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1. Targeted and selective knockout of the TLQP-21 neuropeptide unmasks its unique role in energy homeostasis

Author

Sahu, Bhavani S., Razzoli, Maria, McGonigle, Seth, Pallais, Jean Pierre, Nguyen, Megin E., Sadahiro, Masato, Jiang, Cheng, Lin, Wei-Jye, Kelley, Kevin A., Rodriguez, Pedro, Mansk, Rachel, Cero, Cheryl, Caviola, Giada, Palanza, Paola, Rao, Loredana, Beetch, Megan, Alejandro, Emilyn, Sham, Yuk Y., Frontini, Andrea, Salton, Stephen R., and Bartolomucci, Alessandro

Published
2023
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10. Contributors

Author

Anderson, Sean T., primary, Anderson, Olivia S., additional, Balcerczyk, Aneta, additional, Beacon, Tasnim H., additional, Beetch, Megan, additional, Biesiekierska, Marta, additional, Caporossi, Daniela, additional, Chapman, Christopher G., additional, Crew, Rachael C., additional, Davie, James R., additional, Dimauro, Ivan, additional, DiTacchio, Luciano, additional, Evans, Levi, additional, Ferguson, Bradley S., additional, Greenwood-Van Meerveld, Beverley, additional, Gupta, Subash C., additional, Harandi-Zadeh, Sadaf, additional, Ibay, Iara Cassandra V., additional, Isabelli, Allison, additional, Jahan, Sanzida, additional, Jawaid, Ali, additional, Johnson, Anthony C., additional, Lane, Robert H., additional, Lee, Ho-Sun, additional, Li, Jiao, additional, Louwies, Tijs, additional, Majnik, Amber V., additional, Mansuy, Isabelle M., additional, Mark, Peter J., additional, Martinez-Guryn, Kristina, additional, Mihaylova, Maria M., additional, Needham, Belinda L., additional, Odenwald, Matthew A., additional, Orock, Albert, additional, Osman, Fadumo D.S., additional, Paronetto, Maria Paola, additional, Paschos, Georgios K., additional, Peng, Yong, additional, Pirola, Luciano, additional, Poteres, Elesa, additional, Rai, Vipin, additional, Rehkopf, David H., additional, Ribarič, Samo, additional, Romanick, Samantha, additional, Sant, Karilyn E., additional, Segar, Jeffrey L., additional, Sepehri, Zahra, additional, Shen, Kate, additional, Shinmura, Ken, additional, Shukla, Kamla Kant, additional, Stefanska, Barbara, additional, Stratton, Matthew S., additional, van Steenwyk, Gretchen, additional, Verma, Sumit S., additional, Vialichka, Varvara, additional, Waddell, Brendan J., additional, Xu, Xiangru, additional, Yan, Menghong, additional, Yuan, Tian, additional, Zahnow, Cynthia A., additional, Zhou, Tong, additional, and Zhu, Lei, additional

Published
2019
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12. Targeted and selective knockout of the TLQP-21 neuropeptide unmasks its unique role in energy homeostasis

Author

Sahu, Bhavani, primary, Razzoli, Maria, additional, McGonigle, Seth, additional, Pallais, Jean P, additional, Nguyen, Megin, additional, Sadahiro, Masato, additional, Jiang, Cheng, additional, Lin, Wei-Jye, additional, Kelley, Kevin, additional, Rodriguez, Pedro, additional, Mansk, Rachel, additional, Cero, Cheryl, additional, Caviola, Giada, additional, Palanza, Paola, additional, Rao, Loredana, additional, Beetch, Megan, additional, Alejandro, Emilyn, additional, Sham, Yuk, additional, Frontini, Andrea, additional, Salton, Stephen, additional, and Bartolomucci, Alessandro, additional

Published
2023
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14. List of Contributors

Author

Aggarwal, Neha, primary, Araki, Yasuto, additional, Aref-Eshghi, Erfan, additional, Arima, Takahiro, additional, Bai, Yunfeng, additional, Barani, Bahar, additional, Beetch, Megan, additional, Blake, Georgina E.T., additional, Burdge, Graham C., additional, Carere, Deanna Alexis, additional, Chang, Pearl, additional, Chen, Pao-Yang, additional, Colón-Caraballo, Mariano, additional, Coppedè, Fabio, additional, Dawn, Buddhadeb, additional, Dugué, Pierre-Antoine, additional, El-Heis, Sarah, additional, Fernandez, Eliana Portilla, additional, Flores-Caldera, Idhaliz, additional, Franco, Oscar H., additional, Fuso, Andrea, additional, Ghanbari, Mohsen, additional, Ghosh, Asish K., additional, Gluckman, Peter D., additional, Godfrey, Keith M., additional, Gohain, Moloya, additional, Gray, Steven G., additional, Hanson, Mark A., additional, Hattori, Hiromitsu, additional, Hedrich, Christian M., additional, Hiura, Hitoshi, additional, Hopper, John L., additional, Hosseini, Amir, additional, Hoyo, Cathrine, additional, Hsu, Fei-Man, additional, Karmaus, Wilfried, additional, Kobayashi, Norio, additional, Kocerha, Jannet, additional, Koliada, Alexander K., additional, Larijani, Leila, additional, Lelièvre, Sophie A., additional, Li, Shuai, additional, Lillycrop, Karen A., additional, Lu, Jui-Hsien, additional, Lubecka, Katarzyna, additional, Lushchak, Oleh V., additional, Maekawa, Masato, additional, Mahnke, Amanda H., additional, Mastrototaro, Giuseppina, additional, Milne, Roger L., additional, Mimura, Toshihide, additional, Minarovits, Janos, additional, Minucci, Saverio, additional, Miranda, Rajesh C., additional, Mohan, Vasavi, additional, Muka, Taulant, additional, Mukherjee, Nandini, additional, Mutirangura, Apiwat, additional, Nano, Jana, additional, Nguyen, Khue Vu, additional, Niller, Hans Helmut, additional, Okae, Hiroaki, additional, Park, Sarah S., additional, Pruksananonda, Kamthorn, additional, Rajasingh, Sheeja, additional, Rajasingh, Johnson, additional, Rakoczy, Joanna, additional, Rancourt, Derrick E., additional, Rodenhiser, David I., additional, Sadikovic, Bekim, additional, Saldanha, Sabita N., additional, Salem, Nihal A., additional, Samanta, Saheli, additional, Schenkel, Laila C., additional, Sessa, Alessandro, additional, Skaar, David A., additional, Sorrow, Patricia, additional, Stefanska, Barbara, additional, Takahashi, Souta, additional, Thumoju, Sravya, additional, Tollefsbol, Trygve O., additional, Troup, Jenna, additional, Tseng, Alexander M., additional, Vaiserman, Alexander M., additional, Vaughan, Douglas E., additional, Wang, Sumei, additional, Wang, Ruilan, additional, Wasinarom, Artisa, additional, Watanabe, Yoshihisa, additional, Watson, Erica D., additional, Wu, Wanyin, additional, Zhou, Zhigang, additional, and Ziyab, Ali H., additional

Published
2018
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18. Epigenetic aberrations of gene expression in a rat model of hepatocellular carcinoma

Author

Boycott, Cayla, primary, Beetch, Megan, additional, Yang, Tony, additional, Lubecka, Katarzyna, additional, Ma, Yuexi, additional, Zhang, Jiaxi, additional, Kurzava Kendall, Lucinda, additional, Ullmer, Melissa, additional, Ramsey, Benjamin S., additional, Torregrosa-Allen, Sandra, additional, Elzey, Bennett D., additional, Cox, Abigail, additional, Lanman, Nadia Atallah, additional, Hui, Alisa, additional, Villanueva, Nathaniel, additional, de Conti, Aline, additional, Huan, Tao, additional, Pogribny, Igor, additional, and Stefanska, Barbara, additional

Published
2022
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22. Pterostilbene Changes Epigenetic Marks at Enhancer Regions of Oncogenes in Breast Cancer Cells

Author

Harandi-Zadeh, Sadaf, primary, Boycott, Cayla, additional, Beetch, Megan, additional, Yang, Tony, additional, Martin, Benjamin J. E., additional, Ren, Kevin, additional, Kwasniak, Anna, additional, Dupuis, John H., additional, Lubecka, Katarzyna, additional, Yada, Rickey Y., additional, Howe, LeAnn J., additional, and Stefanska, Barbara, additional

Published
2021
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23. Placental mTOR complex 1 regulates fetal programming of obesity and insulin resistance in mice

Author

Akhaphong, Brian, primary, Baumann, Daniel C., additional, Beetch, Megan, additional, Lockridge, Amber D., additional, Jo, Seokwon, additional, Wong, Alicia, additional, Zemanovic, Tate, additional, Mohan, Ramkumar, additional, Fondevilla, Danica L., additional, Sia, Michelle, additional, Pineda-Cortel, Maria Ruth B., additional, and Alejandro, Emilyn U., additional

Published
2021
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26. DNA hypermethylation of Kiss1rpromoter and reduction of hepatic Kiss1r in female rats with type 2 diabetes

Author

Ziarniak, Kamil, Yang, Tony, Boycott, Cayla, Beetch, Megan, Sassek, Maciej, Grzeda, Emilia, Ma, Yuexi, Sliwowska, Joanna H., and Stefanska, Barbara

Abstract

ABSTRACTKisspeptin, produced from the brain and peripheral tissues, may constitute an important link in metabolic regulation in response to external cues, such as diet. The kisspeptin system is well described in the brain. However, its function and regulation in the peripheral tissues, especially in relation to metabolic disease and sex differences, remain to be elucidated. As Kiss1and Kiss1r, encoding for kisspeptin and kisspeptin receptors, respectively, are altered by overnutrition/fasting and regulated by DNA methylation during puberty and cancer, epigenetic mechanisms in metabolic disorders are highly probable. In the present study, we experimentally induced type 2 diabetes mellitus (DM2) in female Wistar rats using high-fat diet/streptozocin. We analysed expression and DNA methylation of Kiss1and Kiss1rin the peripheral tissues, using quantitative-reverse-transcription PCR (qRT-PCR) and pyrosequencing. We discovered differential expression of Kiss1and Kiss1rin peripheral organs in DM2 females, as compared with healthy controls, and the profile differed from patterns reported earlier in males. DM2 in females was linked to the increased Kiss1mRNA in the liver and increased Kiss1rmRNA in the liver and adipose tissue. However, Kiss1rpromoter was hypermethylated in the liver, suggesting gene silencing. Indeed, the increase in DNA methylation of Kiss1rpromoter was accompanied by a reduction in Kiss1r protein, implying epigenetic or translational gene repression. Our results deliver novel evidence for tissue-specific differences in Kiss1and Kiss1rexpression in peripheral organs in DM2 females and suggest DNA methylation as a player in regulation of the hepatic kisspeptin system in DM2.

Published
2022
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27. Epigenetic mechanisms of anti-cancer effects of dietary stilbenoids

Author

Beetch, Megan

Abstract

Epigenetics refers to control of gene expression without changes to the underlying DNA sequence. DNA methylation, a dynamic epigenetic modification responsive to environmental factors, underlies genomic instability, silencing of tumor suppressor genes (TSGs), and activation of genes driving cancer development. Reversing DNA methylation patterns established during carcinogenesis constitutes a promising anti-cancer strategy. Interestingly, certain dietary polyphenols, such as stilbenoids abundantly found in grapes and blueberries, have been shown to exert anti-cancer effects through epigenetic gene regulation. The overarching objective of my research is to understand epigenetic mechanisms of stilbenoids’ anti-cancer effects. We hypothesize that dietary stilbenoids, resveratrol (RSV) and pterostilbene (PTS), modulate DNA methylation patterns and thereby gene transcription via modifying expression and activity of epigenetic enzymes such as DNA methyltransferases (DNMTs) and transcriptional machinery such as transcription factors (TFs). Stilbenoid-induced changes in DNA methylation and transcriptional machinery could, in turn, lead to reactivation of methylation-silenced TSGs and downregulation of epigenetically-activated oncogenes leading to reduced cancer development. Upon treatment with RSV (15 μM, 9 days), DNA methylation levels in MCF10CA1a breast cancer cells were altered as assessed by genome-wide DNA methylation analysis. Hypermethylated CpG sites corresponded to genes predominantly associated with oncogenic functions, whereas hypomethylated sites were located in genes with potential tumor suppressor roles. Changes in methylation and expression of candidate oncogenes and TSGs were examined using pyrosequencing and qPCR, respectively, upon treatment with RSV or PTS. Further, chromatin immunoprecipitation (ChIP) sequencing assessed DNA binding events, including occupancy of DNMTs and TFs at stilbenoid-mediated differentially methylated sites. Specific putative roles for de novo DNMTs in mediating changes in DNA methylation patterns upon exposure to stilbenoids were established. Based on our findings in cell lines, we turned to an in vivo model of methyl donor deficiency to assess the contribution of methyl donors, another important factor for maintaining normal DNA methylation patterns, to carcinogenesis. Collectively, these findings provide evidence that dietary stilbenoids may exert their anti-cancer effects, at least partially, by impacting DNA methylation machinery, and as a result, this line of evidence has potential to be used to develop novel anti-cancer approaches.

Published
2020
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32. Dietary antioxidants remodel DNA methylation patterns in chronic disease.

Author

Beetch, Megan, Harandi‐Zadeh, Sadaf, Shen, Kate, Lubecka, Katarzyna, Kitts, David D., O'Hagan, Heather M., Stefanska, Barbara, and Harandi-Zadeh, Sadaf

Subjects
*DNA methylation, *CHROMATIN-remodeling complexes, *CHRONIC diseases, *GENE regulatory networks, *ANTIOXIDANTS, *ENZYME regulation, *ANTHOCYANINS
Abstract

Chronic diseases account for over 60% of all deaths worldwide according to the World Health Organization reports. Majority of cases are triggered by environmental exposures that lead to aberrant changes in the epigenome, specifically, the DNA methylation patterns. These changes result in altered expression of gene networks and activity of signalling pathways. Dietary antioxidants, including catechins, flavonoids, anthocyanins, stilbenes and carotenoids, demonstrate benefits in the prevention and/or support of therapy in chronic diseases. This review provides a comprehensive discussion of potential epigenetic mechanisms of antioxidant compounds in reversing altered patterns of DNA methylation in chronic disease. Antioxidants remodel the DNA methylation patterns through multiple mechanisms, including regulation of epigenetic enzymes and chromatin remodelling complexes. These effects can further contribute to antioxidant properties of the compounds. On the other hand, decrease in oxidative stress itself can impact DNA methylation delivering additional link between antioxidant mechanisms and epigenetic effects of the compounds. LINKED ARTICLES: This article is part of a themed section on The Pharmacology of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.6/issuetoc. [ABSTRACT FROM AUTHOR]

Published
2020
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35. Loci-specific differences in blood DNA methylation in HBV-negative populations at risk for hepatocellular carcinoma development

Author

Lubecka, Katarzyna, primary, Flower, Kirsty, additional, Beetch, Megan, additional, Qiu, Jay, additional, Kurzava, Lucinda, additional, Buvala, Hannah, additional, Ruhayel, Adam, additional, Gawrieh, Samer, additional, Liangpunsakul, Suthat, additional, Gonzalez, Tracy, additional, McCabe, George, additional, Chalasani, Naga, additional, Flanagan, James M, additional, and Stefanska, Barbara, additional

Published
2018
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40. Targeted and selective knockout of the TLQP-21 neuropeptide unmasks its unique role in energy homeostasis.

Author

Sahu BS, Razzoli M, McGonigle S, Pallais JP, Nguyen ME, Sadahiro M, Jiang C, Lin WJ, Kelley KA, Rodriguez P, Mansk R, Cero C, Caviola G, Palanza P, Rao L, Beetch M, Alejandro E, Sham YY, Frontini A, Salton SR, and Bartolomucci A

Abstract

Pro-peptide precursors are processed into biologically active peptide hormones or neurotransmitters, each playing an essential role in physiology and disease. Genetic loss of function of a pro-peptide precursor results in the simultaneous ablation of all biologically-active peptides within that precursor, often leading to a composite phenotype that can be difficult to align with the loss of specific peptide components. Due to this biological constraint and technical limitations, mice carrying the selective ablation of individual peptides encoded by pro-peptide precursor genes, while leaving the other peptides unaffected, have remained largely unaddressed. Here, we developed and characterized a mouse model carrying the selective knockout of the TLQP-21 neuropeptide (ΔTLQP-21) encoded by the Vgf gene. To achieve this goal, we used a knowledge-based approach by mutating a codon in the Vgf sequence leading to the substitution of the C-terminal Arginine of TLQP-21, which is the pharmacophore as well as an essential cleavage site from its precursor, into Alanine (R 21 →A). We provide several independent validations of this mouse, including a novel in-gel digestion targeted mass spectrometry identification of the unnatural mutant sequence, exclusive to the mutant mouse. ΔTLQP-21 mice do not manifest gross behavioral and metabolic abnormalities and reproduce well, yet they have a unique metabolic phenotype characterized by a temperature-dependent resistance to diet-induced obesity and activation of the brown adipose tissue.

Published
2023
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