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5. C57BL/6J mice exposed to perfluorooctanoic acid demonstrate altered immune responses and increased seizures after Theiler's murine encephalomyelitis virus infection.

Author

Gómez, Aracely A. Pérez, Wang, Meichen, Kochan, Kelli, Amstalden, Katia, Young, Colin R., Welsh, C. Jane, Phillips, Timothy D., and Brinkmeyer-Langford, Candice L.

Subjects
PERFLUOROOCTANOIC acid, IMMUNE response, EPILEPSY, LABORATORY mice, IMMUNOREGULATION, VIRUS diseases, MYELIN oligodendrocyte glycoprotein
Abstract

Introduction: Neurological diseases can stem from environmental influences such as antecedent viral infections or exposure to potential toxicants, some of which can trigger immune responses leading to neurological symptoms. Theiler's murine encephalomyelitis virus (TMEV) is used to model human neurological conditions associated with prior viral infections, with outcomes partly attributable to improper induction and regulation of the immune response. Perfluorooctanoic acid (PFOA) can alter pathologies known to influence neurological disease such as inflammatory responses, cytokine expression, and glial activation. Co-exposure to TMEV and PFOA was used to test the hypothesis that early life exposure to the potential immunotoxicant PFOA would affect immune responses so as to render TMEV-resistant C57BL/6J (B6) mice susceptible to viral-induced neurological disease. Methods: Neonate B6 mice were exposed to different treatments: non-injected, sham-infected with PBS, and TMEV-infected, with the drinking water of each group including either 70 ppt PFOA or filtered water. The effects of PFOA were evaluated by comparing neurological symptoms and changes in immune-related cytokine and chemokine production induced by viral infection. Immune responses of 23 cytokines and chemokines were measured before and after infection to determine the effects of PFOA exposure on immune response. Results: Prior to infection, an imbalance between Th1, Th2, and Treg cytokines was observed in PFOA-exposed mice, suppressing IL-4 and IL-13 production. However, the balance was restored and characterized by an increase in proinflammatory cytokines in the non-infected group, and a decrease in IL-10 in the PFOA + TMEV group. Furthermore, the PFOA + TMEV group experienced an increase in seizure frequency and severity. Discussion: Overall, these findings provide insight into the complex roles of immune responses in the pathogenesis of virus-associated neurological diseases influenced by co-exposures to viruses and immunotoxic compounds. [ABSTRACT FROM AUTHOR]

Published
2023
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9. Genetic and immunological contributors to virus-induced paralysis

Author

Perez Gomez, Aracely A., primary, Karmakar, Moumita, additional, Carroll, Raymond J., additional, Lawley, Koedi S., additional, Amstalden, Katia, additional, Young, Colin R., additional, Threadgill, David W., additional, Welsh, C. Jane, additional, and Brinkmeyer-Langford, Candice, additional

Published
2021
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11. Host genetic diversity drives variable central nervous system lesion distribution in chronic phase of Theiler’s Murine Encephalomyelitis Virus (TMEV) infection

Author

Lawley, Koedi S., primary, Rech, Raquel R., additional, Elenwa, Faith, additional, Han, Gang, additional, Perez Gomez, Aracely A., additional, Amstalden, Katia, additional, Welsh, C. Jane, additional, Young, Colin R., additional, Threadgill, David W., additional, and Brinkmeyer-Langford, Candice L., additional

Published
2021
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12. The Genome Sequence of Taurine Cattle: A Window to Ruminant Biology and Evolution

Author

Elsik, Christine G., Tellam, Ross L., Worley, Kim C., Gibbs, Richard A., Elsik, Christine G., Tellam, Ross L, Gibbs, Richard A., Muzny, Donna M., Weinstock, George M., Adelson, David L, Eichler, Evan E., Elnitski, Laura, Elsik, Christine G., Guigó, Roderic, Hamernik, Debora L., Kappes, Steve M., Lewin, Harris A, Lynn, David J., Nicholas, Frank W., Reymond, Alexandre, Rijnkels, Monique, Skow, Loren C., Tellam, Ross L, Worley, Kim C., Zdobnov, Evgeny M., Gibbs, Richard A., Kappes, Steve M., Schook, Lawrence, Skow, Loren C., Weinstock, George M., Womack, James, Alioto, Tyler, Antonarakis, Stylianos E., Astashyn, Alex, Chapple, Charles E., Chen, Hsiu-Chuan, Chrast, Jacqueline, Câmara, Francisco, Elsik, Christine G., Ermolaeva, Olga, Guigó, Roderic, Henrichsen, Charlotte N., Hlavina, Wratko, Kapustin, Yuri, Kiryutin, Boris, Kitts, Paul, Kokocinski, Felix, Landrum, Melissa, Maglott, Donna, Pruitt, Kim, Reymond, Alexandre, Sapojnikov, Victor, Searle, Stephen M., Solovyev, Victor, Souvorov, Alexandre, Ucla, Catherine, Weinstock, George M., Wyss, Carine, Alioto, Tyler, Antonarakis, Stylianos E., Chapple, Charles E., Chrast, Jacqueline, Câmara, Francisco, Guigó, Roderic, Henrichsen, Charlotte N., Reymond, Alexandre, Ucla, Catherine, Wyss, Carine, Anzola, Juan M., Gerlach, Daniel, Zdobnov, Evgeny M., Elhaik, Eran, Elsik, Christine G., Graur, Dan, Reese, Justin T., Adelson, David L., Edgar, Robert C., McEwan, John C., Payne, Gemma M., Raison, Joy M., Junier, Thomas, Kriventseva, Evgenia V., Zdobnov, Evgeny M., Chrast, Jacqueline, Eyras, Eduardo, Henrichsen, Charlotte N., Plass, Mireya, Reymond, Alexandre, Donthu, Ravikiran, Larkin, Denis M., Lewin, Harris A., Nicholas, Frank W., Elnitski, Laura, Larkin, Denis M., Lewin, Harris A., Reecy, James, Yang, Mary Q., Adelson, David L, Chen, Lin, Cheng, Ze, Chitko-McKown, Carol G., Eichler, Evan E., Elnitski, Laura, Elsik, Christine G., Liu, George E., Matukumalli, Lakshmi K., Song, Jiuzhou, Zhu, Bin, Elsik, Christine G., Lynn, David J., Reese, Justin T., Bradley, Daniel G., Brinkman, Fiona S.L, Lau, Lilian P.L., Lynn, David J., Whiteside, Matthew D., Tellam, Ross L, Walker, Angela, Wheeler, Thomas T., Casey, Theresa, German, Bruce J., Lemay, Danielle G., Lynn, David J., Maqbool, Nauman J., Molenaar, Adrian J., Rijnkels, Monique, Lewin, Harris A., Seo, Seongwon, Stothard, Paul, Baldwin, Cynthia L., Baxter, Rebecca, Brinkmeyer-Langford, Candice L., Brown, Wendy C., Childers, Christopher P., Connelley, Timothy, Ellis, Shirley A., Fritz, Krista, Glass, Elizabeth J., Herzig, Carolyn T.A., livanainen, Antti, Lahmers, Kevin K., Skow, Loren C., Bennett, Anna K., Childers, Christopher P., Dickens, Michael C., Elsik, Christine G., Gilbert, James G.R., Hagen, Darren E., Reese, Justin T., Salih, Hanni, Aerts, Jan, Caetano, Alexandre R., Dalrymple, Brian, Elsik, Christine G., Fernando Garcia, Jose, Gibbs, Richard A., Gill, Clare A., Hamernik, Debora L, Hiendleder, Stefan G., Memili, Erdogan, Nicholas, Frank W., Reecy, James, Rijnkels, Monique, Skow, Loren C., Spurlock, Diane, Stothard, Paul, Tellam, Ross L, Weinstock, George M., Williams, John L, Worley, Kim C., Alexander, Lee, Brownstein, Michael J., Guan, Leluo, Holt, Robert A., Jones, Steven J.M., Marra, Marco A., Moore, Richard, Moore, Stephen S., Roberts, Andy, Taniguchi, Masaaki, Waterman, Richard C., Chacko, Joseph, Chandrabose, Mimi M., Cree, Andy, Diep Dao, Marvin, Dinh, Huyen H., Ayiesha Gabisi, Ramatu, Hines, Sandra, Hume, Jennifer, Jhangiani, Shalini N., Joshi, Vandita, Kovar, Christie L., Lewis, Lora R., Liu, Yih-shin, Lopez, John, Morgan, Margaret B., Muzny, Donna M., Bich Nguyen, Ngoc, Okwuonu, Geoffrey O., Ruiz, San Juana, Santibanez, Jireh, Wright, Rita A., Buhay, Christian, Ding, Yan, Dugan-Rocha, Shannon, Herdandez, Judith, Holder, Michael, Sabo, Aniko, Egan, Amy, Goodell, Jason, Wilczek-Boney, Katarzyna, Fowler, Gerald R., Edward Hitchens, Matthew, Lozado, Ryan J., Moen, Charles, Steffen, David, Warren, James T., Zhang, Jingkun, Chiu, Readman, Jones, Steven J.M., Marra, Marco A., Schein, Jacqueline E., James Durbin, K., Havlak, Paul, Jiang, Huaiyang, Liu, Yue, Qin, Xiang, Ren, Yanru, Shen, Yufeng, Song, Henry, Weinstock, George M., Worley, Kim C., Nicole Bell, Stephanie, Davis, Clay, Jolivet Johnson, Angela, Lee, Sandra, Nazareth, Lynne V., Patel, Bella Mayurkumar, Pu, Ling-Ling, Vattathil, Selina, Williams, Rex Lee, Jr., Curry, Stacey, Hamilton, Cerissa, Sodergren, Erica, Nazareth, Lynne V., Wheeler, David A., Adelson, David L, Aerts, Jan, Barris, Wes, Bennett, Gary L, Dalrymple, Brian, Eggen, André, Gill, Clare A., Green, Ronnie D., Harhay, Gregory P., Hobbs, Matthew, Jann, Oliver, Kappes, Steve M., Keele, John W., Kent, Matthew P., Larkin, Denis M., Lewin, Harris A., Lien, Sigbjørn, McEwan, John C., McKay, Stephanie D., McWilliam, Sean, Moore, Stephen S., Nicholas, Frank W., Payne, Gemma M., Ratnakumar, Abhirami, Salih, Hanni, Schnabel, Robert D., Smith, Timothy, Snelling, Warren M., Sonstegard, Tad S., Stone, Roger T., Sugimoto, Yoshikazu, Takasuga, Akiko, Taylor, Jeremy F., Tellam, Ross L., Van Tassell, Curtis P., Williams, John L, MacNeil, Michael D., Abatepaulo, Antonio R.R., Abbey, Colette A., Aerts, Jan, Ahola, Virpi, Almeida, Iassudara G., Amadio, Ariel F., Anatriello, Elen, Bahadue, Suria M., Baldwin, Cynthia L., Baxter, Rebecca, Bennett, Anna K., Biase, Fernando H., Boldt, Clayton R., Brinkmeyer-Langford, Candice L, Brown, Wendy C., Caetano, Alexandre R., Carroll, Jeffery A., Carvalho, Wanessa A, Casey, Theresa, Cervelatti, Eliane P., Chacko, Elsa, Chapin, Jennifer E., Cheng, Ye, Childers, Christopher P., Choi, Jungwoo, Colley, Adam J., Connelley, Timothy, de Campos, Tatiana A., De Donato, Marcos, de Miranda Santos, Isabel K.F., de Oliveira, Carlo J.F., Deobald, Heather, Devinoy, Eve, Dickens, Michael C., Donohue, Kaitlin E., Dovc, Peter, Eberlein, Annett, Ellis, Shirley A., Fitzsimmons, Carolyn J., Franzin, Alessandra M., Fritz, Krista, Garcia, Gustavo R., Fernando Garcia, Jose, Genini, Sem, German, Bruce J., Gilbert, James G.R., Gill, Clare A., Gladney, Cody J., Glass, Elizabeth J., Grant, Jason R., Greaser, Marion L., Green, Jonathan A., Hadsell, Darryl L., Hagen, Darren E., Hakimov, Hatam A., Halgren, Rob, Harrow, Jennifer L, Hart, Elizabeth A., Hastings, Nicola, Hernandez, Marta, Herzig, Carolyn T.A., Hiendleder, Stefan G., Hobbs, Matthew, Hu, Zhi-Liang, livanainen, Antti, Ingham, Aaron, Iso-Touru, Terhi, Jamis, Catherine, Jann, Oliver, Jensen, Kirsty, Kapetis, Dimos, Kerr, Tovah, Khalil, Sari S., Khatib, Hasan, Kolbehdari, Davood, Kumar, Charu G., Kumar, Dinesh, Leach, Richard, Lee, Justin C-M, Lemay, Danielle G., Li, Changxi, Liu, George E., Logan, Krystin M., Malinverni, Roberto, Maqbool, Nauman J., Marques, Elisa, Martin, William F., Martins, Natalia F., Maruyama, Sandra R., Mazza, Raffaele, McLean, Kim L, Medrano, Juan F., Memili, Erdogan, Molenaar, Adrian J., Moreno, Barbara T., Moré, Daniela D., Muntean, Carl T., Nandakumar, Hari P., Nogueira, Marcelo F.G., Olsaker, Ingrid, Pant, Sameer D., Panzitta, Francesca, Pastor, Rosemeire C.P., Poli, Mario A., Poslusny, Nathan, Rachagani, Satyanarayana, Ranganathan, Shoba, Razpet, Andrej, Reecy, James, Riggs, Penny K., Rijnkels, Monique, Rincon, Gonzalo, Rodriguez-Osorio, Nelida, Rodriguez-Zas, Sandra L., Romero, Natasha E., Rosenwald, Anne, Sando, Lillian, Schmutz, Sheila M., Seo, Seongwon, Shen, Libing, Sherman, Laura, Skow, Loren C., Southey, Bruce R., Spurlock, Diane, Strandberg Lutzow, Ylva, Sweedler, Jonathan V., Tammen, Imke, Taniguchi, Masaaki, Tellam, Ross L, Telugu, Bhanu Prakash V.L, Urbanski, Jennifer M., Utsunomiya, Yuri T., Verschoor, Chris P., Waardenberg, Ashley J., Walker, Angela, Wang, Zhiquan, Ward, Robert, Weikard, Rosemarie, Welsh, Thomas H., Jr., Wheeler, Thomas T., White, Stephen N., Williams, John L, Wilming, Laurens G., Wunderlich, Kris R., Yang, Jianqi, and Zhao, Feng-Qi

Published
2009

15. A high resolution RH map of the bovine major histocompatibility complex

Author

Womack James E, Raudsepp Terje, Cothran Marian, Gustafson-Seabury Ashley L, Fritz Krista L, Childers Christopher P, Brinkmeyer-Langford Candice L, and Skow Loren C

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background The cattle MHC is termed the bovine leukocyte antigen (BoLA) and, along with the MHCs of other ruminants, is unique in its genomic organization. Consequently, correct and reliable gene maps and sequence information are critical to the study of the BoLA region. The bovine genome sequencing project has produced two assemblies (Btau_3.1 and 4.0) that differ substantially from each other and from conventional gene maps in the BoLA region. To independently compare the accuracies of the different sequence assemblies, we have generated a high resolution map of BoLA using a 12,000rad radiation hybrid panel. Seventy-seven unique sequence tagged site (STS) markers chosen at approximately 50 kb intervals from the Btau 2.0 assembly and spanning the IIa-III-I and IIb regions of the bovine MHC were mapped on a 12,000rad bovine radiation hybrid (RH) panel to evaluate the different assemblies of the bovine genome sequence. Results Analysis of the data generated a high resolution RH map of BoLA that was significantly different from the Btau_3.1 assembly of the bovine genome but in good agreement with the Btau_4.0 assembly. Of the few discordancies between the RH map and Btau_4.0, most could be attributed to closely spaced markers that could not be precisely ordered in the RH panel. One probable incorrectly-assembled sequence and three missing sequences were noted in the Btau_4.0 assembly. The RH map of BoLA is also highly concordant with the sequence-based map of HLA (NCBI build 36) when reordered to account for the ancestral inversion in the ruminant MHC. Conclusion These results strongly suggest that studies using Btau_3.1 for analyses of the BoLA region should be reevaluated in light of the Btau_4.0 assembly and indicate that additional research is needed to produce a complete assembly of the BoLA genomic sequences.

Published
2009
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16. Additional file 5: Figure S3. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Abstract

Plot shows over-represented pathways for genes up-regulated in 6 m GRMD MHG. Statistical significance (smaller p values = larger numbers = greater significance) is shown on the x-axis, and numbers of genes altered per pathway is shown to the right of each bar. (DOCX 32 kb)

Published
2017
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17. Additional file 3: Table S2. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Abstract

Functional analysis results of GRMD-induced gene alterations. MHG = medial head of the gastrocnemius, LV = left ventricle, B-H p val = Benjamini & Hochberg-corrected p value, No. = number of differentially expressed genes in the given functional category, ns = not significant, Dash (“-”) indicates not identified in the analysis. (DOCX 16 kb)

Published
2017
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18. Additional file 8: Figure S6. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Subjects
genetic structures
Abstract

Plot shows over-represented pathways for genes altered in 6 m (light blue bars, top) or 12 m (dark blue bars, bottom) GRMD LV. Statistical significance (smaller p values = larger numbers = greater significance) is shown on the x-axis, and numbers of genes altered per pathway is shown to the right of each bar. AMPK signaling pathway genes are shown below the corresponding pathway bar, colored based on directionality (red for up-regulation and green for down-regulation, respectively in GRMD versus normal dogs). (DOCX 26 kb)

Published
2017
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19. Additional file 2: Figure S1. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Abstract

Hierarchical clustering of 5,835 significantly altered transcripts is shown. Rows represent individual samples, labeled according to group, and columns represent individual transcripts. Bright red, bright blue and gray represent highest, lowest and median normalized and scaled signal intensity values, respectively. (DOCX 116Â kb)

Published
2017
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20. Additional file 6: Figure S4. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Abstract

Plot shows over-represented pathways for genes down-regulated in 6 m GRMD MHG. Statistical significance (smaller p values = larger numbers = greater significance) is shown on the x-axis, and numbers of genes altered per pathway is shown to the right of each bar. (DOCX 35 kb)

Published
2017
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21. Additional file 7: Figure S5. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Subjects
genetic structures
Abstract

Plot shows over-represented pathways for genes up- (red bars) or down-regulated (green bars) in 12 m GRMD MHG. Statistical significance (smaller p values = larger numbers = greater significance) is shown on the x-axis, and numbers of genes altered per pathway is shown to the right of each bar. (DOCX 30 kb)

Published
2017
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22. Additional file 4: Figure S2. of GRMD cardiac and skeletal muscle metabolism gene profiles are distinct

Author

Markham, Larry, Brinkmeyer-Langford, Candice, Soslow, Jonathan, Gupte, Manisha, Sawyer, Douglas, Kornegay, Joe, and Galindo, Cristi

Abstract

Volcano plot is shown highlighting gene expression differences between dystrophic left ventricle (LV) and medial head of the gastrocnemius (MHG) skeletal muscle of golden retriever muscular dystrophy (GRMD) dogs at 6 months. The y-axis displays p values, and fold-differences are plotted on the x-axis for comparison of GRMD LV versus MHG (LV/MHG). Each circle represents an individual probe set (gene) and is colored based on fold-difference (blue for genes with lower expression in GRMD MHG and higher expression in LV, red for genes with higher expression values in LV and lower in MHG, and gray for no change), as shown in the legend. Orange lines mark cut-off values (p value 2). Official gene symbols are indicated to highlight major expression differences between LV and MHG. (PPTX 136 kb)

Published
2017
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24. Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures

Author

Kornegay, Joe N., Bogan, Daniel J., Bogan, Janet R., Dow, Jennifer L., Wang, Jiahui, Fan, Zheng, Liu, Naili, Warsing, Leigh C., Grange, Robert W., Ahn, Mihye, Balog-Alvarez, Cynthia J., Cotten, Steven W., Willis, Monte S., Brinkmeyer-Langford, Candice, Zhu, Hongtu, Palandra, Joe, Morris, Carl A., Styner, Martin A., Wagner, Kathryn R., and Human Nutrition, Foods, and Exercise

Subjects
musculoskeletal system
Abstract

Background Myostatin (Mstn) is a negative regulator of muscle growth whose inhibition promotes muscle growth and regeneration. Dystrophin-deficient mdx mice in which myostatin is knocked out or inhibited postnatally have a less severe phenotype with greater total mass and strength and less fibrosis and fatty replacement of muscles than mdx mice with wild-type myostatin expression. Dogs with golden retriever muscular dystrophy (GRMD) have previously been noted to have increased muscle mass and reduced fibrosis after systemic postnatal myostatin inhibition. Based partly on these results, myostatin inhibitors are in development for use in human muscular dystrophies. However, persisting concerns regarding the effects of long-term and profound myostatin inhibition will not be easily or imminently answered in clinical trials. Methods To address these concerns, we developed a canine (GRippet) model by crossbreeding dystrophin-deficient GRMD dogs with Mstn-heterozygous (Mstn +/−) whippets. A total of four GRippets (dystrophic and Mstn +/−), three GRMD (dystrophic and Mstn wild-type) dogs, and three non-dystrophic controls from two litters were evaluated. Results Myostatin messenger ribonucleic acid (mRNA) and protein levels were downregulated in both GRMD and GRippet dogs. GRippets had more severe postural changes and larger (more restricted) maximal joint flexion angles, apparently due to further exaggeration of disproportionate effects on muscle size. Flexors such as the cranial sartorius were more hypertrophied on magnetic resonance imaging (MRI) in the GRippets, while extensors, including the quadriceps femoris, underwent greater atrophy. Myostatin protein levels negatively correlated with relative cranial sartorius muscle cross-sectional area on MRI, supporting a role in disproportionate muscle size. Activin receptor type IIB (ActRIIB) expression was higher in dystrophic versus control dogs, consistent with physiologic feedback between myostatin and ActRIIB. However, there was no differential expression between GRMD and GRippet dogs. Satellite cell exhaustion was not observed in GRippets up to 3 years of age. Conclusions Partial myostatin loss may exaggerate selective muscle hypertrophy or atrophy/hypoplasia in GRMD dogs and worsen contractures. While muscle imbalance is not a feature of myostatin inhibition in mdx mice, findings in a larger animal model could translate to human experience with myostatin inhibitors. Published version

Published
2016

25. Additional file 3: of Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures

Author

Kornegay, Joe, Bogan, Daniel, Bogan, Janet, Dow, Jennifer, Jiahui Wang, Fan, Zheng, Naili Liu, Warsing, Leigh, Grange, Robert, Mihye Ahn, Balog-Alvarez, Cynthia, Cotten, Steven, Willis, Monte, Brinkmeyer-Langford, Candice, Hongtu Zhu, Palandra, Joe, Morris, Carl, Styner, Martin, and Wagner, Kathryn

Abstract

Table S2. T2 mapping values (Mean ± SD) in non-dystrophic control, GRMD (Mstn +/+ ), and GRippet (Mstn +/− ) Dogs (mean ± SD). (DOCX 369 kb)

Published
2016
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26. Additional file 2: of Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures

Author

Kornegay, Joe, Bogan, Daniel, Bogan, Janet, Dow, Jennifer, Jiahui Wang, Fan, Zheng, Naili Liu, Warsing, Leigh, Grange, Robert, Mihye Ahn, Balog-Alvarez, Cynthia, Cotten, Steven, Willis, Monte, Brinkmeyer-Langford, Candice, Hongtu Zhu, Palandra, Joe, Morris, Carl, Styner, Martin, and Wagner, Kathryn

Abstract

Table S1. MRI volumes in non-dystrophic control, GRMD (Mstn +/+ ), and GRippet (Mstn +/â ) Dogs (Meanâ Âąâ SD). (DOCX 954 kb)

Published
2016
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29. Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures

Author

Human Nutrition, Foods, and Exercise, Kornegay, Joe N., Bogan, Daniel J., Bogan, Janet R., Dow, Jennifer L., Wang, Jiahui, Fan, Zheng, Liu, Naili, Warsing, Leigh C., Grange, Robert W., Ahn, Mihye, Balog-Alvarez, Cynthia J., Cotten, Steven W., Willis, Monte S., Brinkmeyer-Langford, Candice, Zhu, Hongtu, Palandra, Joe, Morris, Carl A., Styner, Martin A., Wagner, Kathryn R., Human Nutrition, Foods, and Exercise, Kornegay, Joe N., Bogan, Daniel J., Bogan, Janet R., Dow, Jennifer L., Wang, Jiahui, Fan, Zheng, Liu, Naili, Warsing, Leigh C., Grange, Robert W., Ahn, Mihye, Balog-Alvarez, Cynthia J., Cotten, Steven W., Willis, Monte S., Brinkmeyer-Langford, Candice, Zhu, Hongtu, Palandra, Joe, Morris, Carl A., Styner, Martin A., and Wagner, Kathryn R.

Abstract

Background Myostatin (Mstn) is a negative regulator of muscle growth whose inhibition promotes muscle growth and regeneration. Dystrophin-deficient mdx mice in which myostatin is knocked out or inhibited postnatally have a less severe phenotype with greater total mass and strength and less fibrosis and fatty replacement of muscles than mdx mice with wild-type myostatin expression. Dogs with golden retriever muscular dystrophy (GRMD) have previously been noted to have increased muscle mass and reduced fibrosis after systemic postnatal myostatin inhibition. Based partly on these results, myostatin inhibitors are in development for use in human muscular dystrophies. However, persisting concerns regarding the effects of long-term and profound myostatin inhibition will not be easily or imminently answered in clinical trials. Methods To address these concerns, we developed a canine (GRippet) model by crossbreeding dystrophin-deficient GRMD dogs with Mstn-heterozygous (Mstn +/−) whippets. A total of four GRippets (dystrophic and Mstn +/−), three GRMD (dystrophic and Mstn wild-type) dogs, and three non-dystrophic controls from two litters were evaluated. Results Myostatin messenger ribonucleic acid (mRNA) and protein levels were downregulated in both GRMD and GRippet dogs. GRippets had more severe postural changes and larger (more restricted) maximal joint flexion angles, apparently due to further exaggeration of disproportionate effects on muscle size. Flexors such as the cranial sartorius were more hypertrophied on magnetic resonance imaging (MRI) in the GRippets, while extensors, including the quadriceps femoris, underwent greater atrophy. Myostatin protein levels negatively correlated with relative cranial sartorius muscle cross-sectional area on MRI, supporting a role in disproportionate muscle size. Activin receptor type IIB (ActRIIB) expression was higher in dystrophic versus control dogs, consistent with physiologic feedback between myostatin and ActRIIB. However, t

Published
2016

32. Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures

Author

Kornegay, Joe N., primary, Bogan, Daniel J., additional, Bogan, Janet R., additional, Dow, Jennifer L., additional, Wang, Jiahui, additional, Fan, Zheng, additional, Liu, Naili, additional, Warsing, Leigh C., additional, Grange, Robert W., additional, Ahn, Mihye, additional, Balog-Alvarez, Cynthia J., additional, Cotten, Steven W., additional, Willis, Monte S., additional, Brinkmeyer-Langford, Candice, additional, Zhu, Hongtu, additional, Palandra, Joe, additional, Morris, Carl A., additional, Styner, Martin A., additional, and Wagner, Kathryn R., additional

Published
2016
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33. Translating golden retriever muscular dystrophy microarray findings to novel biomarkers for cardiac/skeletal muscle function in Duchenne muscular dystrophy

Author

Galindo, Cristi L., primary, Soslow, Jonathan H., additional, Brinkmeyer-Langford, Candice L., additional, Gupte, Manisha, additional, Smith, Holly M., additional, Sengsayadeth, Seng, additional, Sawyer, Douglas B., additional, Benson, D. Woodrow, additional, Kornegay, Joe N., additional, and Markham, Larry W., additional

Published
2015
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35. Aberrant Gene Expression in Humans

Author

Zeng, Yong, primary, Wang, Gang, additional, Yang, Ence, additional, Ji, Guoli, additional, Brinkmeyer-Langford, Candice L., additional, and Cai, James J., additional

Published
2015
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42. Translating golden retriever muscular dystrophy microarray findings to novel biomarkers for cardiac/skeletal muscle function in Duchenne muscular dystrophy

Author

Galindo, Cristi L., Soslow, Jonathan H., Brinkmeyer-Langford, Candice L., Gupte, Manisha, Smith, Holly M., Sengsayadeth, Seng, Sawyer, Douglas B., Benson, D. Woodrow, Kornegay, Joe N., and Markham, Larry W.

Abstract

Background:In Duchenne muscular dystrophy (DMD), abnormal cardiac function is typically preceded by a decade of skeletal muscle disease. Molecular reasons for differences in onset and progression of these muscle groups are unknown. Human biomarkers are lacking.Methods:We analyzed cardiac and skeletal muscle microarrays from normal and golden retriever muscular dystrophy (GRMD) dogs (ages 6, 12, or 47+ mo) to gain insight into muscle dysfunction and to identify putative DMD biomarkers. These biomarkers were then measured using human DMD blood samples.Results:We identified GRMD candidate genes that might contribute to the disparity between cardiac and skeletal muscle disease, focusing on brain-derived neurotropic factor (BDNF) and osteopontin (OPN/SPP1, hereafter indicated as SPP1). BDNF was elevated in cardiac muscle of younger GRMD but was unaltered in skeletal muscle, while SPP1 was increased only in GRMD skeletal muscle. In human DMD, circulating levels of BDNF were inversely correlated with ventricular function and fibrosis, while SPP1 levels correlated with skeletal muscle function.Conclusion:These results highlight gene expression patterns that could account for differences in cardiac and skeletal disease in GRMD. Most notably, animal model-derived data were translated to DMD and support use of BDNF and SPP1 as biomarkers for cardiac and skeletal muscle involvement, respectively.

Published
2016
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44. Consequences of perinatal bisphenol A exposure in a mouse model of multiple sclerosis.

Author

Brinkmeyer-Langford, Candice, Rodrigues, Aline, Kochan, Kelli J., Haney, Rachel, Rassu, Fenan, Steelman, Andrew J., Young, Colin, Riggs, Penny, Storts, Ralph, Meagher, Mary W., and Welsh, C. Jane

Subjects
*BISPHENOL A, *DEMYELINATION, *ENDOCRINE disruptors, *GENE expression, *AUTOIMMUNE diseases, *INFLAMMATION, MULTIPLE sclerosis research
Abstract

Multiple sclerosis (MS) is a complex disease influenced by genetic and environmental contributing factors. Endocrine disrupting compounds (EDCs) such as bisphenol A (BPA) affect gene expression and hormone-regulated systems throughout the body. We investigated the effects of BPA on Theiler's-virus induced demyelination (TVID), a mouse model of MS. Perinatal BPA exposure, combined with viral infection, resulted in a decreased level of viral antibodies, accelerated the onset of TVID symptoms, increased inflammation in both the spinal cord and digestive tract, and amplified immune-related gene expression changes induced by viral infection. These results demonstrate the effect of BPA on the trajectory of TVID, and illustrate how multiple factors collectively influence autoimmune disease. [ABSTRACT FROM AUTHOR]

Published
2014
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45. Additional file 4: of Dystrophin-deficient dogs with reduced myostatin have unequal muscle growth and greater joint contractures

Author

Kornegay, Joe, Bogan, Daniel, Bogan, Janet, Dow, Jennifer, Jiahui Wang, Fan, Zheng, Naili Liu, Warsing, Leigh, Grange, Robert, Mihye Ahn, Balog-Alvarez, Cynthia, Cotten, Steven, Willis, Monte, Brinkmeyer-Langford, Candice, Hongtu Zhu, Palandra, Joe, Morris, Carl, Styner, Martin, and Wagner, Kathryn

Subjects
3. Good health
Abstract

Table S3. Histopathologic, morphometric, and molecular findings in non-dystrophic control, GRMD (Mstn +/+ ), and GRippet (Mstn +/â ) dogs. (DOCX 403 kb)

46. Additive, Epistatic, and Environmental Effects Through the Lens of Expression Variability QTL in a Twin Cohort.

Author

Gang Wang, Ence Yang, Brinkmeyer-Langford, Candice L., and Cai, James J.

Subjects
*GENE expression, *LYMPHOBLASTOID cell lines, *TWIN studies, *SINGLE nucleotide polymorphisms, *GENETIC polymorphism research
Abstract

The expression of a gene can vary across individuals in the general population, as well as between monozygotic twins. This variable expression is assumed to be due to the influence of both genetic and nongenetic factors. Yet little evidence supporting this assumption has been obtained from empirical data. In this study, we used expression data from a large twin cohort to investigate the influences of genetic and nongenetic factors on variable gene expression. We focused on a set of expression variability QTL (evQTL)-- i.e., genetic loci associated with the variance, as opposed to the mean, of gene expression. We identified evQTL for 99, 56, and 79 genes in lymphoblastoid cell lines, skin, and fat, respectively. The differences in gene expression, measured by the relative mean difference (RMD), tended to be larger between pairs of dizygotic (DZ) twins than between pairs of monozygotic (MZ) twins, showing that genetic background influenced the expression variability. Furthermore, a more profound RMD was observed between pairs of MZ twins whose genotypes were associated with greater expression variability than the RMD found between pairs of MZ twins whose genotypes were associated with smaller expression variability. This suggests that nongenetic (e.g., environmental) factors contribute to the variable expression. Lastly, we demonstrated that the formation of evQTL is likely due to partial linkages between eQTL SNPs that are additively associated with the mean of gene expression; in most cases, no epistatic effect is involved. Our findings have implications for understanding divergent sources of gene expression variability. [ABSTRACT FROM AUTHOR]

Published
2014
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