دورية أكاديمية
Class I and II histone deacetylase expression is not altered in human amyotrophic lateral sclerosis: Neuropathological and positron emission tomography molecular neuroimaging evidence.
العنوان: | Class I and II histone deacetylase expression is not altered in human amyotrophic lateral sclerosis: Neuropathological and positron emission tomography molecular neuroimaging evidence. |
---|---|
المؤلفون: | Dios AM; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Babu S; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Granucci EJ; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Mueller KA; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Mills AN; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Alshikho MJ; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA.; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA., Zürcher NR; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA., Cernasov P; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Gilbert TM; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA., Glass JD; Department of Neurology, Emory University, Atlanta, Georgia, USA., Berry JD; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA., Atassi N; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA.; Sanofi-Genzyme, Cambridge, Massachusetts, USA., Hooker JM; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA., Sadri-Vakili G; Sean M Healey & AMG Center for ALS at Mass General, Massachusetts General Hospital, Boston, Massachusetts, USA. |
المصدر: | Muscle & nerve [Muscle Nerve] 2019 Oct; Vol. 60 (4), pp. 443-452. Date of Electronic Publication: 2019 Jul 16. |
نوع المنشور: | Journal Article; Observational Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: John Wiley & Sons Country of Publication: United States NLM ID: 7803146 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4598 (Electronic) Linking ISSN: 0148639X NLM ISO Abbreviation: Muscle Nerve Subsets: MEDLINE |
أسماء مطبوعة: | Publication: <2005-> : Hoboken, NJ : John Wiley & Sons Original Publication: New York, NY : John Wiley & Sons |
مواضيع طبية MeSH: | Amyotrophic Lateral Sclerosis/*genetics , Histone Deacetylases/*genetics , Motor Cortex/*metabolism , Spinal Cord/*metabolism, Adamantane/analogs & derivatives ; Adult ; Aged ; Aged, 80 and over ; Amyotrophic Lateral Sclerosis/diagnostic imaging ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Brain/diagnostic imaging ; Brain/metabolism ; Carbon Radioisotopes ; Case-Control Studies ; Cerebral Cortex/diagnostic imaging ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Cross-Sectional Studies ; Female ; Histone Deacetylases/metabolism ; Histones/metabolism ; Humans ; Hydroxamic Acids ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Molecular Imaging ; Motor Cortex/diagnostic imaging ; Motor Cortex/pathology ; Multimodal Imaging ; Positron-Emission Tomography ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Spinal Cord/diagnostic imaging ; Spinal Cord/pathology |
مستخلص: | Introduction: There is an unmet need for mechanism-based biomarkers and effective disease modifying treatments in amyotrophic lateral sclerosis (ALS). Previous findings have provided evidence that histone deacetylases (HDAC) are altered in ALS, providing a rationale for testing HDAC inhibitors as a therapeutic option. Methods: We measured class I and II HDAC protein and transcript levels together with acetylation levels of downstream substrates by using Western blotting in postmortem tissue of ALS and controls. [ 11 C]Martinostat, a novel HDAC positron emission tomography ligand, was also used to assess in vivo brain HDAC alterations in patients with ALS and healthy controls (HC). Results: There was no significant difference in HDAC levels between patients with ALS and controls as measured by Western blotting and reverse-transcription quantitative polymerase chain reaction. Similarly, no differences were detected in [ 11 C]Martinostat-positron emission tomography uptake in ALS participants compared with HCs. Discussion: These findings provide evidence that alterations in HDAC isoforms are not a dominant pathological feature at the bulk tissue level in ALS. (© 2019 Wiley Periodicals, Inc.) |
References: | Mehta P, Kaye W, Bryan L, Larson T, Copeland T, Wu J, et al. Prevalence of amyotrophic lateral sclerosis-United States, 2012-2013. MMWR Surveill Summ 2016;65(8):1-12. Bensimon G, Lacomblez L, Meininger V. A controlled trial of riluzole in amyotrophic lateral sclerosis. N Engl J Med 1994;330(9):585-591. Lacomblez L, Bensimon G, Leigh PN, Guillet P, Meininger V. Dose-ranging study of riluzole in amyotrophic lateral sclerosis. Amyotrophic Lateral Sclerosis/Riluzole Study Group II. Lancet 1996;347(9013):1425-1431. Abe K, Aoki M, Tsuji S, Itoyama Y, Sobue G, Togo M, et al. Safety and efficacy of edaravone in well defined patients with amyotrophic lateral sclerosis: a randomised, double-blind, placebo-controlled trial. Lancet Neurol 2017;16(7):505-512. Paez-Colasante X, Figueroa-Romero C, Sakowski SA, Goutman SA, Feldman EL. Amyotrophic lateral sclerosis: mechanisms and therapeutics in the epigenomic era. Nat Rev Neurol 2015;11(5):266-279. Belzil VV, Katzman RB, Petrucelli L. ALS and FTD: an epigenetic perspective. Acta Neuropathol 2016;132(4):487-502. Jimenez-Pacheco A, Franco JM, Lopez S, Gomez-Zumaquero JM, Magdalena Leal-Lasarte M, Caballero-Hernandez DE, et al. Epigenetic mechanisms of gene regulation in amyotrophic lateral sclerosis. Adv Exp Med Biol 2017;978:255-275. Valle C, Salvatori I, Gerbino V, Rossi S, Palamiuc L, Rene F, et al. Tissue-specific deregulation of selected HDACs characterizes ALS progression in mouse models: pharmacological characterization of SIRT1 and SIRT2 pathways. Cell Death Dis 2014;5:e1296. Taes I, Timmers M, Hersmus N, Bento-Abreu A, Van Den Bosch L, Van Damme P, et al. HDAC6 deletion delays disease progression in the SOD1G93A mouse model of ALS. Hum Mol Genet 2013;22(9):1783-1790. Chen S, Zhang XJ, Li LX, Wang Y, Zhong RJ, Le W. Histone deacetylase 6 delays motor neuron degeneration by ameliorating the autophagic flux defect in a transgenic mouse model of amyotrophic lateral sclerosis. Neurosci Bull 2015;31(4):459-468. Gal J, Chen J, Barnett KR, Yang L, Brumley E, Zhu H. HDAC6 regulates mutant SOD1 aggregation through two SMIR motifs and tubulin acetylation. J Biol Chem 2013;288(21):15035-15045. Kim SH, Shanware NP, Bowler MJ, Tibbetts RS. Amyotrophic lateral sclerosis-associated proteins TDP-43 and FUS/TLS function in a common biochemical complex to co-regulate HDAC6 mRNA. J Biol Chem 2010;285(44):34097-34105. Cassel JA, McDonnell ME, Velvadapu V, Andrianov V, Reitz AB. Characterization of a series of 4-aminoquinolines that stimulate caspase-7 mediated cleavage of TDP-43 and inhibit its function. Biochimie 2012;94(9):1974-1981. Cook C, Stankowski JN, Carlomagno Y, Stetler C, Petrucelli L. Acetylation: a new key to unlock tau's role in neurodegeneration. Alzheimers Res Ther 2014;6(3):29. Tseng JH, Xie L, Song S, Xie Y, Allen L, Ajit D, et al. The deacetylase HDAC6 mediates endogenous neuritic tau pathology. Cell Rep 2017;20(9):2169-2183. Guo W, Naujock M, Fumagalli L, Vandoorne T, Baatsen P, Boon R, et al. HDAC6 inhibition reverses axonal transport defects in motor neurons derived from FUS-ALS patients. Nat Commun 2017;8(1):861. Janssen C, Schmalbach S, Boeselt S, Sarlette A, Dengler R, Petri S. Differential histone deacetylase mRNA expression patterns in amyotrophic lateral sclerosis. J Neuropathol Exp Neurol 2010;69(6):573-581. Piepers S, Veldink JH, de Jong SW, van der Tweel I, van der Pol WL, Uijtendaal EV, et al. Randomized sequential trial of valproic acid in amyotrophic lateral sclerosis. Ann Neurol 2009;66(2):227-234. Cudkowicz ME, Andres PL, Macdonald SA, Bedlack RS, Choudry R, Brown RH Jr, et al. Phase 2 study of sodium phenylbutyrate in ALS. Amyotroph Lateral Scler 2009;10(2):99-106. Rouaux C, Jokic N, Mbebi C, Boutillier S, Loeffler JP, Boutillier AL. Critical loss of CBP/p300 histone acetylase activity by caspase-6 during neurodegeneration. Embo J 2003;22(24):6537-6549. Rouaux C, Panteleeva I, Rene F, Gonzalez de Aguilar JL, Echaniz-Laguna A, Dupuis L, et al. Sodium valproate exerts neuroprotective effects in vivo through CREB-binding protein-dependent mechanisms but does not improve survival in an amyotrophic lateral sclerosis mouse model. J Neurosci 2007;27(21):5535-5545. Ryu H, Smith K, Camelo SI, Carreras I, Lee J, Iglesias AH, et al. Sodium phenylbutyrate prolongs survival and regulates expression of anti-apoptotic genes in transgenic amyotrophic lateral sclerosis mice. J Neurochem 2005;93(5):1087-1098. Petri S, Kiaei M, Kipiani K, Chen J, Calingasan NY, Crow JP, et al. Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis. Neurobiol Dis 2006;22(1):40-49. Xu Z, Li H, Jin P. Epigenetics-based therapeutics for neurodegenerative disorders. Curr Transl Geriatr Exp Gerontol Rep 2012;1(4):229-236. Haggarty SJ, Koeller KM, Wong JC, Grozinger CM, Schreiber SL. Domain-selective small-molecule inhibitor of histone deacetylase 6 (HDAC6)-mediated tubulin deacetylation. Proc Natl Acad Sci U S A 2003;100(8):4389-4394. Smith BN, Ticozzi N, Fallini C, Gkazi AS, Topp S, Kenna KP, et al. Exome-wide rare variant analysis identifies TUBA4A mutations associated with familial ALS. Neuron 2014;84(2):324-331. Pensato V, Tiloca C, Corrado L, Bertolin C, Sardone V, Del Bo R, et al. TUBA4A gene analysis in sporadic amyotrophic lateral sclerosis: identification of novel mutations. J Neurol 2015;262(5):1376-1378. Clark JA, Yeaman EJ, Blizzard CA, Chuckowree JA, Dickson TC. A case for microtubule vulnerability in amyotrophic lateral sclerosis: altered dynamics during disease. Front Cell Neurosci 2016;10:204. Sadri-Vakili G, Bouzou B, Benn CL, Kim MO, Chawla P, Overland RP, et al. Histones associated with downregulated genes are hypo-acetylated in Huntington's disease models. Hum Mol Genet 2007;16(11):1293-1306. McFarland KN, Das S, Sun TT, Leyfer D, Xia E, Sangrey GR, et al. Genome-wide histone acetylation is altered in a transgenic mouse model of Huntington's disease. PLoS One 2012;7(7):e41423. Mueller KA, Glajch KE, Huizenga MN, Wilson RA, Granucci EJ, Dios AM, et al. Hippo signaling pathway dysregulation in human Huntington's disease brain and neuronal stem cells. Sci Rep 2018;8(1):11355. Brooks BR. El Escorial World Federation of Neurology criteria for the diagnosis of amyotrophic lateral sclerosis. Subcommittee on Motor Neuron Diseases/Amyotrophic Lateral Sclerosis of the World Federation of Neurology Research Group on Neuromuscular Diseases and the El Escorial “Clinical limits of amyotrophic lateral sclerosis” workshop contributors. J Neurol Sci 1994;124(Suppl):96-107. Zurcher NR, Loggia ML, Lawson R, Chonde DB, Izquierdo-Garcia D, Yasek JE, et al. Increased in vivo glial activation in patients with amyotrophic lateral sclerosis: assessed with [(11)C]-PBR28. Neuroimage Clin 2015;7:409-414. Catana C, van der Kouwe A, Benner T, Michel CJ, Hamm M, Fenchel M, et al. Toward implementing an MRI-based PET attenuation-correction method for neurologic studies on the MR-PET brain prototype. J Nucl Med 2010;51(9):1431-1438. Alshikho MJ, Zurcher NR, Loggia ML, Cernasov P, Chonde DB, Izquierdo Garcia D, et al. Glial activation colocalizes with structural abnormalities in amyotrophic lateral sclerosis. Neurology 2016;87(24):2554-2561. Loggia ML, Chonde DB, Akeju O, Arabasz G, Catana C, Edwards RR, et al. Evidence for brain glial activation in chronic pain patients. Brain 2015;138(Pt 3):604-615. Nichols TE, Holmes AP. Nonparametric permutation tests for functional neuroimaging: a primer with examples. Hum Brain Mapp 2002;15(1):1-25. Bruneteau G, Simonet T, Bauche S, Mandjee N, Malfatti E, Girard E, et al. Muscle histone deacetylase 4 upregulation in amyotrophic lateral sclerosis: potential role in reinnervation ability and disease progression. Brain 2013;136(Pt 8):2359-2368. Lazo-Gomez R, Ramirez-Jarquin UN, Tovar YRLB, Tapia R. Histone deacetylases and their role in motor neuron degeneration. Front Cell Neurosci 2013;7:243. Di Pietro L, Baranzini M, Berardinelli MG, Lattanzi W, Monforte M, Tasca G, et al. Potential therapeutic targets for ALS: MIR206, MIR208b and MIR499 are modulated during disease progression in the skeletal muscle of patients. Sci Rep 2017;7(1):9538. Schneider A, Chatterjee S, Bousiges O, Selvi BR, Swaminathan A, Cassel R, et al. Acetyltransferases (HATs) as targets for neurological therapeutics. Neurotherapeutics 2013;10(4):568-588. Ripps ME, Huntley GW, Hof PR, Morrison JH, Gordon JW. Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A 1995;92(3):689-693. Yao Y-L, Yang W-M. Beyond histone and deacetylase: an overview of cytoplasmic histone deacetylases and their nonhistone substrates. J Biomed Biotechnol 2011;2011:146493. Paganoni S, Alshikho MJ, Zurcher NR, Cernasov P, Babu S, Loggia ML, et al. Imaging of glia activation in people with primary lateral sclerosis. Neuroimage Clin 2018;17:347-353. Turner MR, Cagnin A, Turkheimer FE, Miller CC, Shaw CE, Brooks DJ, et al. Evidence of widespread cerebral microglial activation in amyotrophic lateral sclerosis: an [11C](R)-PK11195 positron emission tomography study. Neurobiol Dis 2004;15(3):601-609. Gilbert TM, Zürcher NR, Catanese MC, Tseng CJ, Di Biase MA, Lyall AE, Hightower BG, Parmar AJ, Bhanot A, Wu CJ, Hibert ML, Kim M, Mahmood U, Stufflebeam SM, Schroeder FA, Wang C, Roffman JL, Holt DJ, Greve DN, Pasternak O, Kubicki M, Wey HY, Hooker JM. Neuroepigenetic signatures of age and sex in the living human brain. Nat Commun. 2019 Jul 3;10(1):2945. https://doi.org/10.1038/s41467-019-11031-0. |
معلومات مُعتمدة: | S10 OD023517 United States OD NIH HHS |
فهرسة مساهمة: | Keywords: ALS; HDAC; PET imaging; acetylation; histone; postmortem |
المشرفين على المادة: | 0 (Carbon Radioisotopes) 0 (Histones) 0 (Hydroxamic Acids) 0 (RNA, Messenger) 8JJC99KHGL (martinostat) EC 3.5.1.98 (Histone Deacetylases) PJY633525U (Adamantane) |
تواريخ الأحداث: | Date Created: 20190627 Date Completed: 20200114 Latest Revision: 20230211 |
رمز التحديث: | 20240628 |
DOI: | 10.1002/mus.26620 |
PMID: | 31241177 |
قاعدة البيانات: | MEDLINE |
كن أول من يترك تعليقا!