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3. Interaction between Vitamins C and E When Scavenging the Superoxide Radical Shown by Hydrodynamic Voltammetry and DFT.

Author

Caruso, Francesco, Pedersen, Jens Z., Incerpi, Sandra, Belli, Stuart, Sakib, Raiyan, and Rossi, Miriam

Subjects
VITAMIN C, HYDRODYNAMICS, VOLTAMMETRY, VITAMIN E, DENSITY functional theory, SUPEROXIDES
Abstract

In this study, we examine the cooperative effect between vitamins C and E that mitigates oxidative stress by using experimental and computational methods. We performed superoxide scavenging experiments on each vitamin individually and their combination using rotating ring–disk electrode voltammetry. The results indicate that vitamins E and C together produce more effective scavenging of superoxide as evaluated by a steeper slope in the efficiency graph, −7.2 × 104, compared to that of vitamin E alone, −1.8 × 103, or vitamin C alone, −1.3 × 104. Density Functional Theory calculations agree with our experimental results, and we describe a mechanism for the antioxidant action of individual vitamins E and C, plus the synergistic action when both vitamins interact. This process involves the restoration of vitamin E by vitamin C and includes π-π interactions between superoxide and scavengers. The overall result produces an increase in scavenging superoxide radicals when both vitamins act together. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Nongenomic Actions of Thyroid Hormones

Author

Incerpi, Sandra, Davis, Paul J., Pedersen, Jens Z., Lanni, Antonia, Lenzi, Andrea, Series editor, Jannini, Emmanuele A., Series editor, Belfiore, Antonino, editor, and LeRoith, Derek, editor

Published
2018
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6. Nongenomic Actions of Thyroid Hormone and Intracellular Calcium Metabolism

Author

Incerpi, Sandra, Davis, Paul, De Vito, Paolo, Farias, Ricardo, Lin, Hung-Yun, and Davis, Faith

Abstract

Abstract: Nongenomic actions of thyroid hormone include several that involve or require calcium. Actions of thyroid hormone at the plasma or intracellular membranes include stimulation of membrane glucose transport and of the Na+/H+ antiporter (exchanger) by mechanisms that require liberation of intracellular calcium and stimulation of the cell membrane and sarcoplasmic reticulum calcium pumps (Ca2+-ATPases). These pumps not only transport Ca2+, but also are regulated by the intracellular calmodulin-Ca2+ complex (plasma membrane/sarcolemma) or calmodulin-dependent protein kinase II phosphorylation of phospholamban (sarcoplasmic reticulum). Intracellular calcium ion concentration may also be subject to regulation by other nongenomic effects of iodothyronines, such as those on the Na+/H+ antiporter or sodium current, that secondarily affect the Na+/Ca2+ exchanger. Certain of these nongenomic actions of thyroid hormone, e.g., Na+/H+ exchanger, Ca2+-ATPase, are now recognized to begin at a recently described hormone receptor on a heterodimeric structural membrane protein, integrin αvβ3. The thyroid hormone signal at this receptor is further transduced by the mitogen-activated protein kinase (MAPK; extracellular regulated kinase1/2, ERK1/2) pathway.

Published
2024
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9. Extranuclear effects of thyroid hormones and analogs during development: An old mechanism with emerging roles

Author

Incerpi, Sandra, primary, Gionfra, Fabio, additional, De Luca, Roberto, additional, Candelotti, Elena, additional, De Vito, Paolo, additional, Percario, Zulema A., additional, Leone, Stefano, additional, Gnocchi, Davide, additional, Rossi, Miriam, additional, Caruso, Francesco, additional, Scapin, Sergio, additional, Davis, Paul J., additional, Lin, Hung-Yun, additional, Affabris, Elisabetta, additional, and Pedersen, Jens Z., additional

Published
2022
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10. Heteronemin and tetrac derivatives suppress non-small cell lung cancer growth via ERK1/2 inhibition

Author

Chung, Cheng-Chin, primary, Huang, Tung-Yung, additional, Chu, Hung-Ru, additional, De Luca, Roberto, additional, Candelotti, Elena, additional, Huang, Chi-Hung, additional, Yang, Yu-Chen S.H., additional, Incerpi, Sandra, additional, Pedersen, Jens Z., additional, Lin, Chi-Yu, additional, Huang, Haw-Ming, additional, Lee, Sheng-Yang, additional, Li, Zi-Lin, additional, ChangOu, Chun A., additional, Li, Wen-Shan, additional, Davis, Paul J., additional, Lin, Hung-Yun, additional, Whang-Peng, Jacqueline, additional, and Wang, Kuan, additional

Published
2022
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15. Inhibition by Thyroid Hormones of Cell Migration Activated by IGF-1 and MCP-1 in THP-1 Monocytes: Focus on Signal Transduction Events Proximal to Integrin αvβ3

Author

Candelotti, Elena, primary, De Luca, Roberto, additional, Megna, Roberto, additional, Maiolo, Mariangela, additional, De Vito, Paolo, additional, Gionfra, Fabio, additional, Percario, Zulema Antonia, additional, Borgatti, Monica, additional, Gambari, Roberto, additional, Davis, Paul J., additional, Lin, Hung-Yun, additional, Polticelli, Fabio, additional, Persichini, Tiziana, additional, Colasanti, Marco, additional, Affabris, Elisabetta, additional, Pedersen, Jens Z., additional, and Incerpi, Sandra, additional

Published
2021
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16. L-Thyroxine vs. 3,5,3'-triiodo-L-thyronine and cell proliferation: activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase

Author

Lin, Hung-Yun, Sun, Mingzeng, Tang, Heng-Yuan, Lin, Cassie, Luidens, Mary K., Mousa, Shaker A., Incerpi, Sandra, Drusano, George L., Davis, Faith B., and Davis, Paul J.

Subjects
Cell proliferation -- Genetic aspects, Cell proliferation -- Research, Protein kinases -- Physiological aspects, Protein kinases -- Research, Cellular signal transduction -- Research, Biological sciences
Abstract

3,5,3'-Triiodo-L-thyronine ([T.sub.3]), but not L-thyroxine ([T.sub.4]), activated Src kinase and, downstream, phosphatidylinositol 3-kinase (PI3-kinase) by means of an [[alpha].sub.v][[beta].sub.3] integrin receptor on human glioblastoma U-87 MG cells. Although both [T.sub.3] and [T.sub.4] stimulated extracellular signal-regulated kinase (ERK) 1/2, activated ERK1/2 did not contribute to [T.sub.3]-induced Src kinase or PI3-kinase activation, and an inhibitor of PI3-kinase, LY-294002, did not block activation of ERK1/2 by physiological concentrations of [T.sub.3] and [T.sub.4]. Thus the PI3-kinase, Src kinase, and ERK1/2 signaling cascades are parallel pathways in [T.sub.3]-treated U-87 MG cells. [T.sub.3] and [T.sub.4] both caused proliferation of U-87 MG cells; these effects were blocked by the ERK1/2 inhibitor PD-98059 but not by LY-294002. Small-interfering RNA knockdown of PI3-kinase confirmed that PI3-kinase was not involved in the proliferative action of [T.sub.3] on U-87 MG cells. PI3-kinase-dependent actions of [T.sub.3] in these cells included shuttling of nuclear thyroid hormone receptor-[alpha] (TR[alpha]) from cytoplasm to nucleus and accumulation of hypoxia-inducible factor (HIF)-1[alpha] mRNA; LY-294002 inhibited these actions. Results of studies involving [[alpha].sub.v][[beta].sub.3] receptor antagonists tetraiodothyroacetic acid (tetrac) and Arg-Gly-Asp (RGD) peptide, together with mathematical modeling of the kinetics of displacement of radiolabeled [T.sub.3] from the integrin by unlabeled [T.sub.3] and by unlabeled [T.sub.4], are consistent with the presence of two iodothyronine receptor domains on the integrin. A model proposes that one site binds [T.sub.3] exclusively, activates PI3-kinase via Src kinase, and stimulates TR[alpha] trafficking and HIF-1[alpha] gene expression. Tetrac and RGD peptide both inhibit [T.sub.3] action at this site. The second site binds [T.sub.4] and [T.sub.3], and, via this receptor, the iodothyronines stimulate ERKl/2-dependent tumor cell proliferation. [T.sub.3] action here is inhibited by tetrac alone, but the effect of [T.sub.4] is blocked by both tetrac and the RGD peptide. thyroid hormone; phosphatidylinositol 3-kinase; extracellular signal-regulated kinase 1/2; integrin [[alpha].sub.v][[beta].sub.3]; glioblastoma cells; Src kinase; mitogen-activated protein kinase; intracellular hormone receptor trafficking

Published
2009

17. Short-term effects of thyroid hormones on [Na.sup.+]-[K.sup.+]-ATPase activity of chick embryo hepatocytes during development: focus on signal transduction

Author

Scapin, Sergio, Leoni, Silvia, Spagnuolo, Silvana, Fiore, Anna Maria, and Incerpi, Sandra

Subjects
Thyroid hormones -- Physiological aspects, Adenosine triphosphatase -- Physiological aspects, Cellular signal transduction -- Research, Embryonic development -- Research, Biological sciences
Abstract

Nongenomic effects of thyroid hormones on [Na.sup.+]-[K.sup.+]-ATPase activity were studied in chick embryo hepatocytes at two different developmental stages, 14 and 19 days of embryonal age, and the signal transduction pathways involved were characterized. Our data showed the following. 1) 3,5,3'-Triiodo-L-thyronine ([T.sub.3]) and 3,5-diiodo-L-thyronine (3,5-[T.sub.2]) rapidly induced a transient inhibitory effect on the [Na.sup.+]-[K.sup.+]-ATPase; the extent and duration depended on the developmental age of the cells. 2) 3,5-[T.sub.2] behaved as a true hormone and fully mimicked the effect of [T.sub.3]. 3) Thyroxine had no effect at any of the developmental stages. 4) The inhibition of [Na.sup.+]-[K.sup.+]-ATPase was mediated by activation of protein kinase A, protein kinase C, and phosphoinositide 3-kinase, suggesting several modes of modulation of ATPase activity through phosphorylation at different sites. 5) The MAPK pathway did not seem to be involved in the early phase of hormone treatment. 6) The nonpermeant analog [T.sub.3]-agarose inhibited [Na.sup.+]-[K.sup.+]-ATPase activity in the same way as [T.sub.3], confirming that hormone signaling initiated at a receptor on the plasma membrane. From these results, it can be concluded that the cell response mechanisms change rapidly and drastically within the early phase of embryo growth. The differences found at the two stages probably reflect the different roles of thyroid hormones during development and differentiation. 3,5-diiodothyronine; 3,5,3'-triiodothyronine; protein kinase A; protein kinase C; phosphoinositide 3-kinase

Published
2009

19. Thyroid Hormones Interaction With Immune Response, Inflammation and Non-thyroidal Illness Syndrome

Author

De Luca, Roberto, primary, Davis, Paul J., additional, Lin, Hung-Yun, additional, Gionfra, Fabio, additional, Percario, Zulema A., additional, Affabris, Elisabetta, additional, Pedersen, Jens Z., additional, Marchese, Cinzia, additional, Trivedi, Pankaj, additional, Anastasiadou, Eleni, additional, Negro, Roberto, additional, and Incerpi, Sandra, additional

Published
2021
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20. Antioxidant and Biological Activities of Hydroxytyrosol and Homovanillic Alcohol Obtained from Olive Mill Wastewaters of Extra-Virgin Olive Oil Production

Author

Ricelli, Alessandra, primary, Gionfra, Fabio, additional, Percario, Zulema, additional, De Angelis, Martina, additional, Primitivo, Ludovica, additional, Bonfantini, Veronica, additional, Antonioletti, Roberto, additional, Bullitta, Simonetta Maria, additional, Saso, Luciano, additional, Incerpi, Sandra, additional, and Pedersen, Jens Zacho, additional

Published
2020
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24. Combined Treatment of Heteronemin and Tetrac Induces Antiproliferation in Oral Cancer Cells

Author

Huang, Chi-Hung, primary, Huang, Tung-Yung, additional, Chang, Wong-Jin, additional, Pan, Yi-shin, additional, Chu, Hung-Ru, additional, Li, Zi-Lin, additional, Unson, Sukanya, additional, Chin, Yu-Tang, additional, Lin, Chi-Yu, additional, Huang, Haw-Ming, additional, Hsiung, Chao-Nan, additional, Gionfra, Fabio, additional, De Vito, Paolo, additional, Pedersen, Jens Z., additional, Incerpi, Sandra, additional, Chen, Yi-Ru, additional, Lee, Sheng-Yang, additional, Lin, Hung-Yun, additional, Davis, Paul J., additional, Whang-Peng, Jacqueline, additional, and Wang, Kuan, additional

Published
2020
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25. Antioxidant Properties of Embelin in Cell Culture. Electrochemistry and Theoretical Mechanism of Scavenging. Potential Scavenging of Superoxide Radical through the Cell Membrane

Author

Caruso, Francesco, primary, Rossi, Miriam, additional, Kaur, Sarjit, additional, Garcia-Villar, Emmanuel, additional, Molasky, Nora, additional, Belli, Stuart, additional, Sitek, Joanna D., additional, Gionfra, Fabio, additional, Pedersen, Jens Z., additional, and Incerpi, Sandra, additional

Published
2020
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39. Corrigendum: Tetrac and NDAT Induce Anti-proliferation via Integrin αvβ3 in Colorectal Cancers With Different K-RAS Status

Author

Chin, Yu-Tang, primary, He, Zong-Rong, additional, Chen, Chi-Long, additional, Chu, Hsiao-Ching, additional, Ho, Yih, additional, Su, Po-Yu, additional, Yang, Yu-Chen S. H., additional, Wang, Kuan, additional, Shih, Ya-Jung, additional, Chen, Yi-Ru, additional, Pedersen, Jens Z., additional, Incerpi, Sandra, additional, Nana, André Wendindondé, additional, Tang, Heng-Yuan, additional, Lin, Hung-Yun, additional, Mousa, Shaker A., additional, Davis, Paul J., additional, and Whang-Peng, Jacqueline, additional

Published
2019
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40. Tetrac and NDAT Induce Anti-proliferation via Integrin αvβ3 in Colorectal Cancers With Different K-RAS Status

Author

Chin, Yu-Tang, primary, He, Zong-Rong, additional, Chen, Chi-Long, additional, Chu, Hsiao-Ching, additional, Ho, Yih, additional, Su, Po-Yu, additional, Yang, Yu-Chen S. H., additional, Wang, Kuan, additional, Shih, Ya-Jung, additional, Chen, Yi-Ru, additional, Pedersen, Jens Z., additional, Incerpi, Sandra, additional, Nana, André Wendindondé, additional, Tang, Heng-Yuan, additional, Lin, Hung-Yun, additional, Mousa, Shaker A., additional, Davis, Paul J., additional, and Whang-Peng, Jacqueline, additional

Published
2019
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42. Thyroid Hormones. From Molecular Signaling to Human Disease: An Update

Author

INCERPI, Sandra and Incerpi, Sandra

Abstract

This Thematic Issue presents reviews of recent studies on effects of thyroid hormones and certain metabolites that are linked to human diseases, providing a general update of the topic. I have been the guest editor for thematic issues of IEMAMC for three times, in 2006, 2011 and 2015, and over these 10 years my knowledge of the nongenomic effects of thyroid hormone has improved considerably. First issue was dedicated to the nongenomic effects of various hormones endowed with classical nuclear receptors, and included a chronology of the earliest reported nongenomic effects of thyroid hormones. Second issue was centered on thyroid hormone nongenomic mechanisms in skeletal muscle and nerve cells, mainly, but not exclusively, dealing with effects mediated by integrin alphaVbeta3. In the current issue, the coverage of thyroid hormone actions is wider, including also nuclear classical effects, the cognitive processes and effects of some hormone metabolites that are particularly interesting from pharmacological point of view. Why? When a new surprising discovery is published, such as the seminal paper by Bergh et al., in 2005, showing that the integrin alphaVbeta3 was the long-searched plasma membrane receptor for thyroid hormones, it can of course dominate the scenery for years, and other researchers in this field will use this new piece of information in their studies to understand the physio-pathological effects of thyroid hormones. The Bergh et al. paper showed that binding by thyroxine to the integrin alphaVbeta3 gives rise to a downstream signaling that causes MAPK activation and tumor cell proliferation. This has so to say been the ‘Big Bang’ of nongenomic effects of thyroid hormones. After ten years of the integrin story, we can now observe how many things have changed in our knowledge about the role of thyroid hormones in animal physiology. However, actually the integrin story began before alphaVbeta3 was recognized as a plasma membrane thyroid hormone receptor. The group of Davis and Davis showed, in 2004, that various effects of thyroid hormone on the actions of epidermal growth factor and transforming growth factor-alpha were mediated by cAMP-dependent protein kinase II. The crosstalk between thyroid hormones and growth factors reported in that paper would eventually lead to the integrin; alphaVbeta3 was ‘in nuce’ although it was not clear at that time. Now, this interaction of thyroid hormones with growth factors is coming of age and may lead us far, to different and still unknown aspects of physiology and pathology, as it can be observed from some of the contributions in this issue.

Published
2015

43. Receptor Proteins for Nongenomic Actions of Thyroid Hormone

Author

Davis, PJ, Leonard, JL, Lin, HY, Luidens, MK, Tang, HY, Mousa, SA, INCERPI, Sandra, Davis, Pj, Leonard, Jl, Lin, Hy, Incerpi, Sandra, Luidens, Mk, Tang, Hy, and Mousa, Sa

Abstract

Genomic actions of thyroid hormone require the intranuclear binding by nuclear thyroid hormone receptors (TRs) of 3,5,3’-triiodo-L-thyronine (T3). Nongenomic actions of the hormone have been described that are initiated at the plasma membrane, in cytoplasm or in the mitochondrion. These are complex processes associated with maintenance of the cytoskeleton, control of cell respiration, cell proliferation—including tumor cell proliferation and angiogenesis—and nervous system function. We briefly review here the nature of the proteins which are now appreciated to initiate nongenomic actions of the hormone when they bind T3 or L-thyroxine (T4). These receptor proteins for nongenomic effects include truncated isoforms of TRalpha, cytoplasmic intact TRbeta, certain cytoplasmic enzymes and a structural protein of the plasma membrane, integrin alphaVbeta3.

Published
2015

44. Thyroid hormones crosstalk with growth factors: old facts and new hypotheses

Author

CANDELOTTI, ELENA, INCERPI, Sandra, De Vito, P, Ahmed, RG, Luly, P, Davis, PJ, Pedersen, JZ, Candelotti, Elena, De Vito, P, Ahmed, Rg, Luly, P, Davis, Pj, Pedersen, Jz, and Incerpi, Sandra

Abstract

Nongenomic effects of thyroid hormones typically start at the cell surface and do not primarily involve the classical nuclear receptors, but rather a plasma membrane receptor site identified about ten years ago on the integrin v3. Transduction of the thyroid hormone signal from this integrin receptor involves activation of the MAPK pathway and may lead to events such as angiogenesis or tumor cell proliferation. This review focuses on the interaction of thyroid hormones with growth factors, in fact the integrin v3 has been reported to a be a co-receptor for several growth factors such as EGF, IGF-1 and the FGF family, but also for small molecules like resveratrol. Binding of the ligand to integrin v3 is inhibited by tetrac, a metabolite of L-thyroxine, and by its nanoparticulate formulation nanotetrac. Recent microarray studies on tumor cells have shown that tetrac has antiinflammatory effects that are mediated by integrin v3, and tetrac can downregulate the expression of several interleukin genes. Crosstalk between thyroid hormones and vascular growth factors is important for cell migration, vascular calcification and the angiogenic process. Thyroid hormones also show pleiotropic effects on osteoblast function and differentiation, as well as in early pregnancy. The importance of thyroid hormone interaction with neurotrophins and interleukins has also been examined. With integrin v3 firmly established as the plasma membrane receptor future studies will focus on the crosstalk between thyroid hormones and growth factors in order to verify the efficiency of new pharmacological tools, such as nanotetrac.

Published
2015

46. Tetrac downregulates β-catenin and HMGA2 to promote the effect of resveratrol in colon cancer

Author

Nana, André Wendindondé, primary, Chin, Yu-Tang, additional, Lin, Chi-Yu, additional, Ho, Yih, additional, Bennett, James A, additional, Shih, Ya-Jung, additional, Chen, Yi-Ru, additional, Changou, Chun A, additional, Pedersen, Jens Z, additional, Incerpi, Sandra, additional, Liu, Leroy F, additional, Whang-Peng, Jacqueline, additional, Fu, Earl, additional, Li, Wen-Shan, additional, Mousa, Shaker A, additional, Lin, Hung-Yun, additional, and Davis, Paul J, additional

Published
2018
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49. Protection by extra virgin olive oil against oxidative stress in vitro and in vivo. Chemical and biological studies on the health benefits due to a major component of the Mediterranean diet

Author

Rossi, Miriam, primary, Caruso, Francesco, additional, Kwok, Lorraine, additional, Lee, Grace, additional, Caruso, Alessio, additional, Gionfra, Fabio, additional, Candelotti, Elena, additional, Belli, Stuart L., additional, Molasky, Nora, additional, Raley-Susman, Kathleen M., additional, Leone, Stefano, additional, Filipský, Tomáš, additional, Tofani, Daniela, additional, Pedersen, Jens, additional, and Incerpi, Sandra, additional

Published
2017
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50. Thyroid hormone inhibition in L6 myoblasts of IGF-1-mediated glucose uptake and proliferation: new roles for integrin αvβ3

Author

INCERPI, Sandra, CANDELOTTI, ELENA, LEONE, STEFANO, Hsieh, M. T, Lin, H. Y, Cheng, G. Y, De Vito, P, Fiore, A. M, Ahmed, Rg, Salvia, R, Luly, P, Pedersen, Jz, Davis FB, B., Davis, Pj, Incerpi, Sandra, Hsieh, M. T, Lin, H. Y, Cheng, G. Y, De Vito, P, Fiore, A. M, Ahmed, Rg, Salvia, R, Candelotti, Elena, Leone, Stefano, Luly, P, Pedersen, Jz, Davis FB, B., and Davis, Pj

Subjects
integrin alphavbeta3, Insulin -like growth factor -1, thyroid hormone
Abstract

Thyroid hormones L-thyroxine (T4) and 3,5,3’-triiodo-L-thyronine (T3) have been shown to initiate short- and long-term effects via a plasma membrane receptor site located on integrin vβ3. Also insulin-like growth factor-1 (IGF-1) activity is known to be subject to regulation by this integrin. To investigate the possible cross-talk between T4 and IGF-1 in rat L6 myoblasts, we have examined integrin αvβ3-mediated modulatory actions of T4 on glucose uptake, measured through carrier-mediated 2-deoxy-[3H]-D-glucose uptake, and on cell proliferation stimulated by IGF-1, assessed by cell counting, [3H]-thymidine incorporation and FACS analysis. IGF-1 stimulated glucose transport and cell proliferation via the cell surface IGF-1 receptor (IGF1R) and, downstream of the receptor, by the phosphatidylinositol 3-kinase signal transduction pathway. Addition of 0.1 nM free T4 caused little or no cell proliferation, but prevented both glucose uptake and proliferative actions of IGF1. These actions of T4 were mediated by an Arg-Gly-Asp (RGD)-sensitive pathway, suggesting the existence of crosstalk between IGF1R and the T4 receptor located near the RGD recognition site on the integrin. An RGD-sequence-containing integrin inhibitor, a monoclonal antibody to v3, and the T4 metabolite tetraiodothyroacetic acid all blocked the inhibition by T4 of IGF-1-stimulated glucose uptake and cell proliferation. Western blotting confirmed roles for activated phosphatidylinositol 3-kinase and extracellular regulated kinase 1/2 (ERK1/2) in the effects of IGF-1, and also showed a role for ERK1/2 in the actions of T4 that modified the effects of IGF-1. We conclude that thyroid hormone inhibits IGF-1-stimulated glucose uptake and cell proliferation in L6 myoblasts.

Published
2014

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