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7 results on '"Gregg E, Homanics"'

1. Inter- and transgenerational heritability of preconception chronic stress or alcohol exposure: Translational outcomes in brain and behavior

Author

Rachel C. Rice, Daniela V. Gil, Annalisa M. Baratta, Remy R. Frawley, Shirley Y. Hill, Sean P. Farris, and Gregg E. Homanics

Subjects
Intergenerational, Transgenerational, Epigenetics, Inheritance, Stress, Alcohol, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurology. Diseases of the nervous system, RC346-429, Neurophysiology and neuropsychology, QP351-495
Abstract

Chronic stress and alcohol (ethanol) use are highly interrelated and can change an individual’s behavior through molecular adaptations that do not change the DNA sequence, but instead change gene expression. A recent wealth of research has found that these nongenomic changes can be transmitted across generations, which could partially account for the “missing heritability” observed in genome-wide association studies of alcohol use disorder and other stress-related neuropsychiatric disorders. In this review, we summarize the molecular and behavioral outcomes of nongenomic inheritance of chronic stress and ethanol exposure and the germline mechanisms that could give rise to this heritability. In doing so, we outline the need for further research to: (1) Investigate individual germline mechanisms of paternal, maternal, and biparental nongenomic chronic stress- and ethanol-related inheritance; (2) Synthesize and dissect cross-generational chronic stress and ethanol exposure; (3) Determine cross-generational molecular outcomes of preconception ethanol exposure that contribute to alcohol-related disease risk, using cancer as an example. A detailed understanding of the cross-generational nongenomic effects of stress and/or ethanol will yield novel insight into the impact of ancestral perturbations on disease risk across generations and uncover actionable targets to improve human health.

Published
2024
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2. Murine model of triosephosphate isomerase deficiency with anemia and severe neuromuscular dysfunction

Author

Tracey D. Myers, Carolyn Ferguson, Eric Gliniak, Gregg E. Homanics, and Michael J. Palladino

Subjects
Triosephosphate isomerase (TPI), TPI Deficiency, CRISPR, Genetics, Glycolysis, Metabolism, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Triosephosphate isomerase deficiency (TPI Df) is a rare, aggressive genetic disease that typically affects young children and currently has no established treatment. TPI Df is characterized by hemolytic anemia, progressive neuromuscular degeneration, and a markedly reduced lifespan. The disease has predominately been studied using invertebrate and in vitro models, which lack key aspects of the human disease. While other groups have generated mammalian Tpi1 mutant strains, specifically with the mouse mus musculus, these do not recapitulate key characteristic phenotypes of the human disease. Reported here is the generation of a novel murine model of TPI Df. CRISPR-Cas9 was utilized to engineer the most common human disease-causing mutation, Tpi1E105D, and Tpi1null mice were also isolated as a frame-shifting deletion. Tpi1E105D/null mice experience a markedly shortened lifespan, postural abnormalities consistent with extensive neuromuscular dysfunction, hemolytic anemia, pathological changes in spleen, and decreased body weight. There is a ∼95% reduction in TPI protein levels in Tpi1E105D/null animals compared to wild-type littermates, consistent with decreased TPI protein stability, a known cause of TPI Df. This work illustrates the capability of Tpi1E105D/null mice to serve as a mammalian model of human TPI Df. This work will allow for advancement in the study of TPI Df within a model with physiology similar to humans. The development of the model reported here will enable mechanistic studies of disease pathogenesis and, importantly, efficacy testing in a mammalian system for emerging TPI Df treatments.

Published
2022
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3. Deletion of Ptp4a3 reduces clonogenicity and tumor-initiation ability of colitis-associated cancer cells in mice

Author

Julie M. Cramer, Mark W. Zimmerman, Tim Thompson, Gregg E. Homanics, John S. Lazo, and Eric Lagasse

Subjects
Biology (General), QH301-705.5
Abstract

The PTP4A3 gene is highly expressed in human colon cancer and often associates with enhanced metastatic potential. Genetic disruption of the mouse Ptp4a3 gene reduces the frequency of colon tumor formation in mice treated in a colitis-associated cancer model. In the current study, we have examined the role of Ptp4a3 in the tumor-initiating cell population of mouse colon tumors using an in vitro culture system. Tumors generated in vivo following AOM/DSS treatment were isolated, dissociated, and expanded on a feeder layer resulting in a CD133+ cell population, which expressed high levels of Ptp4a3. Tumor cells deficient for Ptp4a3 exhibited reduced clonogenicity and growth potential relative to WT cells as determined by limiting dilution analysis. Importantly, expanded tumor cells from WT mice readily formed secondary tumors when transplanted into nude mice, while tumor cells without Ptp4a3 expression failed to form secondary tumors and thus were not tumorigenic. These results demonstrate that Ptp4a3 contributes to the malignant phenotype of tumor-initiating cells and supports its role as a potential therapeutic target to inhibit tumor self-renewal and metastasis.

Published
2014
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4. Deletion of Ptp4a3 reduces clonogenicity and tumor-initiation ability of colitis-associated cancer cells in mice

Author

Gregg E. Homanics, Julie M. Cramer, Timothy Thompson, John S. Lazo, Eric Lagasse, and Mark W. Zimmerman

Subjects
Population, Cell, Tumor initiation, Biology, Article, Immediate early protein, Immediate-Early Proteins, Metastasis, Mice, In vivo, Cancer stem cell, medicine, Animals, education, lcsh:QH301-705.5, Medicine(all), Mice, Knockout, education.field_of_study, Cell Biology, General Medicine, Colitis, medicine.disease, In vitro, 3. Good health, Disease Models, Animal, medicine.anatomical_structure, lcsh:Biology (General), Colonic Neoplasms, Immunology, Neoplastic Stem Cells, Cancer research, Protein Tyrosine Phosphatases, Developmental Biology
Abstract

The PTP4A3 gene is highly expressed in human colon cancer and often associates with enhanced metastatic potential. Genetic disruption of the mouse Ptp4a3 gene reduces the frequency of colon tumor formation in mice treated in a colitis-associated cancer model. In the current study, we have examined the role of Ptp4a3 in the tumor-initiating cell population of mouse colon tumors using an in vitro culture system. Tumors generated in vivo following AOM/DSS treatment were isolated, dissociated, and expanded on a feeder layer resulting in a CD133(+) cell population, which expressed high levels of Ptp4a3. Tumor cells deficient for Ptp4a3 exhibited reduced clonogenicity and growth potential relative to WT cells as determined by limiting dilution analysis. Importantly, expanded tumor cells from WT mice readily formed secondary tumors when transplanted into nude mice, while tumor cells without Ptp4a3 expression failed to form secondary tumors and thus were not tumorigenic. These results demonstrate that Ptp4a3 contributes to the malignant phenotype of tumor-initiating cells and supports its role as a potential therapeutic target to inhibit tumor self-renewal and metastasis.

Published
2014

5. GABAA Receptor α1 Subunit Knockout Mice: A Novel Model of Essential Tremor

Author

Tood K. O'Buckley, Jessica L. Osterman, Gregg E. Homanics, A. Leslie Morrow, and Jason E. Kralic

Subjects
Agonist, Benzodiazepine, Neuroactive steroid, Essential tremor, business.industry, medicine.drug_class, GABAA receptor, Allopregnanolone, medicine.disease, nervous system diseases, chemistry.chemical_compound, chemistry, GABAergic, Medicine, business, Kinetic tremor, Neuroscience
Abstract

Deletion of GABA A receptor α1 subunits in mice results in a phenotype of kinetic tremor that mimics certain features of essential tremor disease. The GABA A benzodiazepine receptor agonist diazepam and the GABAergic neuroactive steroid allopregnanolone exacerbate the tremor, whereas ethanol completely inhibits the tremor. Since the etiology of essential tremor is unknown, this animal model of genetic essential tremor may lead to an understanding of the pathophysiology of the disease and provide a valuable model system to develop therapeutic interventions. Although tremor is often associated with neurological conditions, such as Parkinson's disease, it is capable of manifesting itself in many other ways. Essential tremor, the most common of the tremor disorders, is a primary condition independent of any overlying disorder. Tremor is also commonly associated with substance withdrawal, and it is often a side effect of various drug treatments. The current studies investigating the ability of GABAergic drugs to modulate pathological tremor have provided direction for future experimental procedures investigating the pathology of the knockout tremor. Future studies may include drugs that mediate their actions through other sites of ethanol action. With continuing research on the mechanisms for genetic essential tremor and possible experimental treatments, a cure for essential tremor and other tremor behaviors may be realized in the near future.

Published
2005
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6. List of Contributors

Author

Tetsuo Ashizawa, P.C. Baier, Lore Becker, David J. Bennett, Brett Berke, Ranjita Betarbet, Kailash P. Bhatia, Francesco Bibbiani, David T. Blake, David R. Borchelt, Prodip Bose, D. Cristopher Bragg, Allison Brashear, Xandra O. Breakefield, Susan Bressman, Kathleen Burke, Nancy N. Byl, Guy A. Caldwell, Kim A. Caldwell, Songsong Cao, M. Angela Cenci, Marie-Françoise Chesselet, Carlo Colosimo, Mai Dang, Julie A. Dennis, Didier Devys, Paula Dietrich, Ioannis Dragatsis, Ian D'Souza, Rodger J. Elble, Craig Evinger, Pierre-Olivier Fernagut, Hubert H. Fernandez, John K. Fink, Sheila M. Fleming, Colin F. Fletcher, Lyle Fox, Stephen C. Fowler, Joseph H. Friedman, Felix Geser, Imad Ghorayeb, Monica Gorassini, J. Timothy Greenamyre, Philip J. Harvey, Simon J.R. Heales, Peter J. Healy, Dominique Helmlinger, Ellen J. Hess, Ralph Hillman, Gregg E. Homanics, Keith Hyland, Iyare Izevbaye, Vernice Jackson-Lewis, H.A. Jinnah, Anita J. Jurkowski, Iris S. Kassem, Michael D. Kaytor, Jason E. Kralic, Mark LeDoux, Jada Lewis, Yuqing Li, David Lieberman, Gary S. Linn, Irene Litvan, Paul J. Lombroso, Elan D. Louis, Martin Lundblad, J. Lawrence Marsh, Eileen McGowan, T.L. McKerchar, Michael Merzenich, A. Leslie Morrow, Robert Naquet, Richard Nass, Parvoneh Poorkaj Navas, Todd K. O'Buckley, Justin D. Oh, Chihiro Ohye, Harry T. Orr, Jessica L. Osterman, Leo J. Pallanck, Massimo Pandolfo, Robert G. Pendleton, Haixiang Peng, I-Feng Peng, Dianne M. Perez, Susan L. Perlman, Joel S. Perlmutter, Jeremy Petravicz, Ronald F. Pfeiffer, James O. Phillips, Michael R. Pranzatelli, Stefan-M. Pulst, Shirley Rainier, Jayaraman Rao, Angelika Richter, Farrel R. Robinson, Christopher A. Ross, Perminder S. Sachdev, Rachel Saunders-Pullman, Gerard D. Schellenberg, Gabriele Schilling, Peter R. Schofield, Nutan Sharma, Todd B. Sherer, Carmen Silva-Barrat, Harvey S. Singer, Richard Jay Smeyne, Constance Smith-Hicks, Mark Stacy, Nadia Stafanova, David G. Standaert, S.H. Subramony, Samer D. Tabbal, Kwok-Keung Tai, Floyd J. Thompson, Leslie M. Thompson, François Tison, Claudia Trenkwalder, Daniel D. Truong, Atsushi Ueda, Suvi Vartiainen, Hans Weiher, Avery H. Weiss, Gregor Karl Wenning, Alexander J. Whitworth, Peter A. Windsor, Garry Wong, Chun-Fang Wu, and T.J. Zarcone

Published
2005
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7. CONTRIBUTORS

Author

Ernest Abel, George Acquaah-Mensah, Junko Adachi, Giovanni Gasbarrini Addolorato, Bert Aertgeerts, Sara Ahlgren, Emanuele Albano, Katrine Albertsen, Jan Albrecht, Jeffrey W. Allen, Paul Allison, Angelo Ammendola, Carlo Ancona, Gavin E. Arteel, C.P. Arun, Michael Aschner, Angelo Avogaro, A.A.-B. Badawy, Shannon M. Bailey, A.J. Barak, John Barefoot, Nancy P. Barnett, R.G. Batey, Abraham P. Bautista, M.C. Beauvieux, Ulrik Becker, Lawerence J. Beilin, Richard L. Bell, K. Berry, A.A.E. Bertelli, Richard D. Blondell, Daniel J. Bonthius, Adrian Borges, Cleofina Bosco, Robert Boughton, Valeria Bender Braulio, Francesco Bravaccio, Jan Braun, Arthur S. Brecher, George R. Breese, P.J. Brooks, Eli Torild Hellandsjo Bu, Daniel Bunout, Stewart Campbell, Bernard Campillo, Q. Cao, Esmeralda Capristo, K.B. Carey, Carol A. Casey, Steven A. Castellon, Jose A. Castro, Gerardo Castro, Y. Çelik, Christina D. Chambers, Geoff K. Chambers, Dev Chandra, Laura W. Cheever, C.J. Cherpitel, Connie Cheung, Duncan B. Clark, Colleen Clark, Dahn L. Clemens, Joseph Conigliaro, Katherine M. Conigrave, Anastasia Constantinescu, Jocelyn L. Cook, M-A. Cornier, David B. Couch, María Isabel Covas, James A. Crampton, H.E. Criswell, Gerhard Dammann, S.T. Davidge, Darren Day, G. de Gaetano, María Pía De la Maza, A. Di Castelnuovo, Jutta Dierkes, Terrence M. Donohue, Tania Douglas, Robert Dudley, M. Duggal, D.A. Dulli, Gerlinde Egerer, John S. Ellingson, Nobuyuki Enomoto, Romon Estruch, Andrea Fabbri, Jaume Farrés, Joaquim Fernández-Solà, Alessandro Federico, David A. Fiellin, A. Fink, W.M. Freeman, Samuel W. French, Robert A. Frost, J.L. Gallis, B. Gao, Giovanni Gasbarrini, Madeleine C. Geraghty, Chris L. Gibson, Emilio Gonzàlez-Reimers, R.S. Gooch, Adam J. Gordon, Joseph-Maria Grau, M.O. Gray, Diederick E Grobbee, Morten Grønbæk, Petra Grubwieser, Michael J. Haas, Stefan L. Haas, P.S. Haber, Deborah Hasin, Henk F.J. Hendriks, Christian von Heymann, Elisabeth Higgins, Charles H. Hinkin, Sandra Hirsch, Gregg E. Homanics, Ross J. Hunter, John T.P. Hustad, Ana M. Hutton Kahrberg, Kenichi Ikejima, Ernest B. Izevbigie, Hitender Jain, Harold Kalant, Ulrik Kesmodel, Kusum K. Kharbanda, Tsuneo Kitamura, Burghard F. Klapp, Wolfgang Kox, T.F. Kresina, Anja Kroke, José María Ladero, Jason C. Lambert, Charles H. Lang, M. Laposata, Rebecca Lebeau-Craven, Andrew J. Levine, Charles S. Lieber, Carmela Loguercio, Philippe Lunetta, Giulio Marchesini, Stephen J. Marshall, Colin R. Martin, Susana E. Martìnez, William J. McBride, Ross A. McKim, Benita L. McVicker, Ernesta M. Meintjes, Jukka H. Meurman, Laura Mezzani, J. Mitchell Miller, Juan Bautista Miñana, Kenneth P. Mitton, Eckhard Mühlbauer, M. Murata, James Murphy, James M. Murphy, Tatsuo Nakahara, Amin A. Nanji, Raghu G. Nath, A.V. Nemtsov, Josep–María Nicolás, Hideyuki Nushida, P.P. Ogurtsov, Tomonori Okamura, Federico V. Pallardo, Nicholas J. Pantazis, Xavier Parés, Alexandr Parlesak, Valentino Patussi, Marion Pavlic, Camilla K. Pease, Giia-Sheun Peng, Alex R. Piquero, Kari Poikolainen, Sergio Porte, Victor Preedy, Ian B. Puddey, Matthew E. Reilly, Alexander R. Rich, Gonzalo Rivera, Z.A. Rodd, Ramón Rodrigo, H. Rommelspacher, S. Rotondo, Emilio Sacanella, Raneem O. Salem, Michael Sander, Francisco Santolaria-Fernandez, Juan Sastre, Nobuhiro Sato, Emanuele Scafato, Luisa Schiaffonati, Alexander Schneider, Marlene B. Schwartz, Helmut Seitz, S. Shourie, Aafje Sierksma, Holly Sindeler, H.C. Manfred V. Singer, Rajita Sinha, Gordon S. Smith, Offie P. Soldin, Claudia Spies, Lina Steinrud Mørch, Felix Stickel, Y. Suwa, Riitta Suuronen, Yoshiyuki Takei, Dawn L. Thatcher, Jacob A. Theruvathu, Geoffrey M. Thiele, Antonio Tiengo, Peter M. Timms, John R. Trevithick, Dean J. Tuma, Yasuhiro Ueno, Alvaro Urbano-Márquez, Julia Vaglenova, Alberto Vandelli, Judith H. Veis, Holly E. Ventura, Matteo Vidali, José Viña, K.E. Vrana, Marc Walter, Jianhua Wang, Rachel Waxman, David F. Werner, J. Westin, Simon Worrall, T.J. Worst, Shunhei Yamashina, S.J. Yin, Magdalena Zielinska, and Renate R. Zilkens

Published
2005
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