Peterson AB, Xu L, Daugherty J, Breiding MJ. Surveillance report of traumatic brain injury-related emergency department visits, hospitalizations, and deaths. Center for Disease Control and Prevention; United States: U.S. Department of Health and Human Services, 2019.
Hammond FM, Giacino JT, Nakase Richardson R, Sherer M, Zafonte RD, Whyte J, et al. Disorders of consciousness due to traumatic brain injury: functional status ten years post-injury. J Neurotrauma. 2019;36:1136–46.
Google Scholar
Holzer KJ, Carbone JT, DeLisi M, Vaughn MG. Traumatic brain injury and coextensive psychopathology: New evidence from the 2016 Nationwide Emergency Department Sample (NEDS). J Psychiatry Res. 2019;114:149–52.
MacGregor AJ, Dougherty AL, Galarneau MR. Injury-specific correlates of combat-related traumatic brain injury in operation Iraqi freedom. J Head Trauma Rehabil. 2011;26:312–18.
Google Scholar
Rigg JL, Mooney SR. Concussions and the military: Issues specific to service members. PMR. 2011;3:S380–6.
Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA. Mild traumatic brain injury in U.S. soldiers returning from Iraq. N Engl J Med. 2008;358:453–63.
Google Scholar
Schneiderman AI, Braver ER, Kang HK. Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: persistent postconcussive symptoms and posttraumatic stress disorder. Am J Epidemiol. 2008;167:1446–52.
Google Scholar
Kennedy JE, Leal FO, Lewis JD, Cullen MA, Amador RR. Posttraumatic stress symptoms in OIF/OEF servicemembers with blast-related and non-blast-related mild TBI. NeuroRehabilitation. 2010;26:223–31.
Google Scholar
Hill JJ, Mobo BHP, Cullen MR. Separating deployment-related traumatic brain injury and posttraumatic stress disorder in veterans: preliminary findings from the Veterans Affairs traumatic brain injury screening program. Am J Phys Med Rehabil. 2009;88:605–14.
Google Scholar
Carlson KF, Nelson D, Orazem RJ, Nugent S, Cifu DX, Sayer NA. Psychiatric diagnoses among Iraq and Afghanistan war veterans screened for deployment-related traumatic brain injury. J Trauma Stress. 2010;23:17–24.
Google Scholar
Belanger HG, Uomoto JM, Vanderploeg RD. The veterans health administration system of care for mild traumatic brain injury: costs, benefits, and controversies. J Head Trauma Rehabil. 2009;24:4–13.
Google Scholar
Chodobski A, Zink BJ, Szmydynger-Chodobska J. Blood-brain barrier pathophysiology in traumatic brain injury. Transl Stroke Res. 2011;2:492–516.
Google Scholar
Hemphill MA, Dauth S, Yu CJ, Dabiri BE, Parker KK. Traumatic brain injury and the neuronal microenvironment: A potential role for neuropathological mechanotransduction. Neuron. 2015;85:1177–92.
Google Scholar
VSSS Sajja, Hlavac N, VandeVord PJ. Role of glia in memory deficits following traumatic brain injury: Biomarkers of glia dysfunction. Front Integr Neurosci. 2016;10:7.
Wong VS, Langley B. Epigenetic changes following traumatic brain injury and their implications for outcome, recovery and therapy. Neurosci Lett. 2016;625:26–33.
Google Scholar
Shein NA, Shohami E. Histone deacetylase inhibitors as therapeutic agents for acute central nervous system injuries. Mol Med. 2011;17:448–56.
Google Scholar
Kiefer JC. Epigenetics in development. Dev Dyn. 2007;236:1144–56.
Google Scholar
Reik W, Dean W, Walter J. Epigenetic reprogramming in mammalian development. Science. 2001;293:1089–93.
Google Scholar
Majdzadeh N, Morrison BE, D’Mello SR. Class IIA HDACs in the regulation of neurodegeneration. Front Biosci. 2008;13:1072–82.
Google Scholar
Seto E, Yoshida M. Erasers of histone acetylation: The histone deacetylase enzymes. Cold Spring Harb Perspect Biol. 2014;6:a018713, 1–26.
Qureshi IA, Mehler MF. Understanding neurological disease mechanisms in the era of epigenetics. JAMA Neurol. 2013;70:703–10.
Google Scholar
Hahnen E, Hauke J, Tränkle C, Eyüpoglu IY, Wirth B, Blümcke I. Histone deacetylase inhibitors: possible implications for neurodegenerative disorders. Expert Opin Investig Drugs. 2008;17:169–84.
Google Scholar
Jin K, Mao XO, Simon RP, Greenberg DA. Cyclic AMP response element-binding protein (CREB) and CREB binding protein (CBP) in global cerebral ischemia. J Mol Neurosci. 2001;16:49–56.
Google Scholar
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;22:6537–49.
Google Scholar
Gibson CL, Murphy SP. Benefits of histone deacetylase inhibitors for acute brain injury: A systematic review of animal studies. J Neurochem. 2010;115:806–13.
Google Scholar
Dash PK, Orsi SA, Zhang M, Grill RJ, Patil S, Zhao J, et al. Valproate administered after traumatic brain injury provides neuroprotection and improves cognitive function in rats. PLoS ONE. 2010;5:e11383, 1–13.
Kozikowski AP, Chen Y, Gaysin A, Chen B, D’Annibale MA, Suto CM, et al. Functional differences in epigenetic modulators – Superiority of mercaptoacetamide-based histone deacetylase inhibitors relative to hydroxamates in cortical neuron neuroprotection studies. J Med Chem. 2007;50:3054–61.
Google Scholar
Zhang B, West EJ, Van KC, Gurkoff GG, Zhou J, Zhang XM, et al. HDAC inhibitor increases histone H3 acetylation and reduces microglia inflammatory response following traumatic brain injury in rats. Brain Res. 2008;1226:181–91.
Google Scholar
Nikolian VC, Dennahy IS, Weykamp M, Williams AM, Bhatti UF, Eidy H, et al. Isoform 6-selective histone deacetylase inhibition reduces lesion size and brain swelling following traumatic brain injury and hemorrhagic shock in. J Trauma Acute Care Surg. 2019;86:232–9.
Google Scholar
Golay J, Cuppini L, Leoni F, Micò C, Barbui V, Domenghini M, et al. The histone deacetylase inhibitor ITF2357 has anti-leukemic activity in vitro and in vivo and inhibits IL-6 and VEGF production by stromal cells. Leukemia. 2007;21:1892–1900.
Google Scholar
Shein NA, Grigoriadis N, Alexandrovich AG, Simeonidou C, Lourbopoulos A, Polyzoidou E, et al. Histone deacetylase inhibitor ITF2357 is neuroprotective, improves functional recovery, and induces glial apoptosis following experimental traumatic brain injury. FASEB J. 2009;23:4266–75.
Google Scholar
Yang H, Ni W, Jiang H, Lei Y, Su J, Gu Y, et al. Histone deacetylase inhibitor Scriptaid alleviated neurological dysfunction after experimental intracerebral hemorrhage in mice. Behav Neurol. 2018;2018:6583267. https://doi.org/10.1155/2018/6583267.
Wang G, Shi Y, Jiang X, Leak RK, Hu X, Wu Y, et al. HDAC inhibition prevents white matter injury by modulating microglia/macrophage polarization through the GSK3β/PTEN/Akt axis. Proc Natl Acad Sci USA. 2015;112:2853–8.
Google Scholar
Wang G, Jiang X, Pu H, Zhang W, An C, Hu X, et al. Scriptaid, a novel histone deacetylase inhibitor, protects against traumatic brain injury via modulation of PTEN and AKT pathway: scriptaid protects against TBI via AKT. Neurotherapeutics. 2013;10:124–42.
Google Scholar
Lu J, Frerich JM, Turtzo LC, Li S, Chiang J, Yang C, et al. Histone deacetylase inhibitors are neuroprotective and preserve NGF-mediated cell survival following traumatic brain injury. Proc Natl Acad Sci USA. 2013;110:10747–52.
Google Scholar
Gaub P, Tedeschi A, Puttagunta R, Nguyen T, Schmandke A, Di Giovanni S. HDAC inhibition promotes neuronal outgrowth and counteracts growth cone collapse through CBP/p300 and P/CAF-dependent p53 acetylation. Cell Death Differ. 2010;17:1392–408.
Google Scholar
Levenson JM, Sweatt JD. Epigenetic mechanisms in memory formation. Nat Rev Neurosci. 2005;6:108–18.
Google Scholar
Vecsey CG, Hawk JD, Lattal KM, Stein JM, Fabian SA, Attner MA, et al. Histone deacetylase inhibitors enhance memory and synaptic plasticity via CREB: CBP-dependent transcriptional activation. J Neurosci. 2007;27:6128–40.
Google Scholar
Bradner JE, West N, Grachan ML, Greenberg EF, Haggarty SJ, Warnow T, et al. Chemical phylogenetics of histone deacetylases. Nat Chem Biol. 2010;6:238–43.
Google Scholar
Kim MS, Akhtar M, Adachi M, Mahgoub M, Bassel-Duby R, Kavalali ET, et al. An essential role for histone deacetylase 4 in synaptic plasticity and memory formation. J Neurosci. 2012;32:10879–86.
Google Scholar
Cho Y, Sloutsky R, Naegle KM, Cavalli V. Injury-Induced HDAC5 nuclear export is essential for axon regeneration. Cell. 2013;155:894.
Google Scholar
Sando R, Gounko N, Pieraut S, Liao L, Yates J, Maximov A. HDAC4 governs a transcriptional program essential for synaptic plasticity and memory. Cell. 2012;151:821–34.
Google Scholar
Agis-Balboa RC, Pavelka Z, Kerimoglu C, Fischer A. Loss of HDAC5 impairs memory function: Implications for Alzheimer’s disease. J Alzheimer’s Dis. 2013;33:35–44.
Google Scholar
Saha P, Gupta R, Sen T, Sen N. Histone deacetylase 4 downregulation elicits post-traumatic psychiatric disorders through impairment of neurogenesis. J Neurotrauma. 2019;36:3284–96.
Google Scholar
Sagarkar S, Balasubramanian N, Mishra S, Choudhary AG, Kokare DM, Sakharkar AJ. Repeated mild traumatic brain injury causes persistent changes in histone deacetylase function in hippocampus: implications in learning and memory deficits in rats. Brain Res. 2019;1711:183–92.
Google Scholar
Bonomi R, Mukhopadhyay U, Shavrin A, Yeh HH, Majhi A, Dewage SW, et al. Novel histone deacetylase class IIa selective substrate radiotracers for PET imaging of epigenetic regulation in the brain. PLoS ONE. 2015;10:e0133512, 1–19.
Abd-Elfattah Foda MA, Marmarou A. A new model of diffuse brain injury in rats. Part II: Morphological characterization. J Neurosurg. 1994;80:301–13.
Cernak I. Animal models of head trauma. NeuroRx. 2005;2:410–22.
Google Scholar
Bodnar CN, Roberts KN, Higgins EK, Bachstetter AD. A systematic review of closed head injury models of mild traumatic brain injury in mice and rats. J Neurotrauma. 2019;36:1683–706.
Google Scholar
Folkerts MM, Berman RF, Muizelaar JP, Rafols JA. Disruption of MAP-2 immunostaining in rat hippocampus after traumatic brain injury. J Neurotrauma. 1998;15:349–63.
Google Scholar
Kallakuri S, Cavanaugh JM, Özaktay AC, Takebayashi T. The effect of varying impact energy on diffuse axonal injury in the rat brain: a preliminary study. Exp Brain Res. 2003;148:419–24.
Google Scholar
Li Y, Zhang L, Kallakuri S, Zhou R, Cavanaugh JM. Quantitative relationship between axonal injury and mechanical response in a Rodent head impact acceleration model. J Neurotrauma. 2011;28:1767–82.
Google Scholar
Kallakuri S, Bandaru S, Zakaria N, Shen Y, Kou Z, Zhang L, et al. Traumatic brain injury by a closed head injury device induces cerebral blood flow changes and microhemorrhages. J Clin Imaging Sci. 2015;5:52.
Google Scholar
Li Y, Zhang L, Kallakuri S, Cohen A, Cavanaugh JM. Correlation of mechanical impact responses and biomarker levels: a new model for biomarker evaluation in TBI. J Neurol Sci. 2015;359:280–6.
Google Scholar
Zakaria N, Kallakuri S, Bandaru, Cavanaugh JM. Temporal assessment of traumatic axonal injury in the rat corpus callosum and optic chiasm. Brain Res. 2012;1467:81–90.
Google Scholar
Li Y, Zhang L, Kallakuri S, Zhou R, Cavanaugh JM. Injury predictors of traumatic axonal injury in a rodent head impact acceleration model. Stapp Car Crash J. 2011;55:25–47.
Google Scholar
Li Y, Zhang L, Kallakuri S, Zhou R, Cvanaugh JM. Quantitative relationship between axonal injury and mechanical response in a rodent head impact acceleration model. J Neurotrauma. 2011;28:1767–82.
Google Scholar
Beaumont A, Fatouros P, Gennarelli T, Corwin F, Marmarou A. Bolus tracer delivery measured by MRI confirms edema without blood-brain barrier permeability in diffuse traumatic brain injury. Acta Neurochir Suppl. 2006;96:171–4.
Google Scholar
Beaumont A, Marmarou C, Marmarou A. The effects of human corticotrophin releasing factor on motor and cognitive deficit after impact acceleration injury. Neurol Res. 2000;22:665–73.
Google Scholar
Chen X, Chen Y, Xu Y, Gao Q, Shen Z, Zheng W. Microstructural and neurochemical changes in the rat brain after diffuse axonal injury. J Magn Res Imaging. 2019;49:1069–77.
Song Y, Qian Y, Su W, Liu X, Huang J, Gong Z, et al. Differences in pathological changes between two rat models of severe traumatic brain injury. Neural Regen Res. 2019;14:1796–804.
Google Scholar
Li S, Sun Y, Shan D, Feng B, Xing J, Duan Y, et al. Temporal profiles of axonal injury following impact acceleration traumatic brain injury in rats – a comparative study with diffusion tensor imaging and morphological analysis. Int J Leg Med. 2013;127:159–67.
Goda M, Isono M, Fujiki M, Kobayashi H. Both MK801 and NBQX reduce the neuronal damage after impact-acceleration brain injury. J Neurotrauma. 2002;19:1445–56.
Google Scholar
Wang H, Ma Y. Experimental models of traumatic axonal injury. J Clin Neurosci. 2010;17:157–62.
Google Scholar
Marmarou CR, Prieto R, Taya K, Young HF, Marmarou A. Marmarou weight drop injury model. In: Chen J, Xu ZC, Xu XM, Zhang JH, editors. Animal models of acute neurological injuries. Springer Protocols Handbooks. Totowa, New Jersey, USA: Humana Press; 2009. p. 393–407.
Marmarou A, Abd-Elfattah Foda MA, Van den Brink W, Campbell J, Kita H, Demetriadou K. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 1994;80:291–300.
Google Scholar
Guo H, Renaut RA, Chen K. An input function estimation method for FDG-PET human brain studies. Nucl Med Biol. 2007;34:483–92.
Google Scholar
Watson C, Paxinos G. The rat brain in stereotaxic coordinates. San Diego: Academic Press; 2006.
Logan J, Fowler JS, Volkow ND, Wang G, Ding Y, Alexoff DL. Distribution volume ratios without blood sampling from graphical analysis of PET data. J Cereb Blood Flow Metab. 1996;16:834–40.
Google Scholar
Laws MT, Bonomi RE, Kamal SR, Gelovani DJ, Llaniguez J, Potukutchi S, et al. Molecular imaging HDACs class IIa expression-activity and pharmacologic inhibition in intracerebral glioma models in rats using PET/CT/(MRI) with [18F]TFAHA. Sci Rep. 2019;9:3595.
Google Scholar
Logan J, Fowler JS, Volkow ND, Wolf AP, Dewey SL, Schlyer DJ. et al. Graphical analysis of reversible radioligand binding from time-activity measurements applied to [N-11C-methyl]-(-)-cocaine PET studies in human subjects. J Cereb Blood Flow Metab.1990;10:740–7.
Google Scholar
Murakami N, Yamaki T, Iwamoto Y, Sakakibara T, Kobori N, Fushiki S, et al. Experimental brain injury induces expression of amyloid precursor protein, which may be related to neuronal loss in the hippocampus. J Neurotrauma. 1998;15:993–1003.
Google Scholar
Zhang MH, Zhou XM, Cui JZ, Wang KJ, Feng Y, Zhang HA. Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression. Mol Med Rep. 2018;17:8079–86.
Google Scholar
Kim JY, Kim N, Zheng Z, Lee JE, Yenari MA. The 70 kDa heat shock protein protects against experimental traumatic brain injury. Neurobiol Dis. 2013;58:289–95.
Google Scholar
Jassam YN, Izzy S, Whalen M, McGavern DB, El Khoury J. Neuroimmunology of traumatic brain injury: Time for a paradigm shift. Neuron. 2017;95:1246–65.
Google Scholar
Kim N, Kim JY, Yenari MA. Anti-inflammatory properties and pharmacological induction of Hsp70 after brain injury. Inflammopharmacology. 2012;20:177–85.
Google Scholar
Eroglu B, Kimbler D, Pang J, Choi J, Moskophidis D, Yanasak N, et al. Therapeutic inducers of the HSP70/HSP110 protect mice against traumatic brain injury. J Neurochemistry. 2014;130:626–41.
Google Scholar
Kallakuri S, Li Y, Zhou R, Bandaru S, Zakaria N, Zhang L, et al. Impaired axoplasmic transport is the dominant injury induced by an impact acceleration injury device: an analysis of traumatic axonal injury in pyramidal tract and corpus callosum of rats. Brain Res. 2012;1452:29–38.
Google Scholar
Hsieh TH, Kang JW, Lai JH, Huang YZ, Rotenberg A, Chen KY, et al. Relationship of mechanical impact magnitude to neurologic dysfunction severity in a rat traumatic brain injury model. PLoS ONE. 2017;12:e0178186, 1–18.
Ciallella JR, Ikonomovic MD, Paljug WR, Wilbur YI, Dixon CE, Kochanek PM, et al. Changes in expression of amyloid precursor protein and interleukin-1β after experimental traumatic brain injury in rats. J Neurotrauma. 2002;19:1555–67.
Google Scholar
Johnson VE, Stewart W, Smith DH. Axonal pathology in traumatic brain injury. Exp Neurol. 2013;246:35–43.
Google Scholar
Shishido H, Ueno M, Sato K, Matsumura M, Toyota Y, Kirino T, et al. Traumatic brain injury by weight-drop method causes transient amyloid-β deposition and acute cognitive deficits in mice. Behav Neurol. 2019;2019:3248519. https://doi.org/10.1155/2019/3248519.
Elliott MB, Tuma RF, Amenta PS, Barbe MF, Jallo JI. Acute effects of a selective cannabinoid-2 receptor agonist on neuroinflammation in a model of traumatic brain injury. J Neurotrauma. 2011;28:973–81.
Google Scholar
Chen Y, Buck J. Cannabinoids protect cells from oxidative cell death: a receptor-independent mechanism. J Pharmacol Exp Ther. 2000;293:807–12.
Google Scholar
Nikodemova M, Duncan ID, Watters JJ. Minocycline exerts inhibitory effects on multiple mitogen-activated protein kinases and IκBα degradation in a stimulus-specific manner in microglia. J Neurochem. 2006;96:314–23.
Google Scholar
Eljaschewitsch E, Witting A, Mawrin C, Lee T, Schmidt PM, Wolf S, et al. The endocannabinoid anandamide protects neurons during CNS inflammation by induction of MKP-1 in microglial cells. Neuron 2006;49:67–79.
Google Scholar
Donat CK, Scott G, Gentleman SM, Sastre M. Microglial activation in traumatic brain injury. Front Aging Neurosci. 2017;15:349–63.
Madathil SK, Wilfred BS, Urankar SE, Yang W, Leung LY, Shear DA, et al. Early microglial activation following closed-head concussive injury is dominated by pro-inflammatory M-1 type. Front Neurol. 2018;9:964.
Google Scholar
Jin Y, Wang R, Yang S, Zhang X, Dai J. Role of Microglia autophagy in microglia activation after traumatic brain injury. World Neurosurg. 2017;100:351–60.
Google Scholar
Imai Y, Kohsaka S. Intracellular signaling in M-CSF-induced microglia activation: role of Iba1. Glia. 2002;40:164–74.
Google Scholar
Imai Y, Ibata I, Ito D, Ohsawa K, Kohsaka S. A novel gene iba1 in the major histocompatibility complex class III region encoding and EF hand protein expressed in a monocytic lineage. Biochem Biophys Res Commun. 1996;224:855–62.
Google Scholar
Ito D, Tanaka K, Suzuki S, Dembo T, Fukuuchi Y. Enhanced expression of Iba1, ionized calcium-binding adapter molecule 1, after transient focal cerebral ischemia in rat brain. Stroke. 2001;32:1208–15.
Google Scholar
Verdin E, Dequiedt F, Kasler HG. Class II histone deacetylases: versatile regulators. Trends Genet. 2003;19:286–93.
Google Scholar
Cernotta N, Clocchiatti A, Florean C, Brancolini C. Ubiquitin-dependent degradation of HDAC4, a new regulator of random cell motility. Mol Biol Cell. 2011;22:278–89.
Google Scholar
Bolger TA, Yao TP. Intracellular trafficking of histone deacetylase 4 regulates neuronal cell death. J Neurosci. 2005;25:9544–53.
Google Scholar
Fischle W, Dequiedt F, Hendzel MJ, Guenther MG, Lazar MA, Verdin E, et al. Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR. Mol Cell. 2002;9:45–57.
Google Scholar
Fitzsimons HL. The Class IIa histone deacetylase HDAC4 and neuronal function: Nuclear nuisance and cytoplasmic stalwart? Neurobiol Learn Mem. 2015;123:149–58.
Google Scholar
Isaacs JT, Antony L, Dalrymple SL, Brennen WN, Gerber S, Leanderson T, et al. Tasquinimod is an allosteric modulator of HDAC4 survival signaling within the compromised cancer microenvironment. Cancer Res. 2013;73:1386–99.
Google Scholar
Li J, Chen J, Ricupero CL, Hart RP, Schwartz MS, Herrup K, et al. Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia. Nat Med. 2012;18:783–90.
Google Scholar
Wu Q, Yang X, Zhang L, Zhang Y, Feng L. Nuclear accumulation of histone deacetylase 4 (HDAC4) exerts neurotoxicity in models of Parkinson’s disease. Mol Neurobiol. 2017;54:6970–83.
Google Scholar
Atkins CM, Chen S, Alonso OF, Dietrich WD, Hu BR. Activation of calcium/calmodulin-dependent protein kinases after traumatic brain injury. J Cereb Blood Flow Metab. 2006;26:1507–18.
Google Scholar
Chang S, Bezprozvannaya S, Li S, Olson EN. An expression screen reveals modulators of class II histone deacetylase phosphorylation. Proc Natl Acad Sci USA. 2005;102:8120–25.
Google Scholar
Harrison BC, Kim M, van-Rooij E, Plato CF, Papst PJ, McKinsey TA, et al. Regulation of cardiac stress signaling by protein kinase D1. Mol Cell Biol. 2006;26:3875–88.
Google Scholar
Li X, Song S, Liu Y, Ko SH, Kao HY. Phosphorylation of the histone deacetylase 7 modulates its stability and association with 14-3-3 proteins. J Biol Chem. 2004;279:34201–08.
Google Scholar
Lehman JJ, Kelly DP. Transcriptional activation of energy metabolic switches in the developing and hypertrophied heart. Clin Exp Pharmacol Physiol. 2002;73:667–77.
McKinsey TA, Zhang CL, Lu J, Olson EN. Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation. Nature. 2000;408:106–11.
Google Scholar
Vega RB, Harrison BC, Meadows E, Roberts CR, Papst PJ, McKinsey TA, et al. Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5. Mol Cell Biol. 2004;24:8374–85.
Google Scholar
Grozinger CM, Schreiber SL. Regulation of histone deacetylase 4 and 5 and transcriptional activity by 14-3-3-dependent cellular localization. Proc Natl Acad Sci USA. 2000;97:7835–40.
Google Scholar
McKinsey TA, Zhang CL, Olson EN. Activation of the myocyte enhancer factor-2 transcription factor by calcium/calmodulin-dependent protein kinase-stimulated binding of 14-3-3 to histone deacetylase 5. Proc Natl Acad Sci USA. 2000;97:14400–5.
Google Scholar
McKinsey TA, Zhang CL, Olson EN. Identification of a signal-responsive nuclear export sequence in class II histone deacetylases. Mol Cell Biol. 2001;21:6312–21.
Google Scholar
Backs J, Song K, Bezprozvannaya S, Chang S, Olson EN. CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. J Clin Investig. 2006;116:1853–64.
Google Scholar
Backs J, Backs T, Bezprozvannaya S, McKinsey TA, Olson EN. Histone deacetylase 5 acquires calcium/calmodulin-dependent kinase II responsiveness by oligomerization with histone deacetylase 4. Mol Cell Biol. 2008;28:3437–45.
Google Scholar
Song B, Lai B, Zheng Z, Zhang Y, Luo J, Li M, et al. Inhibitory phosphorylation of GSK-3 by CaMKII couples depolarization to neuronal survival. J Biol Chem. 2010;285:41122–34.
Google Scholar
Xu K, Dai XL, Huang HC, Jiang ZF. Targeting HDACs: a promising therapy for Alzheimer’s disease. Oxid Med Cell Longev. 2011;2011:143269. https://doi.org/10.1155/2011/143269.
Majdzadeh N, Wang L, Morrison BE, Bassel-Duby R, Olson EN, D’Mello S. HDAC4 inhibits cell-cycle progression and protects neurons from cell death. Dev Neurobiol. 2008;68:1076–92.
Google Scholar
Sando R, Gounko N, Pieraut S, Liao L, Yates J, Maximov A. HDAC4 governs a transcriptional program essential for synaptic plasticity and memory. Cell. 2012;151:821–34.
Google Scholar
Cho Y, Cavalli V. HDAC5 is a novel injury-regulated tubulin deacetylase controlling axon regeneration. EMBO J. 2012;31:3063–78.
Google Scholar
Agis-Balboa RC, Pavelka Z, Kerimoglu C, Fischer A. Loss of HDAC5 impairs memory function: Implications for Alzheimer’s disease. J Alzheimer’s Dis. 2013;33:35–44.
Google Scholar
Mazzocchi M, Wyatt SL, Mercatelli D, Morari M, Morales-Prieto N, O’Keeffe GW, et al. Gene Co-expression Analysis identifies histone deacetylase 5 and 9 expression in midbrain dopamine neurons and as regulators of neurite growth via bone morphogenetic protein signaling. Front Cell Dev Biol. 2019;7:191.
Google Scholar
Cho Y, Sloutsky R, Naegle KM, Cavalli V. Injury-Induced HDAC5 nuclear export is essential for axon regeneration. Cell. 2013;155:894.
Google Scholar
Vargas-López V, Lamprea MR, Múnera A. Histone deacetylase inhibition abolishes stress-induced spatial memory impairment. Neurobiol Learn Mem. 2016;134:328–38.
Google Scholar
Levenson JM, O’Riordan KJ, Brown KD, Trinh MA, Molfese DL, Sweatt JD. Regulation of histone acetylation during memory formation in the hippocampus. J Biol Chem. 2004;279:40545–59.
Google Scholar
Walz A, Ugolkov A, Chandra S, Kozikowski A, Carneiro BA, Mazar AP, et al. Molecular pathways: Revisiting glycogen synthase kinase-3β as a target for the treatment of cancer. Clin Cancer Res. 2017;23:1891–97.
Google Scholar
Hidaka H, Yokokura H. Molecular and cellular pharmacology of a calcium/calmodulin-dependent protein kinase II (CaM kinase II) Inhibitor, KN-62, and proposal of CaM kinase phosphorylation cascades. Adv Pharmacol. 1996;36:193–219.
Google Scholar
Tokumitsu H, Chijiwa T, Hagiwara M, Mizutani A, Terasawa M, Hidaka H. KN-62, 1-[N,O-Bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]−4-phenylpiperazine, a specific inhibitor of Ca2+/calmodulin-dependent protein kinase II. J Biol Chem.1990;265:4315–20.
Google Scholar
Fleming CL, Ashton TD, Gaur V, McGee SL, Pfeffer FM. Improved synthesis and structural reassignment of MC1568: A class IIa selective HDAC inhibitor. J Med Chem. 2014;57:1132–35.
Google Scholar
Nebbioso A, Manzo F, Miceli M, Conte M, Manente L, Altucci L, et al. Selective class II HDAC inhibitors impair myogenesis by modulating the stability and activity of HDAC-MEF2 complexes. EMBO Rep. 2009;10:776–82.
Google Scholar
Raymond E, Dalgleish A, Damber JE, Smith M, Pili R. Mechanisms of action of tasquinimod on the tumour microenvironment. Cancer Chemother Pharmacol. 2014;73:1–8.
Google Scholar
Benson RR, Gattu R, Sewick B, Kou Z, Zakaria N, Cavanaugh JM, et al. Detection of hemorrhagic and axonal pathology in mild traumatic brain injury using advanced MRI: implications for neurorehabilitation. NeuroRehabilitation. 2012;31:261–79.
Google Scholar
Beaumont A, Marmarou A, Hayasaki K, Barzo P, Fatouros P, Corwin F, et al. The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury. Acta Neurochir Suppl. 2000;76:125–9.
Google Scholar
Barzo P, Marmarou A, Fatouros P, Hayasaki K, Corwin F. Biphasic pathophysiological response of vasogenic and cellular edema in traumatic brain swelling. Acta Neurochir Suppl. 1997;70:119–22.
Google Scholar
Barzo P, Marmarou A, Fatouros P, Hayasaki K, Corwin F. Contribution of vasogenic and cellular edema to traumatic brain swelling measure by diffusion-weighted imaging. J Neurosurg. 1997;87:900–7.
Google Scholar
