun, Loan T. Nguyen, et al. "Improved genomic prediction of clonal performance in sugarcane by exploiting non-additive genetic effects." Theoretical and Applied Genetics 134, no. 7 (April 26, 2021): 2235–52. http://dx.doi.org/10.1007/s00122-021-03822-1.

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Abstract Key message Non-additive genetic effects seem to play a substantial role in the expression of complex traits in sugarcane. Including non-additive effects in genomic prediction models significantly improves the prediction accuracy of clonal performance. Abstract In the recent decade, genetic progress has been slow in sugarcane. One reason might be that non-additive genetic effects contribute substantially to complex traits. Dense marker information provides the opportunity to exploit non-additive effects in genomic prediction. In this study, a series of genomic best linear unbiased prediction (GBLUP) models that account for additive and non-additive effects were assessed to improve the accuracy of clonal prediction. The reproducible kernel Hilbert space model, which captures non-additive genetic effects, was also tested. The models were compared using 3,006 genotyped elite clones measured for cane per hectare (TCH), commercial cane sugar (CCS), and Fibre content. Three forward prediction scenarios were considered to investigate the robustness of genomic prediction. By using a pseudo-diploid parameterization, we found significant non-additive effects that accounted for almost two-thirds of the total genetic variance for TCH. Average heterozygosity also had a major impact on TCH, indicating that directional dominance may be an important source of phenotypic variation for this trait. The extended-GBLUP model improved the prediction accuracies by at least 17% for TCH, but no improvement was observed for CCS and Fibre. Our results imply that non-additive genetic variance is important for complex traits in sugarcane, although further work is required to better understand the variance component partitioning in a highly polyploid context. Genomics-based breeding will likely benefit from exploiting non-additive genetic effects, especially in designing crossing schemes. These findings can help to improve clonal prediction, enabling a more accurate identification of variety candidates for the sugarcane industry.

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29

Moussatche, Patricia, and Thomas J. Lyons. "Non-genomic progesterone signalling and its non-canonical receptor." Biochemical Society Transactions 40, no. 1 (January 19, 2012): 200–204. http://dx.doi.org/10.1042/bst20110638.

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The steroid hormone progesterone regulates many critical aspects of vertebrate physiology. The nuclear receptor for progesterone functions as a ligand-activated transcription factor, directly regulating gene expression. This type of signalling is referred to as the ‘genomic’ pathway. Nevertheless, progesterone also stimulates rapid physiological effects that are independent of transcription. This pathway, termed ‘non-genomic’, is mediated by the mPRs (membrane progesterone receptors). These mPRs belong to a larger class of membrane receptors called PAQRs (progestin and adipoQ receptors), which include receptors for adiponectin in vertebrates and osmotin in fungi. mPRs have been shown to activate inhibitory G-proteins, suggesting that they act as GPCRs (G-protein-coupled receptors). However, PAQRs do not resemble GPCRs with respect to topology or conserved sequence motifs. Instead, they more closely resemble proteins in the alkaline ceramidase family and they may possess enzymatic activity. In the present paper, we highlight the evidence in support of each model and what is currently known for PAQR signal transduction of this non-canonical receptor.

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30

Ning, Ying-Jun, Si-Ying Chen, Xin-Jiang Lu, Jian-Fei Lu, and Jiong Chen. "Glucocorticoid receptor in ayu (Plecoglossus altivelis): Genomic and non-genomic effects on monocytes/macrophages function." Fish & Shellfish Immunology 86 (March 2019): 1151–61. http://dx.doi.org/10.1016/j.fsi.2018.12.065.

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31

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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32

Uhrenholt, T. R., J. Schjerning, L. E. Rasmussen, P. B. Hansen, R. Norregaard, B. L. Jensen, and O. Skott. "Rapid non-genomic effects of aldosterone on rodent vascular function." Acta Physiologica Scandinavica 181, no. 4 (August 2004): 415–19. http://dx.doi.org/10.1111/j.1365-201x.2004.01313.x.

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33

SCHMIDT, B. "Rapid non-genomic effects of aldosterone on the renal vasculature." Steroids 73, no. 9-10 (October 2008): 961–65. http://dx.doi.org/10.1016/j.steroids.2007.12.010.

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34

Dukhanin, A., V. Nikitin, G. Engalicheva, and P. Sergeev. "Rapid non-genomic effects of hydrocortisone on rat mast cells." Inflammation Research 45, S1 (March 1996): S15—S16. http://dx.doi.org/10.1007/bf03354067.

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35

Wehling, M., M. Christ, and R. Gerzer. "Aldosterone-specific membrane receptors and related rapid, non-genomic effects." Trends in Pharmacological Sciences 14, no. 1 (January 1993): 1–4. http://dx.doi.org/10.1016/0165-6147(93)90104-r.

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36

Simoncini, T., and AR Genazzani. "Non-genomic actions of sex steroid hormones." European Journal of Endocrinology 148, no. 3 (March 1, 2003): 281–92. http://dx.doi.org/10.1530/eje.0.1480281.

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Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.

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37

Tavares, R. S., S. Escada-Rebelo, M. Correia, P. C. Mota, and J. Ramalho-Santos. "The non-genomic effects of endocrine-disrupting chemicals on mammalian sperm." REPRODUCTION 151, no. 1 (January 2016): R1—R13. http://dx.doi.org/10.1530/rep-15-0355.

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Exposure to toxicants present in the environment, especially the so-called endocrine-disrupting chemicals (EDCs), has been associated with decreased sperm quality and increased anomalies in male reproductive organs over the past decades. Both human and animal populations are continuously exposed to ubiquitous synthetic and natural-occurring EDCs through diet, dermal contact and/or inhalation, therefore potentially compromising male reproductive health. Although the effects of EDC are likely induced via multiple genomic-based pathways, their non-genomic effects may also be relevant. Furthermore, spermatozoa are transcriptionally inactive cells that can come in direct contact with EDCs in reproductive fluids and secretions and are therefore a good model to address non-genomic effects. This review thus focuses on the non-genomic effects of several important EDCs relevant to mammalian exposure. Notably, EDCs were found to interfere with pre-existing pathways inducing a panoply of deleterious effects to sperm function that included altered intracellular Ca2+oscillations, induction of oxidative stress, mitochondrial dysfunction, increased DNA damage and decreased sperm motility and viability, among others, potentially jeopardizing male fertility. Although many studies have used non-environmentally relevant concentrations of only one compound for mechanistic studies, it is important to remember that mammals are not exposed to one, but rather to a multitude of environmental EDCs, and synergistic effects may occur. Furthermore, some effects have been detected with single compounds at environmentally relevant concentrations.

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38

Roosan, Moom R., Francisco J. Nuñez, and Rennolds S. Ostrom. "Non‐genomic glucocorticoid signaling via G αs contributes to one‐third of their canonical genomic effects." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.06371.

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39

Nappi, Annarita, Melania Murolo, Serena Sagliocchi, Caterina Miro, Annunziata Gaetana Cicatiello, Emery Di Cicco, Rossella Di Paola, et al. "Selective Inhibition of Genomic and Non-Genomic Effects of Thyroid Hormone Regulates Muscle Cell Differentiation and Metabolic Behavior." International Journal of Molecular Sciences 22, no. 13 (July 2, 2021): 7175. http://dx.doi.org/10.3390/ijms22137175.

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Thyroid hormones (THs) are key regulators of different biological processes. Their action involves genomic and non-genomic mechanisms, which together mediate the final effects of TH in target tissues. However, the proportion of the two processes and their contribution to the TH-mediated effects are still poorly understood. Skeletal muscle is a classical target tissue for TH, which regulates muscle strength and contraction, as well as energetic metabolism of myofibers. Here we address the different contribution of genomic and non-genomic action of TH in skeletal muscle cells by specifically silencing the deiodinase Dio2 or the β3-Integrin expression via CRISPR/Cas9 technology. We found that myoblast proliferation is inversely regulated by integrin signal and the D2-dependent TH activation. Similarly, inhibition of the nuclear receptor action reduced myoblast proliferation, confirming that genomic action of TH attenuates proliferative rates. Contrarily, genomic and non-genomic signals promote muscle differentiation and the regulation of the redox state. Taken together, our data reveal that integration of genomic and non-genomic signal pathways finely regulates skeletal muscle physiology. These findings not only contribute to the understanding of the mechanisms involved in TH modulation of muscle physiology but also add insight into the interplay between different mechanisms of action of TH in muscle cells.

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40

Nielsen, Jennifer L., and Scott A. Pavey. "Perspectives: Gene expression in fisheries management." Current Zoology 56, no. 1 (February 1, 2010): 157–56. http://dx.doi.org/10.1093/czoolo/56.1.157.

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Abstract Functional genes and gene expression have been connected to physiological traits linked to effective production and broodstock selection in aquaculture, selective implications of commercial fish harvest, and adaptive changes reflected in non-commercial fish populations subject to human disturbance and climate change. Gene mapping using single nucleotide polymorphisms (SNPs) to identify functional genes, gene expression (analogue microarrays and real-time PCR), and digital sequencing technologies looking at RNA transcripts present new concepts and opportunities in support of effective and sustainable fisheries. Genomic tools have been rapidly growing in aquaculture research addressing aspects of fish health, toxicology, and early development. Genomic technologies linking effects in functional genes involved in growth, maturation and life history development have been tied to selection resulting from harvest practices. Incorporating new and ever-increasing knowledge of fish genomes is opening a different perspective on local adaptation that will prove invaluable in wild fish conservation and management. Conservation of fish stocks is rapidly incorporating research on critical adaptive responses directed at the effects of human disturbance and climate change through gene expression studies. Genomic studies of fish populations can be generally grouped into three broad categories: 1) evolutionary genomics and biodiversity; 2) adaptive physiological responses to a changing environment; and 3) adaptive behavioral genomics and life history diversity. We review current genomic research in fisheries focusing on those that use microarrays to explore differences in gene expression among phenotypes and within or across populations, information that is critically important to the conservation of fish and their relationship to humans

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41

Zhao, X., D. Pfaff, and N. Vasudevan. "Estrogens and Thyroid Hormones: Non-Genomic Effects are Coupled to Transcription." Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry 6, no. 3 (June 1, 2006): 267–80. http://dx.doi.org/10.2174/187152206777435564.

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42

Donati, Simone, Gaia Palmini, Cecilia Romagnoli, Cinzia Aurilia, Francesca Miglietta, Irene Falsetti, Francesca Marini, et al. "In Vitro Non-Genomic Effects of Calcifediol on Human Preosteoblastic Cells." Nutrients 13, no. 12 (November 25, 2021): 4227. http://dx.doi.org/10.3390/nu13124227.

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Several recent studies have demonstrated that the direct precursor of vitamin D3, the calcifediol [25(OH)D3], through the binding to the nuclear vitamin D receptor (VDR), is able to regulate the expression of many genes involved in several cellular processes. Considering that itself may function as a VDR ligand, although with a lower affinity, respect than the active form of vitamin D, we have assumed that 25(OH)D3 by binding the VDR could have a vitamin’s D3 activity such as activating non-genomic pathways, and in particular we selected mesenchymal stem cells derived from human adipose tissue (hADMSCs) for the in vitro assessment of the intracellular Ca2+ mobilization in response to 25(OH)D3. Our result reveals the ability of 25(OH)D3 to activate rapid, non-genomic pathways, such as an increase of intracellular Ca2+ levels, similar to what observed with the biologically active form of vitamin D3. hADMSCs loaded with Fluo-4 AM exhibited a rapid and sustained increase in intracellular Ca2+ concentration as a result of exposure to 10−5 M of 25(OH)D3. In this work, we show for the first time the in vitro ability of 25(OH)D3 to induce a rapid increase of intracellular Ca2+ levels in hADMSCs. These findings represent an important step to better understand the non-genomic effects of vitamin D3 and its role in endocrine system.

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Unsworth, Amanda J., Gagan D. Flora, and Jonathan M. Gibbins. "Non-genomic effects of nuclear receptors: insights from the anucleate platelet." Cardiovascular Research 114, no. 5 (February 14, 2018): 645–55. http://dx.doi.org/10.1093/cvr/cvy044.

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Rauch, Cyril, and Anthony Flint. "Non-genomic steroid effects: Merging membrane fluidity and receptor-mediated responses." Veterinary Journal 176, no. 3 (June 2008): 265–66. http://dx.doi.org/10.1016/j.tvjl.2007.07.010.

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Liu, L., Y. X. Wang, J. Zhou, F. Long, H. W. Sun, Y. Liu, Y. Z. Chen, and C. L. Jiang. "Rapid non-genomic inhibitory effects of glucocorticoids on human neutrophil degranulation." Inflammation Research 54, no. 1 (January 2005): 37–41. http://dx.doi.org/10.1007/s00011-004-1320-y.

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Billing, Anja M., Dominique Revets, Céline Hoffmann, Jonathan D. Turner, Sara Vernocchi, and Claude P. Muller. "Proteomic profiling of rapid non-genomic and concomitant genomic effects of acute restraint stress on rat thymocytes." Journal of Proteomics 75, no. 7 (April 2012): 2064–79. http://dx.doi.org/10.1016/j.jprot.2012.01.008.

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Groeneweg, Femke L., Henk Karst, E. Ron de Kloet, and Marian Joëls. "Rapid non-genomic effects of corticosteroids and their role in the central stress response." Journal of Endocrinology 209, no. 2 (February 28, 2011): 153–67. http://dx.doi.org/10.1530/joe-10-0472.

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In response to a stressful encounter, the brain activates a comprehensive stress system that engages the organism in an adaptive response to the threatening situation. This stress system acts on multiple peripheral tissues and feeds back to the brain; one of its key players is the family of corticosteroid hormones. Corticosteroids affect brain functioning through both delayed, genomic and rapid, non-genomic mechanisms. The latter mode of action has long been known, but it is only in recent years that the physiological basis in the brain is beginning to be unravelled. We now know that corticosteroids exert rapid, non-genomic effects on the excitability and activation of neurons in (amongst others) the hypothalamus, hippocampus, amygdala and prefrontal cortex. In addition, corticosteroids affect cognition, adaptive behaviour and neuroendocrine output within minutes. Knowledge on the identity of the receptors and secondary pathways mediating the non-genomic effects of corticosteroids on a cellular level is accumulating. Interestingly, in many cases, an essential role for the ‘classical’ mineralocorticoid and glucocorticoid receptors in a novel membrane-associated mechanism is found. Here, we systematically review the recent literature on non-genomic actions of corticosteroids on neuronal activity and functioning in selected limbic brain targets. Further, we discuss the relevance of these permissive effects for cognition and neuroendocrine control, and the integration of this novel mode of action into the complex balanced pattern of stress effects in the brain.

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Sethuraman, Arun, Fredric J. Janzen, David W. Weisrock, and John J. Obrycki. "Insights from Population Genomics to Enhance and Sustain Biological Control of Insect Pests." Insects 11, no. 8 (July 22, 2020): 462. http://dx.doi.org/10.3390/insects11080462.

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Biological control—the use of organisms (e.g., nematodes, arthropods, bacteria, fungi, viruses) for the suppression of insect pest species—is a well-established, ecologically sound and economically profitable tactic for crop protection. This approach has served as a sustainable solution for many insect pest problems for over a century in North America. However, all pest management tactics have associated risks. Specifically, the ecological non-target effects of biological control have been examined in numerous systems. In contrast, the need to understand the short- and long-term evolutionary consequences of human-mediated manipulation of biological control organisms for importation, augmentation and conservation biological control has only recently been acknowledged. Particularly, population genomics presents exceptional opportunities to study adaptive evolution and invasiveness of pests and biological control organisms. Population genomics also provides insights into (1) long-term biological consequences of releases, (2) the ecological success and sustainability of this pest management tactic and (3) non-target effects on native species, populations and ecosystems. Recent advances in genomic sequencing technology and model-based statistical methods to analyze population-scale genomic data provide a much needed impetus for biological control programs to benefit by incorporating a consideration of evolutionary consequences. Here, we review current technology and methods in population genomics and their applications to biological control and include basic guidelines for biological control researchers for implementing genomic technology and statistical modeling.

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Chen, Zhi-Qiang, John Baison, Jin Pan, Johan Westin, Maria Rosario García Gil, and Harry X. Wu. "Increased Prediction Ability in Norway Spruce Trials Using a Marker X Environment Interaction and Non-Additive Genomic Selection Model." Journal of Heredity 110, no. 7 (October 2019): 830–43. http://dx.doi.org/10.1093/jhered/esz061.

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Abstract A genomic selection study of growth and wood quality traits is reported based on control-pollinated Norway spruce families established in 2 Northern Swedish trials at 2 locations using exome capture as a genotyping platform. Nonadditive effects including dominance and first-order epistatic interactions (including additive-by-additive, dominance-by-dominance, and additive-by-dominance) and marker-by-environment interaction (M×E) effects were dissected in genomic and phenotypic selection models. Genomic selection models partitioned additive and nonadditive genetic variances more precisely than pedigree-based models. In addition, predictive ability in GS was substantially increased by including dominance and slightly increased by including M×E effects when these effects are significant. For velocity, response to genomic selection per year increased up to 78.9/80.8%, 86.9/82.9%, and 91.3/88.2% compared with response to phenotypic selection per year when genomic selection was based on 1) main marker effects (M), 2) M + M×E effects (A), and 3) A + dominance effects (AD) for sites 1 and 2, respectively. This indicates that including M×E and dominance effects not only improves genetic parameter estimates but also when they are significant may improve the genetic gain. For tree height, Pilodyn, and modulus of elasticity (MOE), response to genomic selection per year improved up to 68.9%, 91.3%, and 92.6% compared with response to phenotypic selection per year, respectively.Subject Area: Quantitative genetics and Mendelian inheritance

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Holick, Michael F., Luciana Mazzei, Sebastián García Menéndez, Virna Margarita Martín Giménez, Fatme Al Anouti, and Walter Manucha. "Genomic or Non-Genomic? A Question about the Pleiotropic Roles of Vitamin D in Inflammatory-Based Diseases." Nutrients 15, no. 3 (February 2, 2023): 767. http://dx.doi.org/10.3390/nu15030767.

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Vitamin D (vit D) is widely known for its role in calcium metabolism and its importance for the bone system. However, various studies have revealed a myriad of extra-skeletal functions, including cell differentiation and proliferation, antibacterial, antioxidant, immunomodulatory, and anti-inflammatory properties in various cells and tissues. Vit D mediates its function via regulation of gene expression by binding to its receptor (VDR) which is expressed in almost all cells within the body. This review summarizes the pleiotropic effects of vit D, emphasizing its anti-inflammatory effect on different organ systems. It also provides a comprehensive overview of the genetic and epigenetic effects of vit D and VDR on the expression of genes pertaining to immunity and anti-inflammation. We speculate that in the context of inflammation, vit D and its receptor VDR might fulfill their roles as gene regulators through not only direct gene regulation but also through epigenetic mechanisms.

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