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4. NMNAT2 is a druggable target to drive neuronal NAD production

Author

Tribble, James R., Jöe, Melissa, Varricchio, Carmine, Otmani, Amin, Canovai, Alessio, Habchi, Baninia, Daskalakis, Evangelia, Chaleckis, Romanas, Loreto, Andrea, Gilley, Jonathan, Wheelock, Craig E., Jóhannesson, Gauti, Wong, Raymond C. B., Coleman, Michael P., Brancale, Andrea, and Williams, Pete A.

Published
2024
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5. Hypoxia-mediated repression of pyruvate carboxylase drives immunosuppression

Author

Coleman, Michael F., Cotul, Eylem Kulkoyluoglu, Pfeil, Alexander J., Devericks, Emily N., Safdar, Muhammad H., Monteiro, Marvis, Chen, Hao, Ho, Alyssa N., Attaar, Numair, Malian, Hannah M., Kiesel, Violet A., Ramos, Alexis, Smith, Matthew, Panchal, Heena, Mailloux, Adam, Teegarden, Dorothy, Hursting, Stephen D., and Wendt, Michael K.

Published
2024
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12. Robust Brain Correlates of Cognitive Performance in Psychosis and Its Prodrome

Author

Ward, Heather Burrell, Beermann, Adam, Xie, Jing, Yildiz, Gulcan, Felix, Karlos Manzanarez, Addington, Jean, Bearden, Carrie E., Cadenhead, Kristin, Cannon, Tyrone D., Cornblatt, Barbara, Keshavan, Matcheri, Mathalon, Daniel, Perkins, Diana O., Seidman, Larry, Stone, William S., Tsuang, Ming T., Walker, Elaine F., Woods, Scott, Coleman, Michael J., Bouix, Sylvain, Holt, Daphne J., Öngür, Dost, Breier, Alan, Shenton, Martha E., Heckers, Stephan, Halko, Mark A., Lewandowski, Kathryn E., and Brady, Roscoe O., Jr.

Published
2025
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16. AuNPs with Cynara scolymus leaf extracts rescue arsenic-induced neurobehavioral deficits and hippocampal tissue toxicity in Balb/c mice through D1R and D2R activation

Author

Cicek, Betul, Hacimuftuoglu, Ahmet, Yeni, Yesim, Kuzucu, Mehmet, Genc, Sidika, Cetin, Ahmet, Yavuz, Emre, Danısman, Betul, Levent, Akin, Ozdokur, Kemal Volkan, Kantarcı, Mecit, Docea, Anca Oana, Siokas, Vasileios, Tsarouhas, Konstantinos, Coleman, Michael D., Tsatsakis, Aristidis, and Taghizadehghalehjoughi, Ali

Published
2024
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22. Associations between near end-of-life flortaucipir PET and postmortem CTE-related tau neuropathology in six former American football players

Author

Alosco, Michael L., Su, Yi, Stein, Thor D., Protas, Hillary, Cherry, Jonathan D., Adler, Charles H., Balcer, Laura J., Bernick, Charles, Pulukuri, Surya Vamsi, Abdolmohammadi, Bobak, Coleman, Michael J., Palmisano, Joseph N., Tripodis, Yorghos, Mez, Jesse, Rabinovici, Gil D., Marek, Kenneth L., Beach, Thomas G., Johnson, Keith A., Huber, Bertrand Russell, Koerte, Inga, Lin, Alexander P., Bouix, Sylvain, Cummings, Jeffrey L., Shenton, Martha E., Reiman, Eric M., McKee, Ann C., and Stern, Robert A.

Published
2023
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26. Cell type-specific manifestations of cortical thickness heterogeneity in schizophrenia

Author

Di Biase, Maria A., Geaghan, Michael P., Reay, William R., Seidlitz, Jakob, Weickert, Cynthia Shannon, Pébay, Alice, Green, Melissa J., Quidé, Yann, Atkins, Joshua R., Coleman, Michael J., Bouix, Sylvain, Knyazhanskaya, Evdokiya E., Lyall, Amanda E., Pasternak, Ofer, Kubicki, Marek, Rathi, Yogesh, Visco, Andrew, Gaunnac, Megan, Lv, Jinglei, Mesholam-Gately, Raquelle I., Lewandowski, Kathryn E., Holt, Daphne J., Keshavan, Matcheri S., Pantelis, Christos, Öngür, Dost, Breier, Alan, Cairns, Murray J., Shenton, Martha E., and Zalesky, Andrew

Published
2022
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27. Brain morphometry in former American football players: findings from the DIAGNOSE CTE research project.

Author

Arciniega, Hector, Baucom, Zachary H, Tuz-Zahra, Fatima, Tripodis, Yorghos, John, Omar, Carrington, Holly, Kim, Nicholas, Knyazhanskaya, Evdokiya E, Jung, Leonard B, Breedlove, Katherine, Wiegand, Tim L T, Daneshvar, Daniel H, Rushmore, R Jarrett, Billah, Tashrif, Pasternak, Ofer, Coleman, Michael J, Adler, Charles H, Bernick, Charles, Balcer, Laura J, and Alosco, Michael L

Subjects
CHRONIC traumatic encephalopathy, FOOTBALL, HEAD injuries, SYMPTOMS, MAGNETIC resonance imaging
Abstract

Exposure to repetitive head impacts in contact sports is associated with neurodegenerative disorders including chronic traumatic encephalopathy (CTE), which currently can be diagnosed only at post-mortem. American football players are at higher risk of developing CTE given their exposure to repetitive head impacts. One promising approach for diagnosing CTE in vivo is to explore known neuropathological abnormalities at post-mortem in living individuals using structural MRI. MRI brain morphometry was evaluated in 170 male former American football players ages 45–74 years (n = 114 professional; n = 56 college) and 54 same-age unexposed asymptomatic male controls (n = 54, age range 45–74). Cortical thickness and volume of regions of interest were selected based on established CTE pathology findings and were assessed using FreeSurfer. Group differences and interactions with age and exposure factors were evaluated using a generalized least squares model. A separate logistic regression and independent multinomial model were performed to predict each traumatic encephalopathy syndrome (TES) diagnosis, core clinical features and provisional level of certainty for CTE pathology using brain regions of interest. Former college and professional American football players (combined) showed significant cortical thickness and/or volume reductions compared to unexposed asymptomatic controls in the hippocampus, amygdala, entorhinal cortex, parahippocampal gyrus, insula, temporal pole and superior frontal gyrus. Post hoc analyses identified group-level differences between former professional players and unexposed asymptomatic controls in the hippocampus, amygdala, entorhinal cortex, parahippocampal gyrus, insula and superior frontal gyrus. Former college players showed significant volume reductions in the hippocampus, amygdala and superior frontal gyrus compared to the unexposed asymptomatic controls. We did not observe Age × Group interactions for brain morphometric measures. Interactions between morphometry and exposure measures were limited to a single significant positive association between the age of first exposure to organized tackle football and right insular volume. We found no significant relationship between brain morphometric measures and the TES diagnosis core clinical features and provisional level of certainty for CTE pathology outcomes. These findings suggested that MRI morphometrics detect abnormalities in individuals with a history of repetitive head impact exposure that resemble the anatomic distribution of pathological findings from post-mortem CTE studies. The lack of findings associating MRI measures with exposure metrics (except for one significant relationship) or TES diagnosis and core clinical features suggested that brain morphometry must be complemented by other types of measures to characterize individuals with repetitive head impacts. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Aggravating mechanisms from COVID-19.

Author

Lee, Jong Hoon, Sergi, Consolato, Kast, Richard E., Kanwar, Badar A., Bourbeau, Jean, Oh, Sangsuk, Sohn, Mun-Gi, Lee, Chul Joong, and Coleman, Michael D.

Subjects
SARS-CoV-2, RETROVIRUS diseases, CYTOTOXIC T cells, VIRUS diseases, ACUTE kidney failure
Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. The pathophysiology of COVID-19 uses the following three mechanisms: (1) inflammasome activation mechanism; (2) cGAS–STING signaling mechanism; and (3) SAMHD1 tetramerization mechanism, which leads to IFN-I production. Interactions between the host and virus govern induction, resulting in multiorgan impacts. The NLRP3 with cGAS–STING constitutes the primary immune response. The expression of SARS-CoV-2 ORF3a, NSP6, NSP7, and NSP8 blocks innate immune activation and facilitates virus replication by targeting the RIG-I/MDA5, TRIF, and cGAS–STING signaling. SAMHD1 has a target motif for CDK1 to protect virion assembly, threonine 592 to modulate a catalytically active tetramer, and antiviral IFN responses to block retroviral infection. Plastic and allosteric nucleic acid binding of SAMHD1 modulates the antiretroviral activity of SAMHD1. Therefore, inflammasome activation, cGAS–STING signaling, and SAMHD1 tetramerization explain acute kidney injury, hepatic, cardiac, neurological, and gastrointestinal injury of COVID-19. It might be necessary to effectively block the pathological courses of diverse diseases. Highlights: 1. DNA-driven immune response connects with NLRP3 and controls its inflammasome activity, which leads to IFN-I production via STING. The NLRP3 with cGAS-STING constitutes the primary immune response. 2. The expression of SARS-CoV-2 ORF3a, NSP6, NSP7, and NSP8 blocks innate immune activation and facilitates virus replication by targeting the RIG-I/MDA5, TRIF, and cGAS-STING signaling. 3. Plastic and allosteric nucleic acid binding of SAMHD1 reduces the magnitude of IFN and induction of virus-specific cytotoxic T cells. SAMHD1-deficient cells detect and activate IFN-I-mediated self ISG gene expression via cGAS–STING. 4. SAMHD1 autonomously controls viral infection through innate and adaptive immunity at the level of the infected cell. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Development and Characterization of Syngeneic Orthotopic Transplant Models of Obesity-Responsive Triple-Negative Breast Cancer in C57BL/6J Mice.

Author

Carson, Meredith S., Rädler, Patrick D., Albright, Jody, VerHague, Melissa, Rezeli, Erika T., Roth, Daniel, French, John E., Perou, Charles M., Hursting, Stephen D., and Coleman, Michael F.

Subjects
BIOLOGICAL models, IN vitro studies, TRANSPLANTATION of organs, tissues, etc., DATA analysis, T-test (Statistics), RESEARCH funding, BREAST tumors, INTERNAL thoracic artery, IMMUNE system, CELLULAR signal transduction, MANN Whitney U Test, DESCRIPTIVE statistics, CELL lines, MICE, METABOLITES, RNA, ANIMAL experimentation, GENE expression profiling, ONE-way analysis of variance, STATISTICS, ANALYSIS of variance, SURVIVAL analysis (Biometry), DATA analysis software, OBESITY, DISEASE progression, SEQUENCE analysis
Abstract

Simple Summary: Transplanting cell lines into the mammary fat pad of lean and obese mice is a powerful tool to understand how breast cancer is promoted by obesity. However, for this approach to be effective, well-characterized and appropriate cell lines are needed. Here, we have developed four readily tumorigenic claudin-low triple-negative breast cancer cell lines from tumors arising from C3-TAg transgenic C57BL6 mice (B6TAg). We employ transcriptomic analysis of in vitro and in vivo samples to delineate distinct transcriptomic signatures in each cell line. We demonstrate that tumor progression of the three most distinct cell lines was accelerated by diet-induced obesity. Taken together, our data establish these B6TAg cell lines as potentially potent tools to delineate how obesity promotes triple-negative breast cancer progression. Obesity is an established risk and progression factor for triple-negative breast cancer (TNBC), but preclinical studies to delineate the mechanisms underlying the obesity-TNBC link as well as strategies to break that link are constrained by the lack of tumor models syngeneic to obesity-prone mouse strains. C3(1)/SV40 T-antigen (C3-TAg) transgenic mice on an FVB genetic background develop tumors with molecular and pathologic features that closely resemble human TNBC, but FVB mice are resistant to diet-induced obesity (DIO). Herein, we sought to develop transplantable C3-TAg cell lines syngeneic to C57BL/6 mice, an inbred mouse strain that is sensitive to DIO. We backcrossed FVB-Tg(C3-1-TAg)cJeg/JegJ to C57BL/6 mice for ten generations, and spontaneous tumors from those mice were excised and used to generate four clonal cell lines (B6TAg1.02, B6TAg2.03, B6TAg2.10, and B6TAg2.51). We characterized the growth of the four cell lines in both lean and DIO C57BL/6J female mice and performed transcriptomic profiling. Each cell line was readily tumorigenic and had transcriptional profiles that clustered as claudin-low, yet markedly differed from each other in their rate of tumor progression and transcriptomic signatures for key metabolic, immune, and oncogenic signaling pathways. DIO accelerated tumor growth of orthotopically transplanted B6TAg1.02, B6TAg2.03, and B6TAg2.51 cells. Thus, the B6TAg cell lines described herein offer promising and diverse new models to augment the study of DIO-associated TNBC. [ABSTRACT FROM AUTHOR]

Published
2024
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47. Targeted Treatment of Individuals With Psychosis Carrying a Copy Number Variant Containing a Genomic Triplication of the Glycine Decarboxylase Gene

Author

Bodkin, J. Alexander, Coleman, Michael J., Godfrey, Laura J., Carvalho, Claudia M.B., Morgan, Charity J., Suckow, Raymond F., Anderson, Thea, Öngür, Dost, Kaufman, Marc J., Lewandowski, Kathryn E., Siegel, Arthur J., Waldstreicher, Elliot, Grochowski, Christopher M., Javitt, Daniel C., Rujescu, Dan, Hebbring, Scott, Weinshilboum, Richard, Rodriguez, Stephanie Burgos, Kirchhoff, Colette, Visscher, Timothy, Vuckovic, Alexander, Fialkowski, Allison, McCarthy, Shane, Malhotra, Dheeraj, Sebat, Jonathan, Goff, Donald C., Hudson, James I., Lupski, James R., Coyle, Joseph T., Rudolph, Uwe, and Levy, Deborah L.

Published
2019
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49. Exogenous Metabolic Modulators Improve Response to Carboplatin in Triple-Negative Breast Cancer.

Author

Ho, Alyssa N., Kiesel, Violet A., Gates, Claire E., Brosnan, Bennett H., Connelly, Scott P., Glenny, Elaine M., Cozzo, Alyssa J., Hursting, Stephen D., and Coleman, Michael Francis

Subjects
TRIPLE-negative breast cancer, SOMATOMEDIN C, CARBOPLATIN, INSULIN-like growth factor receptors, DRUG receptors, INSULIN receptors, CANCER chemotherapy
Abstract

Triple-negative breast cancer (TNBC) lacks targeted therapies, leaving cytotoxic chemotherapy as the current standard treatment. However, chemotherapy resistance remains a major clinical challenge. Increased insulin-like growth factor 1 signaling can potently blunt chemotherapy response, and lysosomal processes including the nutrient scavenging pathway autophagy can enable cancer cells to evade chemotherapy-mediated cell death. Thus, we tested whether inhibition of insulin receptor/insulin-like growth factor 1 receptor with the drug BMS-754807 and/or lysosomal disruption with hydroxychloroquine (HCQ) could sensitize TNBC cells to the chemotherapy drug carboplatin. Using in vitro studies in multiple TNBC cell lines, in concert with in vivo studies employing a murine syngeneic orthotopic transplant model of TNBC, we show that BMS-754807 and HCQ each sensitized TNBC cells and tumors to carboplatin and reveal that exogenous metabolic modulators may work synergistically with carboplatin as indicated by Bliss analysis. Additionally, we demonstrate the lack of overt in vivo toxicity with our combination regimens and, therefore, propose that metabolic targeting of TNBC may be a safe and effective strategy to increase sensitivity to chemotherapy. Thus, we conclude that the use of exogenous metabolic modulators, such as BMS-754807 or HCQ, in combination with chemotherapy warrants additional study as a strategy to improve therapeutic responses in women with TNBC. [ABSTRACT FROM AUTHOR]

Published
2024
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